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Host plant resistance of differentchickpea genotypes against Ascochytarabiei (Pass.) Lab. under tunnelconditionsM. Umar Shahbaza, M. Azhar Iqbala, Azhar Mustafab, M. Intizar ul-Hassanc & Faiz Ahmad Faiza

a Pulses Research Institute, ARRI, Faisalabad, Pakistan.b Rice Research Institute, Kala Shah Kaku, Sheikhupura, Pakistan.c Plant Pathology Section, AARI, Faisalabad, Pakistan.Published online: 11 Jul 2013.

To cite this article: M. Umar Shahbaz, M. Azhar Iqbal, Azhar Mustafa, M. Intizar ul-Hassan & FaizAhmad Faiz (2014) Host plant resistance of different chickpea genotypes against Ascochyta rabiei(Pass.) Lab. under tunnel conditions, Archives Of Phytopathology And Plant Protection, 47:5,529-536, DOI: 10.1080/03235408.2013.813146

To link to this article: http://dx.doi.org/10.1080/03235408.2013.813146

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Host plant resistance of different chickpea genotypes againstAscochyta rabiei (Pass.) Lab. under tunnel conditions

M. Umar Shahbaza*, M. Azhar Iqbala, Azhar Mustafab, M. Intizar ul-Hassanc andFaiz Ahmad Faiza

aPulses Research Institute, ARRI, Faisalabad, Pakistan; bRice Research Institute, Kala ShahKaku, Sheikhupura, Pakistan; cPlant Pathology Section, AARI, Faisalabad, Pakistan

(Received 28 May 2013; final version received 4 June 2013)

Host plant resistance is the most efficient and easy way to manage chickpea blightcaused by Ascochyta rabiei (Pass.) Lab. For this purpose, 374 chickpea lines/varietiesfrom various research organisations were evaluated in plastic tunnels. None of theline showed immune response against the blight; however, one line (K-01005) wasfound to be highly resistant. Moreover, 15 entries were resistant, 136 exhibited mod-erate resistant reaction, 150 were susceptible and 72 showed highly susceptibleresponse. The genotypes found that resistance against blight can serve as a source ofresistance for breeding programmes, and they could be released for commercialproduction directly.

Keywords: resistance; blight; chickpea; Ascochyta rabiei

Introduction

Chickpea (Cicer arietinum L.) is an important pulse crop of Pakistan mainly grown inrain-fed areas, after monsoon. It is cultivated in about 26 countries in the world. Thetotal cultivated area of chickpea in Pakistan is 1066.9 thousand hectares, and annualproduction is about 561.5 thousand tonnes. The average yield per hectare is estimatedto be around 550 kg. Punjab province contributes to the major portion of chickpea culti-vation area and production as 90.6 and 86.9%, respectively (Agriculture statistics2010). In Punjab, 80% of chickpea crop is cultivated in Thal region (Khan et al. 1991).Chickpea plays a vital role in human diet in terms of protein (Hulse 1991). It alsorestores soil fertility and health through the symbiotic fixation of atmospheric nitrogen.

Among the different diseases which limit the production of chickpea, Ascochytablight caused by A. rabiei is the most devastating seedborne disease of chickpea as wet,cool weather favours the disease development (Nene 1982). Since A. rabiei is readilyseedborne, care should be taken when chickpea seeds are sent to various locations(Kaiser 1973; Kaiser & Hannan 1988). The symptoms are circular spots on leaves andpods and as elongated lesions on petiole and stem. Seeds within the pods also developlesions and become shrivelled (Nene 1982).

The occurrence of this disease was first reported by Butler in 1911 in the NorthWestern province (now known as Khyber Pakhtunkhwa in Pakistan) of the UnitedIndia subcontinent (Butler 1918). The disease has always been considered as

*Corresponding author. Email: umar739@yahoo.com

Archives of Phytopathology and Plant Protection, 2014Vol. 47, No. 5, 529–536, http://dx.doi.org/10.1080/03235408.2013.813146

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economically important. The disease causes 50–70% crop loss (Malik et al. 1991),and under conditions conducive for the development of disease losses may run tocomplete failure of the crop (Nene 1984). Chickpea blight epidemics existed in Paki-stan with different frequencies in different years, 1928–1929, 1947–1954 and 1981–1982 (Kausar 1965; Aslam 1984) from mild to severe forms. A. rabiei has severalpathotypes and races which are highly variable in nature (Singh & Reddy 1990,1993). Exploiting genetic potential is the most effective and economical way for themanagement of disease. This research work is about the identification of resistantgenetic sources against A. rabiei.

Materials and methods

For the identification of resistant germplasm to chickpea blight, 374 chickpea accessionsobtained from different sources were evaluated during rabi season 2011–2012 tunnelsof the Pulses Research Institute (PRI), Faisalabad (Figure 1). The germplasm wasobtained from various research institutes like the Arid Zone Research Institute, Bhakkar(AZRI), the Nuclear Institute for Agriculture and Biology, Faisalabad (NIAB) and thePRI, Faisalabad. The test lines were sown in single rows of plot size of 2� 0.30m, andK-850 served as susceptible check. After every two test entries, the check line wassown. The lines were covered with plastic sheet to create humidity and sprayed with A.rabiei culture.

Inoculum was prepared from the old growing culture of A. rabiei, multiplied onsterilised/autoclaved chickpea grains and incubated at 22 °C for 10–15 days (Ilyas &Khan 1986). At the flowering and pod initiation stage, the plants were sprayed with theinoculum. The concentration of the inoculum was adjusted to 5� 105 conidia/ml byusing a haemocytometer. Tap water was continuously sprayed in evenings for providingmore than 90% relative humidity till the appearance of blight. Disease observationswere recorded following the rating scale described in Table 1 to check infection andresponse of genotypes.

Figure 1. Chickpea genotypes under tunnel.

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Results and discussion

Different genotypes of various research institutes under plastic tunnels behaved differ-ently. Nearly all the genotypes showed eye-shaped circular spots on leaves and podsand elongated lesions on petiole and stem (Figures 2–4). None of the test entry gaveimmune response against A. rabiei (Table 2, Figures 5 and 6). Only one line (K-01005)showed highly resistant reaction against the pathogen at 1.5% disease incidence. Theresistant response given by the entries were 15 (K-01001, K-01004, K-01008, K-01009,K-08023, CM739/06, K006-11, TGx219, TGx225, 09AK050, TGxK09, 11107, 11111,11112, 11207) in which disease incidence was 5.1–10%. One hundred and thirty-sixlines possessed moderate resistance and their disease incidence was 10.1–20%. Theentries that carried 20.1–50% of disease incidence were rated as susceptible. The sus-ceptible reaction was present in 150 genotypes. Seventy-two tested lines were highlysusceptible against the A. rabiei in which incidence varied by 50.1–100%.

Out of the 374 entries screened, 189 (51% of total) were of PRI genotypes, 80(21% of the total) were AZRI advance breeding material and 105 (28% of total) werefrom NIAB. Figure 6 illustrated that out of 189 genotypes of PRI, even a single entrydid not show immune reaction; one was highly resistant, seven were resistant, 79 weremoderately resistant, 69 were susceptible and 33 were highly susceptible. From the

Table 1. Disease scale for rating chickpea blight.

Ratingscale Symptoms on plants

Overalldiseaseinfection

(%)Diseaseresponse

0 No lesion and stem girdling on plants 0 Immune1 Small pinhead lesions in upto 5% of plants

without stem girdling0.1–5 Highly

resistant3 Lesions visible in more than 5% plants with stem girdling 5.1–10 Resistant5 Lesions visible in more than 5% plants and

stem girdling on 10% plants with little damage10.1–20 Moderately

resistant7 Lesions present in almost all plants, 50% plants with stem

girdling, death of 10% plants and conspicuous damage20.1–50 Susceptible

9 Lesions very common in all plants, stem girdling on morethan 50% plants and more than 50% damage

50.1–100 Highlysusceptible

Figure 2. Eye-shaped spot on pod.

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AZRI breeding lines, no line gave immune and highly resistant response; four linesshowed resistant reaction, 28 were moderately resistant, 18 were susceptible and 30were highly susceptible. Among the NIAB-sent 105 entries, no line was immune orhighly resistant; four lines were resistant, 29 were moderately resistant, 63 were suscep-tible and nine were highly susceptible. This revealed that 0.27% of advance breedingmaterial was highly resistant, 4% was resistant, 36% was moderately resistant, 40% wassusceptible and 19% was highly susceptible.

Singh et al. (1984) confirmed that A. rabiei pathotypes in Pakistan and India aremore aggressive, and the fungus is highly variable. The fungus remains alive for abouttwo years in infected tissues. The visual disease scoring method can be used for screen-

Figure 3. Elongated lesion on stem.

Figure 4. Eye-shaped spots on leaves.

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Table

2.Reactions

ofdifferentgeno

typesob

tained

from

variou

ssourcesscreened

againstA.rabiei.

Disease

incidence(%

)Disease

respon

seGenotyp

esNo.

ofgeno

types

0Im

mun

e–

–0.1–

5Highlyresistant

PRI:

K-010

051

5.1–

10Resistant

PRI:

K-010

01,K-010

04,K-010

08,K-010

09,K-080

23,CM73

9/06

,K00

6-11.

15

AZRI:

TGx2

19,TGx2

25,09

AK05

0,TGxK

09.

NIA

B:1110

7,11111,

11112,

1120

7.10

.1–20

Mod

eratelyresistant

PRI:

1000

3,10

010,

0901

8,08

018,

0802

5,08

026,

0803

0,08

041,

0805

2,07

007,

0702

0,07

041,

0704

5,07

,057

,06

002,

0600

3,Pb2

008,

Pb1

,AUG78

6,03

009,

Bittal98

,K0110

2,K0110

4,K0110

6,K0110

7,K01

002,

K01

003,

K01

006,

K01

007,

K01

010,

K01

011,

K01

013,

K01

014,

K01

015,

K01

016,

K01

017,

K01

018,

K01

020,

K09

010,

K09

011,

K09

012,

K09

013,

K09

015,

K09

023,

CM57

9/06

,CM60

1/06

,CM75

9/06

,K-080

02,CM77

0/06

,6K

CC-

122,

K-060

05,CM95

6/06

,CM10

04/06,

CM68

7/06

,CM73

1/06

,CM79

5/06

,CM84

8/06

,CM15

28-14/03

,21

24,K00

2-10

,K00

3-10

,K00

5-10

,K01

4-10

,K01

6-10

,K01

7-10

,K02

7-10

,K03

0-10

,K03

1-10

,K03

2-10

,K03

7-10

,K04

2-10

,K05

2-10

,K06

3-10

,K06

6-10

,K06

8-10

,K06

9-10

,09

AG00

2,08

AG01

5,D08

5-10

.

136

AZRI:

TGx2

20,TGx2

21,TGx2

22,TGx2

26,TG1102

,TG1105

,TG1108

,Tg110

9,TG1110

,TG1111,TG1112

,TGx2

03,TGx2

04,05

A01

5,06

A011,

93A37

5,05

A02

0,06

A01

6,09

AG01

3,09

AK05

3,09

AK05

7,09

AK06

1,TGxK

01,Noo

r200

9,TG1117

,TG1122

,TG1123

,TG1125

.NIA

B:1110

1,1110

2,1110

3,11,110

,11113,

1112

3,1112

4,1112

5,1112

6,1114

9,1115

0,1115

1,1115

2,1120

1,1120

2,1120

6,1121

6,1122

3,1122

4,1122

6,1122

7,1122

8,1122

9,11,230

,1123

1,1123

2,1123

7,1123

8,1124

7.

(Con

tinued)

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Table

2.(Con

tinued).

Disease

incidence(%

)Disease

respon

seGenotyp

esNo.

ofgeno

types

20.1–50

Susceptible

PRI:

1000

1,10

002,

1000

4,10

005,

1000

7,10

008,

10011,

1001

8,10

020,

1002

3,10

026,

0901

0,09

013,

0902

3,09

027,

0903

6,09

043,

0904

4,08

006,

0801

0,08

016,

0801

7,07

008,

0700

9,07

012,

0605

2,K0110

1,K0110

8,K0110

9,K01114,

K01115,

K01116,

K01117,

K01

012,

K01

019,

CM-200

8,K09

002,

K09

003,

K09

005,

K09

006,

K09

009,

K09

014,

K09

017,

K09

018,

CM64

/06,

K-080

20,K-080

04,K-080

03,K-080

01,K-06,00

6,CM70

9/06

,CM77

6/06

,09

AK05

5,K01

0-10

,K01

2-10

,K01

3-10

,K01

9-10

,K02

4-10

,K02

6-10

,09

AG01

9,09

AG01

5,08

AG00

4,08

AG01

6,09

AG00

6,D00

78-10,

D00

79-10,

D08

0-10

,K00

4-11,K00

5-11.

150

AZRI:

TG21

6,TG21

7,TG22

3,TG22

8,TG1101

,TG1104

,TG1113

,93

A00

2,93

A25

6,06

A00

3,06

A01

7,06

A05

5,08

AG00

7,04

A01

3,TG1120

,TG1124

,TG1128

,09

AG00

6.NIA

B:1110

6,1110

8,11114,

11115,

11116,

11117,

11118,

11119,

1112

0,1112

1,1112

2,1112

7,1112

8,1113

1,1113

2,1113

3,1113

4,1113

7,1113

8,1113

9,1114

0,1114

1,1114

2,1114

3,1114

4,1114

5,1114

6,1114

7,1114

8,1120

3,1120

5,1120

8,1120

9,1121

0,11211,

1121

2,1121

3,1121

4,1121

5,1121

7,1121

8,1121

9,1122

0,1122

1,1122

2,1122

5,1123

3,1123

4,1123

5,1123

6,1123

9,1124

0,1124

1,1124

2,1124

3,1124

4,1124

5,1124

6,1124

8,1124

9,1125

0,1125

1,1125

2.50

.1–100

Highlysusceptib

lePRI:

1000

6,10

012,

1001

6,10

030,

1003

5,10

036,

1003

9,09

015,

0902

4,09

028,

0902

9,09

042,

0904

5,AUG1129

,K0110

3,K0110

5,K01110,

K01111,

K01112,

0021

75,00

2204

,K00

4-10

,K00

8-10

,K04

9-10

,D08

1-10

,D09

1-10

,D09

4-10

,D09

6-10

,D09

7-10

,D09

9-10

,K00

1-11,K00

2-11,K00

3-11.

72

AZRI:

TGx2

15,TGx2

18,TGx2

27,TG1107

,TG20

1,TG20

2,TG20

5,TG20

6,TG20

9,TG21

2,09

AG00

3,09

AG01

5,09

AG01

8,09

AG02

1,BK20

11,08

AG01

4,08

AG01

5,09

AK05

4,09

AK05

5,09

AK05

6,09

AK05

8,TGK02

,TGK03

,TGK04

,TGK05

,TGK06

,TGK07

,TGK08

,TG1121

,TG1130

.NIA

B:1110

4,1110

5,1110

9,1112

9,1113

0,1113

5,1113

6,1120

4,K-850

.

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ing chickpea genotypes under plastic tunnels. Many other researchers also used thisscoring method to identify resistance in chickpea against A. rabiei (Ready & Singh1984; Singh et al. 1984; Haware et al. 1995; Hussain et al. 2002; Toker & Canci 2003;Iqbal & Ghafoor 2005; Bokhari et al. 2011; Kaur et al. 2011).

But, most of the cultivars in farmer fields throughout the world have lost resistancedue to the forming of new races of this fungus. So, there is a need to develop more andmore resistant cultivars for the farmers. The resistant cultivars should be suitable forlarge geographical area because climate is changing day by day. Moreover, it is alsocompulsory to screen advance breeding material year to year so that the lines showresistance for a number of years which can be used in breeding and can also bereleased directly to farmer fields for production.

Figure 5. Disease ratings of genotypes.

Figure 6. Frequency of germplasm obtained from various sources for disease ratings.

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AcknowledgementsThe authors acknowledge the support from the breeders of Pulses Research Institute, Faisalabad,Arid Zone Research Institute, Bhakkar and Nuclear Institute for Agriculture and Biology,Faisalabad, for providing advanced chickpea genotypes for screening against the blight.

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