RESISTANCE TO ASCOCHYTA BLIGHT IN CHICKPEA - GENETIC-BASIS

Authors
Citation
Sk. Dey et G. Singh, RESISTANCE TO ASCOCHYTA BLIGHT IN CHICKPEA - GENETIC-BASIS, Euphytica, 68(1-2), 1993, pp. 147-153
Citations number
23
Categorie Soggetti
Plant Sciences",Agriculture
Journal title
ISSN journal
00142336
Volume
68
Issue
1-2
Year of publication
1993
Pages
147 - 153
Database
ISI
SICI code
0014-2336(1993)68:1-2<147:RTABIC>2.0.ZU;2-L
Abstract
Genetic regulation of host resistance in chickpea-Ascochyta rabiei int eraction system is governed by two dominant complementary genes each i n the genotypes GLG 84038 and GL 84099, whereas the resistance in a bl ack seeded genotype ICC 1468 was controlled by one dominant and one re cessive independent gene. In all the genotypes, resistance is operated by inter-allelic interactions. The genes conferring resistance in GLG 84038 were found to be different to those operating in GL 84099 and I CC 1468. Among the five dominant genes dispersed in 3 genotypes under study, at least one has been reported for the first time, as to date, only three dominant genes have been reported in the literature. The fo ur identified dominant genes in GLG 84038 and GL 84099 have been named as Arc1, Arc2 (in GLG 84038) and ArC3, Arc4 (in GL 84099). The undist inguished dominant gene in ICC 1468 has been named as Arc5(3,4) as it could not be equated or differentiated from Arc3 or Arc4. The recessiv e gene in ICC 1468 has been named as Arc1. Generation mean analysis of the 6 resistant x susceptible crosses involving the same genotypes, r evealed that the genes conferring resistance in any of the 3 genotypes did not follow simple Mendelian inheritance but were influenced by in ter allelic interactions. Additive gene effect along with dominance we re operative in all the 3 genotypes under study in conferring resistan ce. However, the mechanism of resistance in GLG 84038 and GL 84099 wer e primarily additive in nature while that in ICC 1468, dominance as we ll as dominance x dominance interactions were more important than addi tive gene action.