Review - J-Stage

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Copyright , Japan Poultry Science Association.

http://www.jstage.jst.go.jp/browse/jpsa

doi: . /jpsa. .

Received: April , , Accepted: April ,

Correspondence: Dr. M. Tsudzuki, Graduate School of Biosphere

Science, Hiroshima University, Higashi-Hiroshima, Hiroshima

, Japan. (E-mail: [email protected])

Graduate School of Biosphere Science, Hiroshima University, Higashi-Hiroshima , Japan

Japanese quail ( ) is a valuable bird for both research and production. From a mainly biomedical

research point of view, this article describes characteristics of mutations of Japanese quail that have been found in the last

years, along with the recent ( or years) advances in molecular genetics of Japanese quail. In the years following the

first report of a mutation in Japanese quail in , approximately mutations were found, and during the subsequent

years, approximately mutations have been added to the list of mutations in Japanese quail to date. Based on advances in

molecular genetics of Japanese quail, two main genetic linkage maps have been constructed, mostly using microsatellite DNA

and amplified fragment length polymorphism (AFLP) markers, and several mutations have been solved at the molecular level

for their causative genes. It is anticipated that molecular studies will further reveal the nature of Japanese quail in the near

future and enhance its value as a laboratory research animal and agricultural (industrial) animal.

: causative gene, gene mapping, genetic linkage map, Japanese quail, mutation

other kinds of DNA markers were developed in the s,

quail is also used as an experimental animal. The first

report in which Japanese quail was genetically examined

Wild Japanese quail ( ), belonging to was published by Shimakura ( ). Shimakura ( )

the order Galliformes and the family Phasianidae, inhabits reported the first plumage color mutation in Japanese

the eastern part of the Eurasian continent, including quail, brown-splashed white, and recognized the advan-

Hainan and Taiwan, and the islands of Japan. In each of tages of using Japanese quail as a laboratory research

the continent and the islands of Japan, this species mi- animal. However, his proposal was not widely recognized

grates from the northern area to the southern area in throughout the world, probably because the paper was

winter season and from the southern area to the northern written in Japanese and submitted to a Japanese journal.

area in summer season (Yamashina, ; Taka-Tsukasa, About years later, Padgett and Ivey ( ) and Wilson

; Kawahara, ; Wakasugi, ). It is generally ( ) again proposed the advantages of Japanese

thought that Japanese quail was first domesticated in quail as a laboratory research animal. Since then, use of

Japan around the th century as a pet song bird. Al- Japanese quail has become wide spread in the biomedical

though the true origin and onset of domestication are research fields (Homma, ; Minvielle, ). The

unclear (Kawahara, ; Wakasugi, ; Crawford, merits of this bird are found in its small body size, short

), it is apparently documented that domesticated generation turnover, and high egg production.

Japanese quail were reared in Japan around the th In the genetic research fields employing Japanese quail,

century as a pet bird for song and plumage colors a number of morphological, biochemical, and other muta-

(Soseidoh-Syujin, ). Thereafter, at the beginning of tions have been discovered (Somes, ; Cheng and

the s, the improvement and use of Japanese quail for Kimura, ). The studies on biochemical ( iso-

egg production began in Japan (Oda, ; Ohmori, zymes) and immunological ( blood types) traits were

). Today, it is widely reared for egg and meat performed from the s to the s with the zenith in

production not only in Japan, but also in several countries the s. Morphological mutants were also actively

of Asia, Europe, and America (Minvielle, ). studied from the s to the s, but the number of

Besides rearing for eggs/meat production, Japanese studies on classical mutants decreased after . Instead

of these classical studies, modern molecular techniques

began to be adapted to quail genomes from the s

onwards. In chickens, a number of microsatellite and

and a comprehensive genetic linkage map was constructed

Masaoki Tsudzuki

The Journal of Poultry Science, : ,

Coturnix japonica

J. Poult. Sci., : ,

Coturnix japonica

et al.

e.g.,

e.g.,

Key words

Review

Introduction

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(Groenen ; Schmid ). On the other feathers, the whole pigmentation is diluted and the wheat-

hand, over microsatellite markers and a number of straw colored shaft streak is narrower than the wild type.

other kinds of DNA markers were also developed in Furthermore, the transversal bars in individual feathers

Japanese quail from to , and later in chickens, are completely missing. The dotted white is a bottom

genetic linkage maps based on these markers were con- recessive allele at the panda ( ) locus (Mizutani

structed (Kayang ; Sasazaki a). ; Tsudzuki ). The panda is also a mutant

Biochemical and immunological variants of Japanese that shows white plumage with dark patches on the head,

quail have been well summarized by Kimura ( ), cheek, back, wing, and tail. In contrast with the dotted

Somes ( ), and Cheng and Kimura ( ), along with white, in the panda mutant the feathers from the dark

morphological, behavioral (neurological), and other kinds patches are similar to the wild type in both color and

of mutations by Somes ( ) and Cheng and Kimura markings (Tsudzuki ).

( ). It is now years since these reviews were done. ( ) (Tsudzuki ): This is an auto-

During this years however, there are very few biochem- somal incompletely dominant mutation that occurred at

ical and immunological variants that have been newly the yellow ( ) locus (Homma ). The neonatal

discovered. Therefore in this article, the author mostly plumage of the homozygote shows a creamy yellow color

reviews morphological, behavioral (neurological), and all over the body with three dark brownish obscure stripes

other kinds of mutants that have been discovered in on the back, and no stripes on the head. However, faint

Japanese quail during the past years, along with recent dark pigmentation is observed at the tip of some head

developments in molecular genetics for Japanese quail. plumules. In the chicks heterozygous for this mutation,

the creamy color is slightly deeper than that of the homo-

zygote. The three stripes on the back are more blackish in

Table is a list of morphological, behavioral, and some color and clearer than those of the homozygote. Sex

other mutations in Japanese quail that have so far been di erences are large in adult plumage of both the homozy-

discovered. Among the loci controlling these mutations, gote and heterozygote. The homozygous male shows

some are multiple-allelic loci, which are also summarized whitish light-brown plumage with a few small black speck-

in Table . The author herein describes features of the les on the back, while the homozygous female shows more

Japanese quail mutations that were found during the last creamy plumage than the male and has a relatively large

years, with those of some older mutations. Mutations number of black speckles on the back. Irrespective of the

have been categorized as morphological, behavioral or yellow mutant, the homozygote of the fawn- mutant is

muscular, and other mutations. Morphological mutations fully viable. The face of the homozygous male is rusty

have been further classified into plumage color, plumage with the crown composed of dark and creamy feathers,

system, eggshell color, and morphogenetic mutations. while the face of the homozygous female is creamy with

Gene symbols presented here are according to those sparsely dotted black pigmentation. In the heterozygote,

described in each original report, although there is some the primary plumage pattern is basically the same as tha

confusion in nomenclature of mutant genes.

( ) (Tsudzuki ): This

autosomal recessive plumage color mutation was found in

. The neonatal mutant chick has the same striped

plumage pattern as the wild type. However, the plumage

color is slightly lighter than the wild type. The brownish

stripes of the wild type are replaced by slightly lighter

brownish or yellowish colored stripes. In the wings and

thighs of the mutant chick, blurry black markings replace

the dense black markings of the wild type. Besides the

down color abnormality, of the mutant chicks have

bent digits. All the mutant chicks die within three days of

hatching.

( ) (Tsudzuki ): This is an

autosomal recessive plumage color mutation discovered in

. The mutant chick has creamy yellow down plu-

mules with a brown spot on the head and/or back.

of the mutant chicks have no colored spot. The creamy

yellow and brown plumules of the chick replace white and

dark feathers respectively in their adulthood. In the dark

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Morphological Mutations

Fawn-

Plumage Color Mutations

Dilute down lethal

Dotted white

Mutations in Japanese Quail

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J. Poult. Sci., ( )

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of the homozygote, but the brown color is deeper in the

heterozygote than in the homozygote in each sex. The

female plumage of the heterozygote has a much larger

amount of black pigmentation than the homozygous

female, somewhat similar to the yellow mutant plumage.

The phenotype and mode of inheritance of the fawn-

mutant are similar to those of the fawn mutant (Nichols

and Cheng, ) that is an allele at the yellow locus

(Cheng and Kimura, ). Furthermore, Minvielle

( ) described that the beige mutant is also similar to

the fawn mutant both in the phenotype and mode of

inheritance. Thus, there is a possibility that these three

(fawn, fawn- , and beige) are identical mutants, or alleles

at the yellow locus.

(formerly bleu) ( formerly, )

(Minvielle , ): This is one of the dilution

mutations that was renamed by Minvielle ( ,

). The previous mutant name was bleu (Cheng and

Kimura, ). The adult mutant shows bluish gray all

over the body with the same primary plumage pattern as

the wild type. The secondary plumage pattern (the mark-

ing in individual feathers) is also the same as that of the

wild type. However, in individual contour feathers, the

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Mode ofCategory of traits Mutant names Gene symbols References

inheritance

Morphological mutations

Plumage color Beige AD Minvielle ( )

Black AD Chikamune and Kanai ( ), Somes ( )

Black at hatch AD Minezawa and Wakasugi ( )

Brown-splashed white AR Shimakura ( )

Bu AR Sittmann ( )

Cinnamon AR Fulton ( a)

Complete albino AR Homma ( )

Dilute down lethal AR Tsudzuki ( )

Dotted white AR Tsudzuki ( , )

Extended brown AD Somes ( ), Truax and Johnson ( )

Fawn AD Cheng and Kimura ( )

Fawn- AD Tsudzuki ( )

Imperfect albinism SR Lauber ( ), Homma ( )

Lavender (Bleu) AR Minvielle ( , )

Light down AD Ito and Tsudzuki ( )

Light down lethal AR Tsudzuki ( b)

Marbled plumage AR Yakovlev ( )

Orange AR Ito and Tsudzuki ( )

Panda AR Mizutani ( )

Pansy AR Tsudzuki ( )

Recessive black AR Fujiwara ( ), Hiragaki ( )

Recessive silver AR Homma ( )

Recessive white AR Roberts ( ), Somes ( )

Redhead AR Truax ( )

Roux SR Minvielle ( )

Rusty AR Minvielle ( a)

Sex-linked brown SR Wakasugi and Kondo ( )

Sex-linked cinnamon SR Wakasugi and Kondo ( )

Silver AD Homma ( )

White AD Wakasugi and Kondo ( )

White bib (white crescent) AR ( ) Roberts ( )

White breasted AR Roberts ( )

White primaries AR Somes ( )

White-feathered down AR Sittmann and Abplanalp ( )

Yellow AD Homma ( )

Plumage system Curly AR Minvielle ( a)

Defective feathers AD, AR Fulton ( )

Downless AR Savage and Collins ( a)

Fray AD, AR Tsudzuki ( c)

Partial featherlessness AD This article

Porcupine AR Fulton ( b)

Rough-textured AR Roberts and Fulton ( )

Ru e AR Somes ( )

Short barb AR Fulton ( c)

Eggshell color Celadon AR Ito ( )

Red eggshell AD Hardiman ( )

White eggshell AR Poole ( )

Tsudzuki: Mutations and Modern Genetics in Quail

brownish color area is replaced with bluish gray and the eter of the pupils is much larger than that of the heterozy-

wheat-straw color markings with a whitish appearance. gotes. Consequently, the iris area of the homozygotes

( ) (Ito and Tsudzuki, ): This plum- is extremely small. All of the homozygous chicks that

age color mutation is controlled by an incompletely dom- hatched show behavioral abnormalities with variable ex-

inant autosomal gene. The homozygotes, a third of which pressivity. Mildly a ected chicks slowly shake their heads

die before hatching, show creamy yellow down plumules. right and left, while severely a ected chicks rigidly bend

The eye of the homozygotes is not reddish, but the diam- the neck inward and subsequently, either draw backward

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Summary of mutations found in Japanese quail ( )Coturnix japonica

Light down

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Table .

Mode ofCategory of traits Mutant names Gene symbols References

inheritance

Morphogenesis Abnormal head AD Morse and Abplanalp ( ), Somes ( )

Arostroperocephaly AR Dodson and Coleman ( )

Chondrodystrophy AR Collins ( )

Chondrodystrophy- AR Hermes ( )

Crooked neck dwalf AR Sittmann and Craig ( )

Deformed beak AR Cheng and Kimura ( )

Ear tuft AR Tsudzuki and Wakasugi ( b)

Hereditary multiple malformation AR Tsudzuki ( a)

Long beak AR Cheng and Kimura ( )

Micromelia AR Hill ( )

Short beak AR Tsudzuki ( b)

Short lower beak AR Nakane and Tsudzuki ( c)

Stumpy limb AR Tsudzuki ( a)

Throat tuft AR Tsudzuki and Wakasugi ( )

Zazen AD, SR Nakane and Tsudzuki ( b)

Behavioral or Back drawer AR Tsudzuki and Wakasugi ( a)

muscular Circular AR Mizutani ( )

mutations Congenital loco AR Sittmann ( )

Crooked neck unknown Dodson and Coleman ( )

Dark feather nervous disorder AR Kawahara ( , ), Ueda ( )

Hypotrophic axonopathy AR Mizutani ( )

Muscular disorder AD Braga ( a, b)

Star gazing AR Savage and Collins ( )

Wry neck AR Savage and Collins ( b)

Other mutations Clench AR Nakane and Tsudzuki ( a)

Diabetes insipidus AR Minvielle ( a)

Glycogenosis type-II AR Nunoya ( )

Twinning AD Sittmann ( )

Biochemical and immunological variants are not included.

AD autosomal dominant over the wild-type allele, AR autosomal recessive to the wild-type allele, SR sex-linked recessive to the

wild-type allele. Almost all AD essentially are incompletely dominant.

Including some symbols that were not proposed in each original paper but thereafter proposed by Cheng and Kimura ( ) and this

article.

There is a possibility that the three mutations are identical or alleles at the same locus.

It is very likely that the two mutations are identical.

There is a possibility that the three mutations are identical or alleles at the same locus.

There is a possibility that the two mutations are identical or alleles at the same locus.

There is a possibility that the two mutations are identical or alleles at the same locus.

There are two synonyms for this mutation, such as red-eyed brown and dark-eyed dilute (Cheng and Kimura, ).

There are three synonyms for this mutation, such as dominant white, autosomal dilute, and dominant dilute (Cheng and Kimura,

).

J. Poult. Sci., ( )

or roll forward. Some severely a ected chicks draw the feathers, this mutant has four pairs of transversal bars,

head backward with the beak pointing upward. All homo- while the wild type has three pairs.

zygous chicks that could hatch die within a week of ( ) (Tsudzuki, b): This plum-

hatching. The neonatal plumage of the heterozygotes is age color mutant is an autosomal recessive with nearly

similar to that of the wild type. However, the black stripes total lethality. The neonatal plumage pattern of this

on the head and back are somewhat narrower than those mutant is the same as that of the wild type. However,

of the wild type, and their color is slightly diluted. Conse- black and tan stripes of the wild type are replaced with

quently, the brownish (yellowish) stripes are broader than blurry black and dilute tan stripes, respectively. Almost

those of the wild type, and the color is also lighter. The all of these mutants that could hatch die by three weeks of

whole plumage of the adult heterozygotes is also similar to age, with the majority dying within one week. Moreover,

that of the wild type, but its color is slightly diluted all prehatch mortality is high ( ) in this mutant. Among

over the body just like in the chicks (Fig. A). In the the light down lethal chicks, only two males survived

individual feathers of the adult heterozygotes, the number to adulthood and reproduced normally. The adult mutant

of transversal bars is increased. For example, in the back phenotype is very similar to that of the wild type.

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(Continuation) Summary of mutations found in Japanese quail ( )Coturnix japonica

Light down lethal

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Table .

Loci Alleles References

Black

Extended brown

Hyomandibular furrow closure defect

Imperfect a

( ) (Ito and Tsudzuki, ): This is an auto- small number of black spots. The pansy mutant is con-

somal recessive mutation. The plumage pattern of this trolled by a bottom recessive allele ( ) at the black ( )

mutant is the same as that of the wild type, but the locus (Chikamune and Kanai, ; Somes, ). The

pigmentation is obviously lightened in both chicks and pansy plumage resembles the redhead plumage which is a

adults. The mutant chicks have chocolate brown and light bottom recessive allele ( ) at the extended brown ( )

brownish-yellow stripes on the head and back. In the locus (Somes, ; Truax ). As described in

adult orange males, light reddish-brown is predominant on a later section, the black mutant will be identical to the

the whole body (Fig. B). The color is especially conspic- extended brown mutant. Thus, there is a possibility that

uous on the face and breast. In contrast, in the adult the pansy and redhead mutants are identical mutants, and

orange females, the light reddish-brown color is less that at least these two are alleles.

marked. The eye of the orange mutant is reddish when ( ) (Fujiwara ): This

held to the light. Hatchability of the orange mutant is mutant was first reported by Fujiwara ( ), and

significantly lower than that of the wild type because of the gene symbol was assigned. Later, Hiragaki

the increased prehatching mortality, but fertility in this ( ) found the allelism of this mutation at the yellow

mutant is normal. Furthermore, posthatch mortality ( ) locus (Homma ). This is a bottom reces-

within five weeks of age is greatly increased in the orange sive allele at the yellow locus. Both sexes of this mutant

mutant over that of the wild type ( ). There is exhibit blackish (or dark brownish) plumage throughout

a possibility that the orange mutant is identical to the bu the body that is very similar to the plumage of the black

(Sittmann ) or the cinnamon mutant (Fulton (Chikamune and Kanai, ; Somes, ) or the ex-

a). Ito and Tsudzuki ( ) did not propose a tended brown mutant (Somes, ; Truax ).

gene symbol for this mutation in their report. Here, for In individual feathers on the back of this mutant, the

the sake of convenience, the author proposes the gene wheat-straw colored shaft stream seen in the wild-type

symbol because this mutation was first reported in feathers is missing, although transversal bars are present

. The symbol may be when adopting the as in the wild type. However, the width of the transversal

new nomenclature proposed by Crittenden ( ). bars becomes narrower when compared with that of the

( ) (Tsudzuki and Wakasugi, ; Tsudzuki wild type, which gives it a blackish or dark brownish

): The mutant chicks have light yellow plumules appearance in this mutant. This is the first black colored

with three black stripes on the back. The black stripes are mutation occurring at the agouti signaling protein ( )

narrower and more obscure than those of the wild type. locus in poultry (Hiragaki ), and is also de-

The head plumules are brownish when compared to the scribed in a later section.

light yellow color seen on the back. The plumage pattern ( ) (Minvielle b, ): This is a

of the adults is totally di erent from that of the wild type. sex-linked mutation that belongs to the sex-linked brown

A shaft stream and transversal bars seen in the wild-type ( or recently ) locus (Wakasugi and Kondo, ;

feathers are absent in the pansy mutant. Adult plumage Cheng and Kimura, ) with a bottom recessive e ect.

shows a mixture of rust, black, and white (Fig. C). In The brown locus is linked to the imperfect albinism locus,

the male plumage, the face, chin, and throat are brown or and the recombination rate of was first reported by

heavy rust in color. There are large variations in neonatal Wakasugi and Kondo ( ) and of by Minvielle

and adult plumage. The neonatal plumage in some chicks ( b) between the two loci. The plumage color of

is somewhat similar to that of the fawn- (Tsudzuki the roux mutant is also brownish as is the brown mutant,

), and consequently some adult males resemble homo- but is paler than that of the brown mutant. Judging from

zygous fawn- males in plumage color. Such a type of the the color photo by Minvielle ( b), the plumage

pansy male shows fawn color all over the back with a color of the roux mutant is grayish light brown, rather

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A list of multiple-allelic loci on morphological characters

Orange

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Tsudzuki ( )

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Tsudzuki and Wakasugi ( )

lbinism Wakasugi and Kondo ( ), Cheng and Kimura ( )

Panda Tsudzuki ( )

Sex-linked brown Minvielle ( b, )

Yellow Tsudzuki ( ), Hiragaki ( )

Cheng and Kimura ( )

The black locus is very likely to be identical to the extended brown locus.

Descriptions of the gene symbols are based on those that appeared in each original report.


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Fig. .

J. Poult. Sci., ( )

(A) Comparison of the wild-type (left)and light-down ( / ) mutant (right) quail. (B) A male of the orange ( / ) mutant quail. (C) A female (left)and male (right) of the pansy ( / ) mutant quail. (D) The homozygote for the white mutation ( / ). (E)The heterozygote for the white mutation ( / ). (F) Homozygous (middle) and heterozygous (left and right)chicks for the white ( ) mutation. (G) Wild-type (left) and mutant chicks (others) heterozygous for themutation. The neonatal mutant plumage is variable in color. (H) The fray mutant ( / , / ) with mildexpressivity. (I) The fray mutant with intermediate expressivity. (J) The fray mutant with severe expressivity.(K) A black-at-hatch mutant male. (L) The ventral surface of the partial featherlessness mutants. (M)Comparison of the normal (left) and stumpy-limb ( / ) mutant (right) quail. (N) The back-drawer ( /

/ ) mutant exhibiting severe abnormality. (O) The heterozygote (left) and homozygote (right) forthe silver ( ) mutation. (P) The red-eyed brown ( sex-linked cinnamon, ) mutant.

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Several morphological and behavioral mutants in Japanese quail.

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(continued)

165

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similar to that of the sex-linked cinnamon. The roux plumules or feathers and are almost totally bare. This

plumage shows significant association with lower body mutant trait is controlled by the combination of an auto-

weight and less abdominal fat pad. Egg production somal dominant mutant gene ( ) and another autosomal

ability is normal, although egg weight is lower recessive modifier gene ( ). The gene has a com-

(Minvielle ). plete lethal e ect in the homozygous condition. The re-

( ) (Minvielle a): This auto- cessive modifier ( ) is epistatic to and the homo-

somal recessive plumage color mutant shows reddish- zygous state of the modifier allows the expression of the

brown (rusty) color all over the body. The individual gene; that is, only the / / genotype exhib-

contour feathers show rusty color in the pennaceous por- its the fray mutant phenotype. Furthermore, the and

tion. However, the plumulaceous portion shows a slate are closely linked on the same chromosome

like color as in the wild type, di ering from the roux (Tsudzuki c). The fray mutant is similar to the

mutant (Minvielle b, ) in which rusty defective feathers mutant in the phenotype and mode of

color is seen all over the contour feather. The rusty color inheritance of two-locus control (Fulton ).

is heavier in the rusty mutant than in the roux mutant. However, the two loci controlling the defective feathers

Hatchability of the rusty mutant is normal. mutant trait seem to be located at di erent chromosomes

( ) (Wakasugi and Kondo, ): This is an (Fulton ). Therefore, the two mutants are

autosomal dominant plumage color mutation. The mu- di erent.

tant name is assigned to the plumage appearing in the ( ): In , the author dis-

homozygotes (Fig. D). Very few homozygotes for this covered phenotypically unusual chicks among the black-

mutation survive to adulthood and show white plumage all at-hatch ( ) mutant (Minezawa and Wakasugi, )

over the body. However, according to the observations quail (Fig. K) flock kept by the Department of Labora-

made by the author, the white is not pure white but has tory Animal Science, Faculty of Agriculture, Osaka Pre-

extremely diluted gray tinges in the outer margin of indi- fecture University. In the mutant chicks, feather buds did

vidual contour feathers. The adult plumage color of the not extend in the limited areas of the hind head, back,

heterozygotes, which is fully viable, is brownish gray with abdomen, thigh, and chin (Fig. L). Although such

the wild-type plumage pattern (Fig E). The density of chicks showed high mortality, some survived to adulthood

the color is variable from individual to individual. Some and were able to reproduce. No feathers grew in the areas

are similar to that of the wild type and cannot be distin- that were bare at the neonatal chick days. From the

guishable from the wild-type plumage. In the most gray- matings with the wild-type colored normal birds and the

ish case, the wild-type plumage pattern becomes obscure. birds that have the black-at-hatch plumage and partial

The chicks homozygous for this mutation have dusty featherlessness, wild-type colored chicks that have partial

creamy yellow plumules accompanied by dark skin and featherlessness appeared with low incidence, although par-

crooked toes (Fig. F). Almost all homozygotes die tial featherlessness was nearly always exhibited ac-

around hatching. In the heterozygous chicks, the plumage companied by black-at-hatch plumage.

pattern is the same as that of the wild type, but black and

tan stripes seen in the wild type are replaced with grayish

and dusty yellowish stripes, respectively (Fig G). Ac-

cording to Cheng and Kimura ( ), the white mutant is

homologous to the autosomal dilute mutant (Somes,

) and the dominant dilute mutant (Truax and John-

son, ).

( ) (Minvielle a): This is an

autosomal recessive mutation. The adult plumage of the

curly mutant shows a flu er appearance than the wild-

type plumage. The curly phenotype results from the con-

nected calamus of the growing wing feathers at chick

days. The expressivity of the mutant plumage is variable

and the penetrance of the mutant gene is not complete.

Postnatal survivability of this mutant is normal.

( ) (Tsudzuki c): This mutant is

characterized by curly, short, and sparse plumules in

chicks and underdevelopment of barbs and barbules in

adults. There is a large variability in the degree of severity

of the mutant phenotype (Fig. H, I, J). In the most

severe case (Fig. J), both chicks and adults have no

Fr

mod Fr

et al.,

RU*R et al., mod Fr,

Fr Fr fr mod mod

Fr

mod

et al.,

et al.,

et al.,

W et al.,

Pf

Bh

CU*C et al.,

Fr, mod et al.,

Rusty

White

Partial featherlessness

Plumage System Mutations

Curly

Fray

--

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J. Poult. Sci., ( )

This result strong-

ly suggests that the mutant locus controlling the partial

featherlessness is closely linked to the locus, and that

the gene is an autosomal dominant.

( ) (Ito ): The name was assigned

to this eggshell color mutation because of the similarity of

the eggshell color to that of the porcelain in the time of the

Sung, China. This mutation is controlled by an autosomal

recessive gene and is hypostatic to the white eggshell ( )

mutation (Poole, ). The celadon eggshell possesses

the pigments protoporphyrin and biliverdin, as does the

wild-type eggshell. However, the amount of the pro-

toporphyrin in the celadon eggshell is much smaller than

in the wild type ( . of the wild type). The biliverdin

content of the celadon eggshell is of that in the

wild-type eggshell.

( ) (Tsudzuki and Wakasugi, b): This is

a morphogenetic mutation controlled by an autosomal

recessive gene (hyomandibular furrow closure defect)

with incomplete penetrance. The is a bottom recessive

Bh

ce et al.,

we

hfd

hfd

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Eggshell Color Mutations

Celadon

Morphogenetic Mutations

Ear tuft

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allele at the locus (Tsudzuki and Wakasugi, ). This mutant is not allelic to a similar mutant, stumpy limb

This mutation is characterized by ear-opening abnormali- ( ) (Tsudzuki, a)

ty and an ear tuft, which is composed of an epidermal ( ) (Nakane and Tsudzuki,

peduncle and covering feathers, protruding within or c): This mutant was found in . This morpho-

below the abnormal ear opening. Abnormal ear openings genetic mutant dies during late embryonic stages. The

are oval-shaped and accompanied by fissures of varying mutant embryos at days of incubation are first char-

size on the ventral margin. The incidence of the ear tuft acterized by a shortened lower beak. The severity of the

and ear-opening abnormality is and respectively shortening varies largely. In the most severe case, the

in the homozygotes. These abnormalities are attrib- length of the lower beak is approximately one third of the

uted to the hyomandibular furrow closure (or visceral upper beak, and in mild cases the lower beak is slightly

arch) defect occurring at five days of incubation. The shorter than the upper beak. Almost all mutant embryos

incidence of the hyomandibular furrow closure defect is keep the mouth wide open. In the skull of the mutant

in the homozygotes. However, the defect that oc- embryos, the Meckel’s cartilage of the mandible is abnor-

curred at five days of incubation is rapidly repaired by six mally bent downward in its proximal portion, and ossifica-

days of incubation in approximately a half of the a ected tion of the mandibular bone occurs around the abnormal

embryos, which results in the low ( ) incidence of the Meckel’s cartilage, which seems to be responsible for the

ear-opening abnormality at later stages (Tsudzuki and shortened lower beak and the opened mouth. In addition

Wakasugi, d). The early embryonic abnormalities to these abnormalities, this mutant shows hypoplasia or

occurred around the visceral arch region also give rise to partial lack of the hyoid apparatus, abnormal formation

head skeletal abnormalities; that is, partial deletion or and/or fusion of the sternal ribs, and increased number of

irregularity is seen in the mandible, basiparasphenoid, cervical vertebrae. This mutant trait seems to be con-

quadratojugal, squamosal, and quadrate bones. The inci- trolled by two autosomal recessive genes that are linked on

dence of the head skeletal abnormalities is in the the same chromosome, the recombination rate of which is

homozygotes (Tsudzuki and Wakasugi, c). approximately . However, further genetic studies will

( ) (Tsudzuki be needed to confirm the mode of inheritance of this

a): This autosomal recessive mutation is the first mutation.

polydactyl mutation found in Japanese quail. No mutant ( ) (Tsudzuki ; Tsudzuki,

embryos survive beyond days of incubation, with the a): This mutation was discovered in as an embryonic

peak of death at the sixth day of incubation. Mutant completely lethal mutation. However, changing of genetic

embryos at late incubation stages ( days) show an backgrounds gave rise to viable adult mutants (Fig. M)

early embryo-like body shape, and have no plumules, al- (Tsudzuki, a). Late embryos an

though feather buds are seen in their body. In the mutant

head, the eyelid is left wide open. The upper and lower

beaks are greatly deformed and set apart. The wings and

legs are stumpy and showed syndactylous polydactyly. In

the abdomen, a part of the ventriculus, liver, and small

intestine protrudes out of the umbilicus region. The

skeleton of the mutant embryos shows underdevelopment

and/or morphogenetic abnormalities all over the body. In

the mutant skeleton, ossification is generally delayed, and

cartilage is predominant throughout the body except the

head. Delay of the ossification is most remarkable in the

fore and hind limbs.

( ) (Tsudzuki b): This mutant

was found in . The majority of the short beak mu-

tants die at the late embryonic stages and within three

days of hatching. In this mutant, the length of the beak,

shanks, and digits is shortened to approximately of

that of the wild type, although there is no significant

di erence in body weight between the mutant and wild

type. Irrespective of the shortening, the shank is

thickened to approximately of the wild type. The

shortened beak shows no parrot-like shape, contrasting

with other poultry condrodystrophic mutants (Hays,

; Collins ; Nestor, ; Hermes

; Tsudzuki ). Some of the mutants

( . ) reach sexual maturity and are able to reproduce.

hfd

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al.,

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et al., et al.,

et al., sbk

Short lower beak

Hereditary multiple malformation

Stumpy limb

Short beak

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d chicks are charac-

terized by brachycephaly, short beak, thick neck, and

short and thick extremities. At the skeleton level, the

mutant exhibits globular skull, unusual curvature of the

of the upper beak, and

shortening and thickening of the appendicular bones.

Some embryos show a bending of the humerus, femur

and/or tibiotarsus. Abnormalities are more conspicuous

in the leg bones than in the wing bones. In the UOP-WT

genetic background (Ito and Tsudzuki, ), of the

a ected embryos could hatch out of the eggshell with no

assistance, and could walk in a relatively smooth manner.

of the chicks that could hatch died at various ages

before reaching maturity with a mortality peak at three

days of age. Of these, the birds that survived for relatively

long periods started showing di culty in walking around

two weeks of age and subsequently died at various ages.

The remaining ( ) survived maturity, but the birds

that sexually matured were only of the hatched mu-

tant chicks. Although reproductive ability of these sexual-

ly matured mutant birds varied from individual to individ-

ual due to the degree of the di culty in walking, sper-

matogenesis and oogenesis seemed to progress normally

in the gonads of the sexually developed mutants.

( ) (Tsudzuki and Wakasugi, ):

This mutant shows ear-opening abnormality and a feath-

ered tuft as seen in the ear-tufted ( ) mutant (Tsudzuki

Tt

Processus palatinus maxillaris

sl

hfd

hfd

Throat tuft

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and Wakasugi, b), and is autosomally recessive to the abnormalities, some mutants show shortening of the lower

wild type and dominant over the mutation. As seen in beak with upward bending of its tip, lack of the edges

the case of the the penetrance of the allele is also around the basal part of the upper beak, and lateral

not complete. The tuft originates in the throat region and curvature of the upper beak. In the legs, all the mutant

is composed of an epidermal peduncle and covering feath- embryos have full-length fibula from the stifle articulation

ers. Some birds possessing these throat tufts exhibit to the tibiotarsal-tarsometatarsal articulation. The femur

abnormal ear-openings, in which either a wide cleft or a of the mutant embryos is articulated with the proximal

short fissure is formed at the ventral margin. The inci- end of the fibula, whereas in the normal embryos the

dence of the throat tuft and ear-opening abnormality is femur is articulated with the tibia. In the mutant head, the

and , respectively. Throat tufts are usually ac- maxillary and the palatine processes of the premaxilla are

companied by normal ear openings, contrasting with the extremely reduced in length, which seems to result in the

case of the ear-tuft mutant. Furthermore, the position lack of the basal edges of the upper beak. Almost all zazen

from which peduncles protrude in the mutant is mutants show lack of the parietal and abnormally formed

di erent from that of the mutant. There is also a dif- ribs. The joint between the sternal and vertebral ribs is

ference in abnormal morphology of the ear opening be- fused and/or ossified. The vertebral ribs gain or lose one

tween the two. The ear-tuft mutants exhibit a fissure rib in number, and the ribs themselves are abnormally

below the ear opening, whereas the throat-tuft mutants shaped and/or deformed. This mutation seems to be

express a wide cleft, much wider than the fissure of the controlled by two genes; one is an autosomal dominant

ear-tuft mutants, at the ventral margin. Throat tufts and mutant gene ( ) and the other is a sex-linked recessive

ear-opening abnormalities are also attributed to visceral modifier (epistatic) gene ( ) that allows the expression

arch defects seen in the embryos at five days of age, as in of the in the / state. However, further genetic

the case of the ear-tuft mutants. The incidence of the studies will be necessary to confirm the mode of inherit-

defects is , greatly lower than that of the ear-tuft ance of this mutation.

mutant. Incomplete closure of the hyomandibular furrow

is also repaired in some a ected embryos. However,

abnormal morphology in the visceral arch regions is dif- ( ) (Tsudzuki and Wakasugi,

ferent between the two mutants, which leads to partial de- a): The onset of the expression of the abnormal be-

letion or irregularity in the head skeleton of the throat- havior varies from hatching to eight weeks of age. All

tuft mutant with di erent severity and incidence of each individuals that exhibit the abnormality at hatching die

bone from the case of the ear-tuft mutant (Tsudzuki and within five days. Severely a ected birds crouch and draw

Wakasugi, b). Irrespective of the di erent incidence backward wi

of each bone abnormality, the whole incidence of the head

skeletal abonormality of the throat-tuft mutant is ,

similar to that ( ) of the ear-tuft mutant (Tsudzuki

and Wakasugi, a, b). Comparative studies on the

head skeletal abnormalities in the ear-tuft and throat-tuft

mutants suggested that the gene influences the dorsal

region of the visceral archs with stronger intensity than its

allele In contrast, appears to have a greater

e ect than on developmental events associated with

the third arch and the ventral or median ventral regions of

the first and second arches (Tsudzuki and Wakasugi,

b). Interestingly, the incidence of the head skeletal ab-

normality is significantly lower in the / heterozy-

gotes than in the / and / homozygotes

(Tsudzuki and Wakasugi, ).

( ) (Nakane and Tsudzuki, b): This

mutation was found in . The mutant name is based

on the leg condition that is similar to the figure of religious

meditation ( zazen) in the Zen sect of Buddhism. This

mutant shows complete lethality at the late embryonic

stages. The -day mutant embryos cross their legs in the

front of the abdomen around the yolk sack. In about half

the mutant embryos, the crus is joined to the shank at an

abnormal angle, which results in the shank turning toward

the backside. In almost all ( ) of the mutant embryos,

the eyelid is left wide open. In addition to the leg and eye

Tt

Tt

Tt Tt

Tt

Tt Tt

hfd

hfd, hfd

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Zn

moz

Zn moz moz

bkd- , bkd-

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hfd

hfd hfd

hfd hfd hfd hfd

Zn, moz

Behavioral or Muscular Mutations

Back drawer

Zazen

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J. Poult. Sci., ( )

th the head pressing on the floor and the beak

pointing toward the abdomen (Fig. N). Such birds

occasionally roll forward. Intermediately a ected birds

usually walk forward with neck bending downward and

occasionally draw backward or roll forward. Mildly af-

fected birds direct their heads downward slightly and

neither draw backward nor roll forward. The mild and

intermediate abnormalities appear before and/or after the

period of the severe abnormality. Some severely a ected

birds survive for a long period comparable to normal

birds, with gradual recovery from the abnormality. The

reproductive ability of the mutants is reduced in both

sexes, particularly the laying ability of females. Although

this mutation is controlled by two independent autosomal

recessive genes, Tsudzuki and Wakasugi ( a) did not

propose a gene symbol for this mutation. Later, Cheng

and Kimura ( ) assigned the symbols and

to the genes.

( ) (Mizutani, ): This behavioral mutant

shakes its neck and subsequently shows a turning move-

ment right or left. Although the cause of the abnormal

behavior is unknown, it has been revealed that in the

mutant brain the total amount of proteins is less than that

of the normal quail. This mutation is controlled by an

autosomal recessive gene. So far, no gene symbol has been

assigned to this mutation. Here, the author tentatively

assigns the symbol to this mutation.

bkd- bkd-

cr

cr

Circular

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have

been frequently utilized as biomedical animal models,

( ) (Mizutani ): the first nephrogenic diabetes insipidus mutation reported

This is an autosomal recessive mutation characterized by in Japanese quail. This mutation is inherited as an auto-

neurofilament deficiency. The quail that shows the neuro- somal recessive trait. Minvielle ( a) found the

filament deficiency (hypotrophic axonopathy) is usually quail showed excessive drinking and excessive urination,

known as quiver (Quv) quail (Yamasaki ; and carried out experiments on plasma levels and brain

Mizutani, ). The mutants exhibit quivering at the mRNA contents for avian Arg vasotocin. As a result,

neonatal stage. In mildly a ected birds, the quivering is they found that these were a ected little by the mutation,

observed only in the head and neck, whereas in severely however plasma avian Arg vasotocin was -fold higher

a ected birds it is manifested in the entire body. This and brain mRNA contents were significantly increased in

symptom is more marked when the a ected birds are both normal and mutant quail following a -hour water

frightened by some visual or auditory stimuli. Fertility, deprivation. The mutant quail shows similar performance

hatchability, and posthatch mortality are . , . , to the normal quail in the traits such as egg production

and . , respectively. Light microscopic morphometry and quality, feed intake, and gross carcass traits. Howev-

revealed that the mutant has significantly smaller cross- er, residual feed consumption is higher in the mutant.

sectional areas of the cervical spinal cord and the optic

and sciatic nerves. Furthermore, electron microscopic

morphometry indicated that in the cervical spinal cord, Among the Japanese quail mutants that are listed in

myelinated axons in the a ected birds are significantly Table or described in this article, black-at-hatch (Fig.

smaller in size than normal, though greater in density. K), glycogenesis type-II, hypotrophic axonopathy, imper-

Electron microscopically and immunohistochemically, fect albinism, muscular disorder, and silver (Fig. O)

neurofilaments are not detected in the axons or neuronal as

cell bodies (Yamasaki ). Later on, through reported in Ono and Wakasugi ( a, b), Kubota

electrophoresis and Western blot analysis, Yamasaki ( ), Satoh ( ), Shiojiri ( ), and

( ) revealed that low, middle, and high molecular Niwa ( ) for the black-at-hatch; Matsui

mass neurofilament subunits are markedly deficient in the ( ), Tsujino ( , ), Kikuchi ( ),

brain, cervical spinal cord, and sciatic nerves of the a ect- Yang ( ), Lin ( ), and McVie-Wylie

ed quail. Immunohistochemically, the spinal cord of the ( ) for the glycogenesis type-II; Zhao ( ,

mutant has no immunoreactive products corresponding to , ), Takahashi ( , ), Hasegawa

low molecular mass neurofilament. ( , ), Hirai ( a, b), Toyoshima

( ) (Braga a, b): The ( ) and Sheykholeslami ( ) for the hypotro-

mutant quail with this disorder is usually known as LWC phic axnopathy; Dkhissi ( , ) a

quail (Mizutani, ). This mutation is characterized by

generalized myotonia, muscle sti ness, and muscle weak-

ness, and is classifiable as a type of progressive muscular

disorder. A ected birds are externally identified by their

inability to lift their wings upward and by their inability to

stand upright when placed on their dorsum. These symp-

toms are clinically observed as early as days of age.

The mutant skeletal muscles include characteristic histo-

logical lesions found in sarcoplasmic masses, ringed fibers,

internal migration of nuclei, and fiber size variation.

These lesions appear first in the pectoral region and later

in the muscles of the thoracic and pelvic limbs. This

mutation is an autosomal dominant with homozygous

lethality, but no gene symbol has been assigned to this

mutation. Here, the author tentatively assigns the symbol

to this mutation.

( ) (Nakane and Tsudzuki, a): This muta-

tion was discovered in . The abnormality exhibited

by this mutant is limited to the toes. The mutants have

rigidly clenched toes in both legs at hatching, which gives

rise to a human fist-like appearance in the distal end of the

legs. Both chicks and adults can stand and walk. In spite

of such abnormality, this mutant can reproduce normally.

( ) (Minvielle a): This is

hax et al.,

et al.

et al.,

et al., et al.

et al. et al. et al.

et al. et al.

et al. et al.

et al. et al. et

al. et al.

et al. et

al. et al. et al.

Md et al., et al.

et al.

Md

cl

di et al.,

Practical Utilization of Quail Mutants

Other Mutations

Hypotrophic axonopathy

Muscular disorder

Clench

Diabetes insipidus

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nd Schrodl

( ) for the imperfect albinism; Braga ( a,

b) and Tanaka ( a, b) for the muscular disorder;

and Araki ( , ), Tsukamoto ( )

and Kawaguchi ( ) for the silver. Besides the

mutants mentioned above, other mutants are also poten-

tially powerful resources in biomedical fields to elucidate

the regulatory mechanisms for pigmentation, morpho-

genesis, nervous systems, and metabolism.

In addition to these biomedical uses, the growth and

productive ability have also been investigated for the re-

cessive white (Petek ), roux (Minvielle

, a), and yellow (Minvielle b) from

the view point of possible use in agricultural (industrial)

fields.

In , an integrated comprehensive linkage map was

constructed in chickens (Groenen ; Schmid

) on the basis of modern molecular techniques,

including linkage groups. This generally resulted from

the development of DNA markers, especially with the

development of a large number of microsatellite DNA

markers. Today, over microsatellite loci have been

mapped in the integrated map with chromosomes and

et

al. et al.

et al.

et al. et al.

et al.

et al., et al.,

et al.,

et al., et

al.,

Development of DNA Markers and Genetic Linkage Maps

169

Modern Advances of Molecular Genetics

for Japanese Quail

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+332 ,**, +333,**+

,**.+333 ,*** ,**1

,***,***

,***/+

3**-+

between loci of . cM. Furthermore, Kayang ( )

linkage groups (Schmid ). On the other ( ) and Sasazaki ( a) assigned some Japanese

hand, in , only linkage groups ( autosoms and Z quail AFLP linkage groups to chicken chromosomes. In

chromosome) were known in Japanese quail, with a few addition, with the same reference family used by Kikuchi

loci in each linkage group, due to the absence of DNA ( ), Mannen ( ), and Sasazaki

markers (Wakasugi and Kondo, ; Ito a, b; ( a), Sasazaki ( b) mapped the orthologous

Cheng and Kimura, ; Shibata and Abe, ). genes/ESTs of chickens on the Japanese quail genome,

To obtain microsatellite markers for Japanese quail, a and made direct comparisons between the Japanese quail

few trials were performed by adapting already developed linkage groups and chicken chromosomes. However,

chicken microsatellite markers to the genome of Japanese there are some discrepancies between the studies (Kikuchi

quail (Pang ; Inoue-Murayama ; ; Mannen ; Sasazaki a, b)

Kayang ). From these trials however, it was in assigning Japanese quail AFLP linkage groups to chick-

concluded that the chicken microsatellite marker primers en chromosomes. Apart from the correctness of the as-

for polymerase chain reaction (PCR) are not e cient in signment, the AFLP linkage map, which was first reported

amplifying Japanese quail microsatellites, therefore micro- by Kikuchi ( ), has become a map of cM in

satellite markers for Japanese quail should be generated total length, with an average marker interval of . cM, by

from Japanese quail genome itself. Kayang ( , the work of Sasazaki ( b). This map is composed

, ) developed microsatellite markers directly of markers, including AFLP markers, three

from the Japanese quail genome and constructed a first- phenotypic loci, and genes/ESTs. These are assigned

generation microsatellite linkage map that included to linkage groups including W chromosome (Sasazaki

microsatellite markers (Kayang ). The total b). As mentioned earlier, there are at present

length of the map was cM, with an average spacing of two main genetic linkage maps for Japanese quail in the

cM between loci. Besides the microsatellite linkage world. It is desired that the two maps should be integrated

map, Roussot ( ) developed a number of amin the near future.

plified fragment length polymorphism (AFLP) markers

and constructed an AFLP-based linkage map with

linkage groups ( autosomal, and Z and W chromo-

somes), in which the number of AFLP markers included, Table summarizes linkage relationships between loci

the total length of the map, and the average spacing (markers) that were revealed on the basis of modern

between markers were , cM, and . cM, respec- molecular techniques, along with classical linkage rela-

tively. Later, Kayang ( ) integrated the micro- tionships. As mentioned earlier, in there were only

satellite map of Kayang ( ) and the AFLP map three autosomal linkage groups and a Z-chromosamal

to one linkage map of . cM, with an average spacing linkage group composed of a small number of classical

mutant phenotypic loci and bi

assigned the Japanese quail chromosomes (CJA) to chick-

en chromosomes (GGA) by a comparative mapping be-

tween the two species. As a result, CJA to , , ,

, , , , and Z have been assigned to GGA to

, , , , , , , and Z, respectively.

Besides the linkage map of Kayang ( ),

Kikuchi ( ) constructed a genetic linkage map

based on a large number of AFLP markers, together with

several orthologous chicken microsatellite markers to Jap-

anese quail and two phenotipic loci, and tried some com-

parisons between the Japanese quail AFLP linkage groups

and chicken chromosomes. The total length of the AFLP

linkage map was cM with an average marker inter-

val of . cM. Subsequently, Sasazaki ( a) im-

proved the AFLP map by increasing the number of AFLP

markers. Moreover, in addition to the AFLP markers,

Sasazaki ( a) developed expressed sequence tag

(EST) markers by using chicken gene sequence informa-

tion on the web site, and located the EST markers on the

AFLP map. Mannen ( ) also developed micro-

satellite markers on the basis of the sequence of cDNA,

and mapped them on the same AFLP map. With the

mapping information of the EST markers and the micro-

satellite markers derived from cDNA, Mannen

et al.

et al., et al.

et al. et al. et al.

et al., et al.

et al., et al., et al., et al., et al.,

et al.,

et al.

et al. et al.

et al., et al.,

et al.

et al.

et al.

et al.

et al.

et al.

et al.

et al.

et al.

Linkage Groups for Phenotypic Loci, Functional Genes,

and ESTs

3 1 ,**0

,, ,**/ ,**/ ,**0,*** . -

,**/ ,**/+31- +322 ,**0 ,**0

+33* +330

+333 ,**+ ,**/ ,**/ ,**0,**-

$,**/ -+33

/ *,*** ,**0

,**, ,**. +** +33/ +3--/3

1, 00,**. ,**0

/10+*

,**-

.+-3

-

,/2 +/+0 1 0,**0 ,***

,**.3*. -

*+ *1 *3 +*+- +. +2 ,* ,1 *+*1 *3 +* +- +. +2 ,* ,1

,**0,**/

,2+0/ / ,**0

,**0

,**/

J. Poult. Sci., ( )

ochemical trait loci, and the

locus order in each linkage group, and the chromosome

number, were unclear. The linkage relationships that had

been known in are: extended brown ( ) and phos-

phoglucose isomerase ( ) (Ito a); panda ( ),

serum albumin ( ), and vitamin D binding protein

( ) (Ito b; Shibata and Abe, ); Yellow

( ) and white breasted ( ) (Cheng and Kimura, );

and imperfect albinism ( ) and sex-linked brown ( )

(Wakasugi and Kondo, ). Today, the number of

linkage groups that include phenotypic traits, genes, and

ESTs is approximately , and the chromosome number

has already been assigned to the linkage groups in most

cases. However, it is di cult to declare the exact number

of linkage groups, because there are some discrepancies in

the assignment of linkage groups to chromosomes as

mentioned before. The classical phenotypic loci that have

been mapped with DNA markers are black-at-hatch plum-

age ( ), panda plumage ( ), yellow plumage ( ), hy-

potrophic axonopathy ( ), transferring ( ), haemo-

globin ( ), and prealbumin- ( ). They, respec-

tively, were mapped on chromosomes/linkage groups CJA

(Niwa ; Miwa ), CJA (Miwa

), CJA (Miwa ; Kayang

), JQG (Kikuchi ), CJA (Miwa

E

PGI et al., s

ALB

GC et al.,

Y wb

al br

Bh s Y

hax Tf

Hb- Pa-

et al., et al.,


et al., et al.,

170 ./ -

,***+322

+322 +330+33*

+31-

,*

$

+

*+ ,**- ,**/ *.,**0 ,* ,**/

,**0 */ ,**/ *3

+ +

��

�

�

Table .

Chromosomes/Loci/markers mapped References

linkage groups

CJA Niwa ( ), Miwa ( ),

Kayang ( ), Sasazaki ( b),

This article

CJA Shibusawa ( ), Sasazaki ( b),

Kayang ( )

CJA Sasazaki ( b)

CJA Ito ( b), Shibata and Abe ( )

Miwa ( ), Sasazaki ( b)

CJA Sasazaki ( b), Kayang ( )

CJA Sasazaki ( b)

CJA Sasazaki ( b), Kayang ( )

CJA Sasazaki ( b)

CJA Miwa ( ), Kayang ( )

CJA Miwa ( )

CJA Kayang ( )

CJA Cheng and Kimura ( ), Miwa ( )

Kayang ( )

QL Miwa ( )

JQG ( ), Mannen ( ), Sasazaki ( a)

JQG Sasazaki ( a)

JQG Sasazaki ( a)

JQG ( ) Kikuchi ( )

JQG Sasazaki ( a)

JQG Sasazaki ( a)

JQG Sasazaki ( a)

JQG Mannen ( )

JQG Sasazaki ( a)

JQG Mannen ( )

unknown Ito ( a)

Z Wakasugi and Kondo ( ),

Minvielle ( b)

There are some discrepancies between studies in assignment of linkage groups to chromosomes. JQG corresponds to CJA or .

JQG corresponds to CJA or . Similarly, JQG to CJA or ; JQG to CJA , , or ; and JQG to CJA , , or .

Including microsatellite markers derived from genes and ESTs.


; Kayang ), CJA (Miwa ), and egg production traits (Schreiweis ; Wright

and QL (Miwa ). In the future, the number ), disease resistance or immune response traits

of mutant phenotypic loci, genes, and ESTs that are (Cheng ; Heifetz ), and behavior

mapped will dramatically increase by using DNA markers traits (Buitenhuis ; Jensen ). The

and their linkage maps, along with the use of comparative author also reported chicken QTLs for shank length and

mapping methods between Japanese quail and other spe- body weight, which are related to the broiler industry

cies, especially chickens. (Tsudzuki ).

Contrastingly, in Japanese quail there are at present

only a few reports concerning QTLs, although QTL

In chickens, the first report for QTL mapping appeared mapping is possible with DNA markers in addition to the

in on the basis of microsatellite DNA markers mapping of loci for qualitative traits. Beaumont

(Vallejo ; van Kaam ). Since then, ( ) tried to identify QTLs for body weight and

about QTLs have been discovered for economic traits kinds of fearfulness-related traits with AFLP markers

of chickens (Abasht ); for example, for growth developed by Roussot ( ), and detected ex-

and carcass traits (Abasht and Lamont, ; Rao periment-wide significant QTLs for five traits; namely,

), meat quality traits (Nadaf ), egg quality body weight at weeks of age, the logarithm of tonic im-

Bh, Pf, SEMA E, IFR , HAL, FLIK, DMD, LOC , et al. et al.

ChEST p , GLUR /D, WNT , TYR et al. et al.

CVIPR, PON , ER , AHR, LOC , PRL, ChEST k , et al. et al.

IKAROS, LOC , CDH , LOC , MT -MMP, CDH , et al.

VIPR, BCL , PRKDC, ROCK , ZFP , CATA , CEBPD,

RGS , MOS, PENK, COPS , GDAP , EYA , PKIA

LOC , UGP , LOC , LOC , LOC , et al.

TLX, LOC

s, ALB, GC, BTK, LOC , PGK, IRF- , RPK- , PCM- , et al.

CEX et al. et al.

DKK , IGF , TN , IP KA, PSEN , ChEST , MJD , et al. et al.

STK , CKB

LOC , LOC , LOC , GDNFRALPHA, BEK et al.

LOC , LOC , GCG, GIRK , LOC , ABCB et al. et al.

LOC , LOC , LOC , LOC , DAB , LEPR et al.

Tf et al. et al.

Hb- et al.

FASN et al.

Y, wb et al.

et al.

Pa- et al.

JGH , JQH TNA LOC et al. et al.

LOC , CDH et al.

EST et al.

hax Quv or NEFL et al.

DKK, LOC et al.

LOC et al.

LOC et al.

JQE - et al.

EST et al.

JQE - et al.

E, PGI et al.

al, br

et al.


et al., et al.,

et al., et al.,

et al., et al.,

et al.,

et al.

et al., et al.,

et al., et al.

et al.,

et al.,

A list of linkage groups for phenotypic traits, genes, and ESTs in Japanese quail

Quantitative Trait Locus (QTL) Mapping

171

-

,+

+

,

*+ ,**- ,**/,**0 ,**0

*, ,**+ ,**0,**0

*- ,**0

*. +322 +330,**0 ,**0

*/ ,**0 ,**0

*0 ,**0*1 ,**0 ,**0*2 ,**0*3 ,**/ ,**0+. ,**/+2 ,**0,* +33* ,**/

,**0+- ,**/

*+ ,**/ ,**0*, ,**0*- ,**0*/ ,**/*0 ,**0*2 ,**0+/ ,**0+3 ,**/., ,**000 ,**/

+322+31-

,***

*+ *+ *,*, *, */ */ */ ,, *0 */ *0 *1 *2 *1 *2 +/

,**/ ,**0 +. ,**/ ,**0+- ,**/ ,**0

,**1 ,**1,**. ,**/

,**1

+332+332 +332 ,**/ ++

1**,**0 ,**-

,**1,**1 ,**1 ,

- + -3//-*2- +. . ++

, 2+ -3/-20 ,3- 2.,+*-- , .,*+33 - ,

, + +0+ 0,* / + +-30*,/ , -30,.* -3//-+ -30+3,

.,+221-30+1- , + +

,- , + - + /0-+, +,3.,-0+, -3/0*, -3/2-.-30.,* -30/.2 + -3/.** 0-3/,03 .,./-- .,./.1 -3/3.* +

+

+-3 0 .+22.-.,+*-- ,.

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� �

mobility, the number of indictions, the number of jumps, The extended brown mutant shows blackish (or dark

and dejections. Furthermore, Minvielle ( b) brownish) plumage throughout the body (Somes, ;

carried out QTL analysis using microsatellite markers Truax and Johnson, ). Nadeau ( ) se-

developed by Kayang ( ) for traits responsible quenced an bp segment of the -bp single coding

for growth, feed consumption, egg production, tonic im- exon of melanocortin receptor ( ) gene of the

mobility, and body temperature. They found experiment- extended brown from a French flock, and observed perfect

wide significant QTLs for five traits, egg clutch length, association between a non-synonymous substitution (Glu

eggshell weight, egg number, feed intake, and residual Lys) and the mutant plumage. The “black” plumage

feed intake. color mutation (Chikamune and Kanai, ; Somes,

) also exhibits similar phenotype to the extended

brown. Nadeau ( ) also sequenced extended

With the exception of two examples, the causative genes brown from a Japanese flock, and found the same

for mutant phenotypes of Japanese quail were unclear at substitution as in the case of the extended brown from a

the molecular level in the th century, although detection French flock. The “extended brown” from a Japanese

of causative genes has continually been reported on and flock examined by Nadeau ( ) is thought to be

after . The first and second Japanese quail mutations, the “black” mutant discovered in Japan. Thus, it is very

on which molecular basis of the abnormality was dis- likely that the extended brown and black are the same

covered in the last decade of the th century, are “hy- mutants.

potrophic axonopathy ( )” (Mizutani ) and Pansy ( ), which exhibits tri-colored mutant plum-

“silver ( )” (Homma ). age, is a bottom recessive allele at the black ( ) locus

The mutant quail is characterized by quivering (Tsudzuki and Wakasugi, ; Tsudzuki ).

behavior and neurofilament deficiency in the axons of Additionally, it has been revealed that the pansy has a

the cervical spinal cord and the optic and sciatic nerves mutation in the locus (Wada and Tsudzuki, un-

(Yamasaki ). Ohara ( ) found a non- published data; accession no. AB in DDBJ). The

sense mutation in the neurofilament-L (NF-L) gene of the pansy mutant has insertion of two extra nucleotides (CG)

mutant quail. A point mutation from C to T resides at codon (nt insCG), which leads to a premature stop

at the nucleotide residue , resulting in a stop codon at codon and produces truncated transcript by a shift of the

the position corresponding to amino acid residue of reading frame. The redhead mutant ( ) (Truax

the NF-L protein. The expression level of NF-L mRNA ) is similar to the pansy in the phenotype, and it is

in the brain drastically decreases to of that in phenotypically unclear whether the two are identical

the wild-type quail. mutants. It is desired to investigate mutation in

The homozygote for the silver mutation ( / ) has pure the redhead, which will precisely determine the sameness

white plumage and eye defects (Homma ). In or di erence between the two mutations.

the / eyes, transdi erentiation from the retinal pigment Panda ( ) (Mizutani ) and do

epithelium into the neural retina occurs at the central

area (Fuji and Wakasugi, ). Mochii ( )

indicated that the microphthalmia-associated transcrip-

tion factor ( ) gene mutation is responsible for the

silver mutation. They revealed that there are two kinds of

nucleotide changes leading to amino acid changes in the

gene by complete sequencing of the cDNA from the

/ retinal pigment epithelial cells. One leads to a substi-

tution from histidine to arginine in the basic region of

MITF protein, and the other is a two-base deletion result-

ing in frame shift and a premature termination of the

polypeptide in the region following the zipper region. In

spite of having such mutations, the retinal pigment epithe-

lial cells of the / embryos express normal size

mRNA, but do not express normal MITF protein, which

causes a partial loss of function of the transactivation of

the promoter of the -kDa melanosomal matrix protein

( ) gene, a kind of pigment-cell-specific genes.

Other Japanese quail mutants, for which the causative

molecular mutations were revealed in this century, are

extended brown ( ), pansy ( ), panda ( ), imperfect

albinism ( ), sex-linked cinnamon ( ), roux ( ),

yellow ( ), and recessive black ( ).

ps

rh

ps

c

et al.

et al.

et al.

MC R

i.e.

et al.

MC R

et al.

hax et al., d

B et al., D

hax et al.,

MC R

et al., et al.

hax

e et al.,

hax

MC R

B B

et al.,

B B s et al.,

et al.

Mitf

Mitf

B B

B B Mitf

mmp

E d s

al al BR*R

Y Y*RB

Causative Genes for Mutant Phenotypes

,**/ +313+313 ,**0

,**. +- 2/ 3./+

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+303+321 +33*

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,0 10-/,

++.+313

/

+303 ## +31.

+33- +332

++/

+

+

+

+

++/

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J. Poult. Sci., ( )

tted white ( )

(Tsudzuki ) mutants show white plumage all

over the body with colored spots. The panda is dominant

over the dotted white (Tsudzuki ). Based on

the mapping result of the panda ( ) locus on Japanese

quail chromosome (CJA ) and the comparative mapp-

ing between Japanese quail and chickens, Miwa

( ) first suggested the endothelin receptor B (

) gene to be a candidate gene for the locus. According

to this finding, Miwa ( ) subsequently confirmed

that the causative gene for the locus is The

panda phenotype is associated with a missense mutation at

the nucleotide position (c. G A) in the

which leads to amino acid substitution (arginine to

histidine change) at the position (p. R H). On the

other hand, no amino acid substitution was found for the

dotted white phenotype. The expression level of the

mRNA was lower and drastically lower in the

panda and dotted-white mutants respectively, than in the

wild-type quail. In spite of the depression of

mRNA expression level and the amino acid change in

EDNRB protein, no significant di erence was observed

in the number or migration pattern of neural crest cells

between the wild-type and panda quail in . -day embryos.

dws

et al.,

et al.,

s

et al.

EDNRB

s

et al.

s EDNRB .

EDNRB

,

EDNRB

EDNRB

172 ./ -

+33,

+33-

. .

,**0

,**1

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, #

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Abasht B, Dekkers JCM and Lamont SJ. Review of quantitative

trait loci identified in the chicken. Poultry Science, :

. .

Abasht B and Lamont SJ. G

molecular level. In future, more numbers of DNA markers

Imperfect albinism ( ) and sex-linked cinnamon ( ) a cysteine residue, and removed the normal stop codon.

(Fig. P) are plumage color mutations and alleles at the On the other hand, the fawn- had two synonymous single

locus on Z chromosome. The is dominant over the nucleotide polymorphisms (c. T C and c. C T),

(Cheng and Kimura, ). Gunnarsson ( ) which raised the possibility that there might be another

found that the solute carrier family , member , protein regulatory mutation in the fawn- as seen in the yellow.

( ) gene, is the causative gene for the mutations The expression level of the recessive black is sig-

at the locus. In the imperfect albinism, a transversion nificantly lower than that of the wild type, whereas that of

from G to T resides at the splice acceptor site just preced- the fawn- is drastically higher than the wild-type and

ing exon . The splice site mutation leads to an in-frame yellow quail. The wild-type and yellow quail showed a

skipping of exon of and amino acids are similar level of expression of to each other as ob-

missing in the mature protein. Gunnarson ( ) served by Nadeau ( ).

also observed an association of a transition from C to A at As mentioned earlier, genetic studies of Japanese quail

nt (Ala Asp) in exon of with the sex- accelerated at the beginning of the st century at the

linked cinnamon allele.

The roux ( ) is a recessive allele to the brown and genes both for qualitative and quantitative traits will

mutation at the brown ( ) locus on Z chromosome, and be mapped on the further integrated map, and further

exhibits slightly lighter brown color than the brown numbers of causative genes for mutant phenotypes will be

(Wakasugi and Kondo, ; Minvielle ). revealed. Such work will raise the value of Japanese quail

Nadeau ( ) revealed that the roux phenotype is to a higher level as a research model in the biomedical

expressed by the non-synonymous point mutation that fields, and as a bird of economic importance.

occurred at the nucleotide position (c. T C) of

the tyrosinase-related protein ( ) gene. The T

C results in a change of phenylalanine to serine at amino The author is deeply indebted to T. Goto, S. Onitsuka,

acid (p. Phe Ser). The expression level of and M. Yoshida for their great help in preparation of the

is the same between the dorsal skins of the wild-type and manuscript. The author is also grateful to F. Kanyinji for

roux quail, suggesting that the mutation is not due to a proof reading the manuscript. The author further wishes

regulatory mutation. to express gratitude to T. Maeda and Y. Yoshimura for

Yellow is a plumage color mutant that shows wheat- their encouragement. The author, M. Tsudzuki, was

straw color throughout the body with basically the same awarded the Scientist Prize of Japan Poultry Science

markings as the wild type (Homma, ). Nadeau Association for genetic studies on Japanese quail mutants.

( ) revealed that the yellow is a mutation of the reg-

ulatory region of agouti signaling protein ( ) gene,

and is not a mutation caused by coding sequence variation

at The yellow mutation lacks almost the entire

coding sequence of two upstream loci, hnRNP associated

with lethal yellow ( ) and eukaryotic translation

initiation factor B ( ), which results in the produc-

tion of a new transcript, because expression is con-

trolled by the promoter. These genotypic condi-

tions in the yellow mutant quail are quite similar to those

in the yellow mutant ( ) mouse (Michaud ).

Unlike the yellow mouse however, no significant di erence

was observed in the ASIP mRNA expression level in the

skins of the yellow and wild-type quail (Nadeau

).

Besides the study of Nadeau ( ) for the yellow

mutant quail, Hiragaki ( ) also investigated the

coding sequence of the gene in the yellow, fawn-

(Tsudzuki ), and recessive black (Fujiwara

) mutants and wild-type quail. The three mutants

are alleles at the locus, and the order of dominance is

fawn- yellow wild type recessive black (Tsudzuki

; Hiragaki ). The yellow mutant

showed no variation in the coding region, which is consis-

tent with the result of Nadeau ( ). The recessive

black showed -bp deletion (c. del), causing a

frame shift that changes the last six amino acids, including

c

c

y

al al

al

al al

et al.

SLC A ASIP

al

SLC A , ASIP

et al. et al.

SLC A

BR*R

br

et al.,

et al.

TYRP

TYRP

et al.

ASIP

ASIP.

RALY

EIF B

ASIP

RALY

A et al.,

et al.,

et al.

et al.

ASIP

et al., et

al.,

Y

et al., et al.,

et al.

Acknowledgments

References

2/,*13 ,*30 ,**0

+ ,-+ +**

+33* ,**1./ , ,

,.

. .1,**1 ,**2

,21 1, + ,+

+31- ,**-,**1

2./ 2./+ 2./

,2, ,2,

,**0+301

,**2

,

+33-#

,**2,**2

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+330,**/

,+330 ,**2

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./ ,

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, �

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Coturnix coturnix japonica

SLC A

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Silver

++- +-+ +.- +33/ 0+ ,-+3 ,-,+ +32,- #

1. +2. +22 +32--, -/+ -0* +33/

+* +-1 +.1 ,***-. -,/ --- ,**.

+1/ 201++1 -+- -+2 ,**1 211 ,**1

--- -0, 00 +.+ +.- +31/+33*

++1 +*/- +*// +33.

+/ ,-0 ,.+ +312

/3 ,.2 ,/* +302,2 ,,+ ,,3 +330

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