Identification of two RAPD markers genetically linked to a recessive allele of a Fusarium wilt resistance gene in pigeonpea (Cajanus cajan L. Millsp.)

Author： Kotresh H. Fakrudin B. Punnuri S. Rajkumar B. Thudi M. Paramesh H. Lohithswa H. Kuruvinashetti M.

Publisher： Springer Publishing Company

ISSN： 0014-2336

Source： Euphytica, Vol.149, Iss.1-2, 2006-05, pp. : 113-120

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Abstract

Fusarium wilt (Fusarium udum Butler) is a soil borne disease of pigeonpea which causes substantial yield losses. The disease can occur at any stage of plant development, from the young seedling to the pod filling stage. Though resistance is simply inherited, transfer to locally adapted cultivars has been difficult due to linkage drag and difficulty in accurate phenotyping, except in sick plots. An attempt was made to identify RAPD markers associated with wilt phenotype by using F2 populations derived from contrasting parents; GSl (susceptible) ‘ICPL87119 (resistant) and GS1’ ICP8863 (resistant). Parents and F₂s were grown in a national _Fusarium sick-plot at Gulbarga, India and phenotyped as resistant or susceptible during the entire crop growth period. In both the crosses, resistance to wilt segregated as a monogenic dominant character. DNA samples extracted from sick plot grown, early seedling stage plants of parents and 254 F₂ plants of GS1 × ICPL87119 were held separately for marker identification. PCR reactions using 340 random decamer primers with genomic DNA of parents resulted in detection of 45 polymorphic amplicons from 39 primers. PCR testing of bulked DNA from subsets of resistant and susceptible plants revealed the presence of two amplicons at 704 bp and 500 bp (OPM03704 and OPAC11500) with susceptibility. Analysis of individual F₂ plants showed a segregation ratio of 3: 1 for the presence: absence of the amplicon in both crosses. Considering the wilt reaction and susceptibility-linked RAPD marker, it was possible to deduce genotype of every F₂ plant and the genotypic ratio for wilt reaction was 1RR: 2Rr: 1rr, as expected.