Rumdeep K. Rangi,
Debabrata Basu, and
First, second, third, and fifth authors: Plant Molecular and Cellular Genetics, Bose Institute, Centenary Campus, P1/12 C.I.T. Scheme VII M, Kankurgachi, Kolkata-700054, India; and fourth author: Botany Department, Bose Institute, Main Campus, 93/1, A.P.C. Road, Kolkata-700009, India.
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Accepted for publication 25 April 2009.
Wilt of chickpea caused by Fusarium oxysporum f. sp. ciceris is one of the most severe diseases of chickpea throughout the world. Variability of pathotypes of F. oxysporum f. sp. ciceris and breakdown of natural resistance are the main hindrances to developing resistant plants by applying resistant breeding strategies. Additionally, lack of information of potential resistant genes limits gene-transfer technology. A thorough understanding of Fusarium spp.--chickpea interaction at a cellular and molecular level is essential for isolation of potential genes involved in counteracting disease progression. Experiments were designed to trigger the pathogen-challenged disease responses in both susceptible and resistant plants and monitor the expression of stress induced genes or gene fragments at the transcript level. cDNA amplified fragment length polymorphism followed by homology search helped in differentiating and analyzing the up- and downregulated gene fragments. Several detected DNA fragments appeared to have relevance with pathogen-mediated defense. Some of the important transcript-derived fragments were homologous to genes for sucrose synthase, isoflavonoid biosynthesis, drought stress response, serine threonine kinases, cystatins, arginase, and so on. Reverse-transcriptase polymerase chain reaction performed with samples collected at 48 and 96 h postinfection confirmed a similar type of differential expression pattern. Based on these results, interacting pathways of cellular processes were generated. This study has an implication toward functional identification of genes involved in wilt resistance.
© 2009 The American Phytopathological Society