Inheritance of resistance to anthracnose at fruiting and seedling stages was studied in two F 2 populations from a cross between Capsicum annuum cv. ÔBangchangÕ and Capsicum chinense ÔPBC932Õ. The first F 2 was used to study anthracnose resistance at fruiting stage on mature green and ripe red fruit, and the second F 2 was used to study the resistance at both seedling and fruiting stages. Fruit inoculation was performed on detached fruit using a microinjector. Disease severity was assessed on a 0-9 scale at 7 days after inoculation. Seedling inoculation was performed using a drop method on detached leaves of 4-week-old seedlings. Disease severity was assessed on a 1-9 scale at 3 days after inoculation. The distribution of the disease scores of green and red fruit, and seedlings in both F 2 populations suggested a single gene model for each trait. Three different recessive genes were responsible for the three resistances from this cross. Linkage analysis suggested that the resistances at green and red fruit were linked (recombination frequency 0.25), and that the seedling resistance was not linked to the fruit resistances.
Resistance to anthracnose, caused by Colletotrichum capsici and C. acutatum, was investigated in Capsicum baccatum PBC80 and PBC1422 and C. chinense PBC932. Mature green and ripe fruit were inoculated with 13 isolates of the two Colletotrichum species PBC80 contained the broadest spectrum of resistance to both Colletotrichum species because none of the isolates were able to infect the genotype. At both fruit maturity stages, PBC1422 was infected by only Colletotrichum acutatum. PBC932 at ripe fruit stage was infected by both C. capsici and C. acutatum, except for one isolate, 158ci, that did not infect PBC932. PBC932 at the mature green fruit stage was infected by only C. acutatum. An intraspecific cross between PBC80 and PBC1422 was developed to determine inheritance of resistance to C. acutatum. Anthracnose resistance was assessed at mature green and ripe fruit stages using 0 to 9 disease severity scores. Frequency distribution of the disease scores in the F(2) and BC(1) populations suggested a single recessive gene responsible for the resistance at mature green fruit stage and a single dominant gene for the resistance at ripe fruit stage. Linkage analysis between the two genes identified in both fruit maturity stages showed the genes to be independent. Based on phenotypic data, the two newly identified genes, co4 and Co5, from PBC80 appeared to be different loci from the co1 and co2 previously identified from PBC932 and will be valuable sources of resistance to anthracnose in chili breeding programs.
Chili anthracnose, caused by Colletotrichum spp., is one of the major diseases to chili production in the tropics and subtropics worldwide. Breeding for durable anthracnose resistance requires a good understanding of the resistance mechanisms to different pathotypes and inoculation methods. This study aimed to investigate the inheritances of differential resistances as responding to two different Colletotrichum pathotypes, PCa2 and PCa3 and as by two different inoculation methods, microinjection (MI) and high pressure spray (HP). Detached ripe fruit of Capsicum baccatum ‘PBC80’ derived F2 and BC1s populations was assessed for anthracnose resistance. Two dominant genes were identified responsible for the differential resistance to anthracnose. One was responsible for the resistance to PCa2 and PCa3 by MI and the other was responsible for the resistance to PCa3 by HP. The two genes were linked with 16.7 cM distance.
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