Necrotrophic pathogens of the cool season food legumes (pea, lentil, chickpea, faba bean and lupin) cause wide spread disease and severe crop losses throughout the world. Environmental conditions play an important role in the development and spread of these diseases. Form of inoculum, inoculum concentration and physiological plant growth stage all affect the degree of infection and the amount of crop loss. Measures to control these diseases have relied on identification of resistant germplasm and development of resistant varieties through screening in the field and in controlled environments. Procedures for screening and scoring germplasm and breeding lines for resistance have lacked uniformity among the various programs worldwide. However, this review highlights the most consistent screening and scoring procedures that are simple to use and provide reliable results. Sources of resistance to the major necrotrophic fungi are summarized for each of the cool season food legumes. Marker-assisted selection is underway for Ascochyta blight of pea, lentil and chickpea, and Phomopsis blight of lupin. Other measures such as fungicidal control and cultural control are also reviewed. The emerging genomic information on the model legume, Medicago truncatula, which has various degrees of genetic synteny with the cool season food legumes, has promise for identification of closely linked markers for resistance genes and possibly for eventual map-based cloning of resistance genes. Durable resistance to the necrotrophic pathogens is a common goal of cool season food legume breeders.
Two recombinant inbred line (RIL) populations derived from intraspecific crosses with a common parental line (JG62) were employed to develop a chickpea genetic map. Molecular markers, flower colour, double podding, seed coat thickness and resistance to fusarium wilt race 0 (FOC-0) were included in the study. Joint segregation analysis involved a total of 160 markers and 159 RILs. Ten linkage groups (LGs) were obtained that included morphological markers and 134 molecular markers (3 ISSRs, 13 STMSs and 118 RAPDs). Flower colour (B/b) and seed coat thickness (Tt/tt) appeared to be linked to STMS (GAA47). The single-/double-podding locus was located on LG9 jointly with two RAPD markers and STMS TA80. LG3 included a gene for resistance to FOC-0 (Foc0(1)/foc0(1)) flanked by RAPD marker OPJ20(600) and STMS marker TR59. The association of this LG with FOC-0 resistance was confirmed by QTL analysis in the CA2139 x JG62 RIL population where two genes were involved in the resistance reaction. The STMS markers enabled comparison of LGs with preceding maps.
The inheritance of resistance to fusarium wilt race 0 of chickpea and linked random amplified polymorphic DNA (RAPD) markers were studied in two F6:7 recombinant inbred line (RIL) populations. These RILs were developed from the crosses CA2156 × JG62 (susceptible × resistant) and CA2139 × JG62 (resistant × resistant), and were sown in a field infected with fusarium wilt race 0 in Beja (Tunisia) over 2 years. A1:1 resistant to susceptible ratio was found in the RIL population from the CA2156 × JG62 cross, indicating that a single gene with two alleles controlled resistance. In the second RIL population (CA2139 × JG62) a 3:1 resistant to susceptible ratio indicated that two genes were present and that either gene was sufficient to confer resistance. Linkage analysis showed a RAPD marker, OPJ20600, linked to resistance in both RIL populations, which is present in the resistant parent JG62.
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