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Cercospora zeae-maydis  causes gray leaf spot of maize, which has become one of the most widespread and destructive diseases of maize in the world.  C. zeae-maydis  infects leaves through stomata, which is predicated on the ability of the pathogen to perceive stomata and reorient growth accordingly. In this study, the discovery that light was required for  C. zeae-maydis  to perceive stomata and infect leaves led to the identification of  CRP1 , a gene encoding a putative blue-light photoreceptor homologous to White Collar-1 (WC-1) of  Neurospora crassa . Disrupting  CRP1  via homologous recombination revealed roles in multiple aspects of pathogenesis, including tropism of hyphae to stomata, the formation of appressoria, conidiation, and the biosynthesis of cercosporin.  CRP1  was also required for photoreactivation after lethal doses of UV exposure. Intriguingly, putative orthologs of  CRP1  are central regulators of circadian clocks in other filamentous fungi, raising the possibility that  C. zeae-maydis  uses light as a key environmental input to coordinate pathogenesis with maize photoperiodic responses. This study identified a novel molecular mechanism underlying stomatal tropism in a foliar fungal pathogen, provides specific insight into how light regulates pathogenesis in  C. zeae-maydis , and establishes a genetic framework for the molecular dissection of infection via stomata and the integration of host and pathogen responses to photoperiod.

Regulation of Stomatal Tropism and Infection by Light in Cercospora zeae-maydis: Evidence for Coordinated Host/Pathogen Responses to Photoperiod?