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  • 1 Biotechnology Laboratory, Sugarcane Breeding Institute, School of Agricultural Biotechnology, Seoul National University, Coimbatore-641-007, India Seoul 151-742, Korea
  • 2 Biotechnology Laboratory, Sugarcane Breeding Institute, Coimbatore-641-007, India
  • 3 School of Agricultural Biotechnology, Seoul National University, Seoul 151-742, Korea
  • 4 Fungal Plant Pathology Laboratory, School of Agricultural Biotechnology, College of Agriculture and Life Sciences, San 56-1 Sillim-dong, Gwanak-gu, Seoul, 151-742, Korea
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Colletotrichum falcatum Went, the causal agent of red rot of sugarcane produces a specialized infection structure called appressorium, for penetrating the host. Environmental cues like surface hydrophobicity and hardness tend to break the dormancy of the conidia and initiate conidial germination. Conidial attachment is generally stronger on hydrophobic surfaces, while hydrophilic surfaces do not permit conidial attachment of C. falcatum. In vitro studies on conidial germination and appressorium development were made to examine whether the Ca2+/calmodulin dependent pathways are involved in appressorium formation in C. falcatum. Effects of calcium chelator (EGTA), calcium channel blocker (methoxy verampamil), calmodulin antagonists (chloropromazine, phenoxy benzamine and W-7) and phospholipase C inhibitor (neomycin) were also examined to see whether they can impair conidial germination and appressorium development. All these chemicals were found to inhibit conidial germination and or appressorium formation in C. falcatum. Chloropromazine and W-7 specifically inhibited appressorium formation at the µM level. Exogenous addition of Ca2+ was found to restore the inhibition of conidial germination and appressorium development by EGTA. These results suggest that the Ca2+/calmodulin signal transduction pathway play an important role in the conidial morphogenesis and appressorium development in C. falcatum.

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