Fusarium wilt of chickpea: physiological specialization, genetics of resistance and resistance gene tagging

Abstract

Chickpea wilt caused by Fusarium oxysporum f. sp. ciceris is one of the major yield limiting factors in chickpea. The disease causes 10–90% yield losses annually in chickpea. Eight physiological races of the pathogen (0, 1A, 1B/C, 2, 3, 4, 5 and 6) are reported so far whereas additional races are suspected from India. The distribution pattern of these races in different parts of the world indicates regional specificity for their occurrence leading to the perception that F. oxysporum f. sp. ciceris evolved independently in different regions. Pathogen isolates also exhibit differences in disease symptoms. Races 0 and 1B/C cause yellowing syndrome whereas 1A, 2, 3, 4, 5 and 6 lead to wilting syndrome. Genetics of resistance to two races (1B/C and 6) is yet to be determined, however, for other races resistance is governed either by monogenes or oligogenes. The individual genes of oligogenic resistance mechanism delay onset of disease symptoms, a phenomenon called as late wilting. Slow wilting, i.e., slow development of disease after onset of disease symptoms also occurs in reaction to pathogen; however, its genetics are not known. Mapping of wilt resistance genes in chickpea is difficult because of minimal polymorphism; however, it has been facilitated to great extent by the development of sequence tagged microsatellite site (STMS) markers that have revealed significant interspecific and intraspecific polymorphism. Markers linked to six genes governing resistance to six races (0, 1A, 2, 3, 4 and 5) of the pathogen have been identified and their position on chickpea linkage maps elucidated. These genes lie in two separate clusters on two different chickpea linkage groups. While the gene for resistance to race 0 is situated on LG 5 of Winter et al. (Theoretical and Applied Genetics 101:1155–1163, 2000) those governing resistance to races 1A, 2, 3, 4 and 5 spanned a region of 8.2 cM on LG 2. The cluster of five resistance genes was further subdivided into two sub clusters of 2.8 cM and 2.0 cM, respectively. Map-based cloning can be used to isolate the six genes mapped so far; however, the region containing these genes needs additional markers to facilitate their isolation. Cloning of wilt resistance genes is desirable to study their evolution, mechanisms of resistance and their exploitation in wilt resistance breeding and wilt management.