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Subject: Biology and Biotechnology × End date: 2009 × Start date: 2007 ×
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    ThesisItemOpen Access
    Molecular mechanism(s) associated with fungal development and pathogenicity of karnal bunt (Tilletia indica) in wheat (Triticum aestivum L.)
    (G.B. Pant University of Agriculture and Technology, Pantnagar - 263145 (Uttarakhand), 2008-04) Seneviratne, J.M.; Anil Kumar
    T. indica, the causal agent of Karnal bunt in wheat exhibits very high variation amongst its isolates as well as monosporidial cultures. This variability is reflected in all morphological, developmental, biochemical as well as in genetic forms. Microscopic examinations suggest that the variability is not an age dependent phenomenon, but predominantly originated through genetic means. Some slow growing monosporidial strains (KB9ms5) were isolated from fast growing isolates (KB9). KB3 isolates showed slow growth however, monosporidial strains (KB3msa and KB3msc) generated from this showed significantly fast growth. Different monosporidial groups show different levels of variability indicating the vast genetic diversity among them. RAPD marker system exhibited a better resolution over ISSR when excavating the genetic variability of the pathogen. Host factor(s) plays a significant role in generating this variability and the effect of host factor(s) is much pronounced in monosporidial strains with narrow genetic base. The most plausible explanation of genetic variation under natural and induced conditions are the recombinations of genetic material from two different mycelial/sporidia through sexual mating as well as through para-sexual means. The observations on onset of Fus3 gene at the early stage of mycelial growth provide the proof for induction of heterothallism which leads to subsequent mating between two different mycelia. Host factor(s) extracted from wheat spikes are partially dialyzable and heat labile, indicating the host factor(s) is comprised with multiple components which produce nutritional as well as hormonal effects on the pathogen. Host factor(s) treatment increase the pathogenic mycelination by reducing the onset of sporidia. Increase protein content in the mycelia as well as in spent media was detected with the host factor(s) treatment. Changes in antigenic properties in different monosporidial strains as well as on induced mycelia with host factors were noticed and this can be used as a very effective bio assay in grouping an unknown population of T. indica in to their pathogenic levels. MAP kinase signal transduction pathway plays an important role in development of pathogenicity in T.indica. RT PCR amplification of cDNA suggest the clear involvement of PMK gene (MAPK) which responsible for invasive filamentous growth and host colonization, Fus3 gene (MAPK) which modulate mating type switching and Mapkk-1 (MAPKK) gene important in cell wall integrity in the development of pathogenicity in T. indica. It is quite evident that host factor(s) trigger the MAP kinase machinery in order to provide signal for induced mycelination, suppression of sporidia formation and alteration of genetic and surface properties. This intern leads to alteration in fungal development and pathogenicity influenced by interaction of host molecular signal(s) derived from the host. All the findings above provide a clear clue to reconfirm that T.indica is a good model organism in-order to detect the molecular mechanism(s) of a pathogenic fungus.