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ARS Home » Midwest Area » West Lafayette, Indiana » Crop Production and Pest Control Research » Research » Publications at this Location » Publication #225190

Title: Regulation of pathogenesis by light in Cercospora zeae-maydis: Identification of a photoreceptor required for infection of maize

Author
item BLUHM, BURTON - UNIV. OF ARKANSAS
item Dunkle, Larry

Submitted to: Phytopathology
Publication Type: Abstract Only
Publication Acceptance Date: 3/25/2008
Publication Date: 6/1/2008
Citation: Bluhm, B.H., Dunkle, L.D. 2008. Regulation of pathogenesis by light in Cercospora zeae-maydis: Identification of a photoreceptor for infection of maize. Phytopathology. 98(6):S23.

Interpretive Summary:

Technical Abstract: Cercospora zeae-maydis causes gray leaf spot, one of the most prevalent and damaging foliar diseases of maize throughout the world. Light plays a key role in the virulence of C. zeae-maydis by inducing the biosynthesis of cercosporin, a photosensitizing, non-host-specific phytotoxin. We determined that blue light induces cercosporin biosynthesis but represses conidiation in C. zeae-maydis. To understand how light regulates pathogenesis at the molecular level, we identified and characterized two genes encoding putative blue-light receptors in the fungus: Phl1, a putative member of the cryptochrome-photolyase family of photoreceptors, and Crp1, an ortholog of White Collar-1 from Neurospora crassa. Disruption of PHL1 abolished photoreactivation, the light-induced DNA repair after exposure to lethal doses of UV light, but had no discernible effect on the ability of the fungus to infect and colonize maize leaves. Disruption of CRP1, however, nearly eliminated the ability of the fungus to form appressoria over stomata, thus rendering the mutants virtually non-pathogenic. Surprisingly, disruption of CRP1 neither abolished the production of cercosporin nor fully derepressed conidiation in blue light, suggesting the existence of a novel, undescribed fungal blue-light photoreceptor. Based on our findings, we propose a working model to explain the molecular regulation of pathogenesis in C. zeae-maydis in response to light.