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Over recent decades, many pathogenicity genes of Magnaporthe oryzae have been identified but only a very limited number of genes have been identified that encode components of the conidiogenesis pathway. We report here a T-DNA insertional mutant that completely lost conidiation ability. Further investigation revealed that this mutant did not develop any conidiophore, and that the T-DNA was integrated into an annotated gene designated as conidiophore stalk-less1 or COS1. Complementation experiments suggested that COS1 may be a determinant of conidiation. Sequence analysis revealed that COS1 putatively encodes a 491-amino-acid zinc-finger protein and the protein was revealed localized to nucleus. Reverse-transcriptase polymerase chain reaction (RT-PCR)-based expression analysis indicated that two homologues of conidiophore-related genes were affected by the cos1 mutation, suggesting that Cos1 may function as a transcriptional regulator controlling genes responsible for conidiation. Inoculations of rice roots and wounded leaves with mycelia suggested that COS1 is not required for pathogenicity. Moreover, mutation of COS1 may aggravate infection of wounded leaves. Interestingly, different from the wild-type strain, mycelia of the cos1 mutant successfully infected host cells and caused visible symptoms on unwounded leaf blades and sheaths, indicating that Cos1 may have a role in some unknown mechanism of mycelial infection of M. oryzae.

molecular plant-microbe interactions

<i>Conidiophore Stalk-less1</i> Encodes a Putative Zinc-Finger Protein Involved in the Early Stage of Conidiation and Mycelial Infection in <i>Magnaporthe oryzae</i>

Conidiophore Stalk-less1 Encodes a Putative Zinc-Finger Protein Involved in the Early Stage of Conidiation and Mycelial Infection in Magnaporthe oryzae