Format

Send to

Choose Destination
See comment in PubMed Commons below
Mol Plant Pathol. 2012 Sep;13(7):677-89. doi: 10.1111/j.1364-3703.2011.00779.x. Epub 2012 Feb 9.

MoSwi6, an APSES family transcription factor, interacts with MoMps1 and is required for hyphal and conidial morphogenesis, appressorial function and pathogenicity of Magnaporthe oryzae.

Author information

1
Department of Plant Pathology, College of Plant Protection, Nanjing Agricultural University, and Key Laboratory of Integrated Management of Crop Diseases and Pests, Ministry of Education, Nanjing 210095, China.

Abstract

The Magnaporthe oryzae mitogen-activated protein kinase (MAPK) MoMps1 plays a critical role in the regulation of various developmental processes, including cell wall integrity, stress responses and pathogenicity. To identify potential effectors of MoMps1, we characterized the function of MoSwi6, a homologue of Saccharomyces cerevisiae Swi6 downstream of MAPK Slt2 signalling. MoSwi6 interacted with MoMps1 both in vivo and in vitro, suggesting a possible functional link analogous to Swi6-Slt2 in S. cerevisiae. Targeted gene disruption of MoSWI6 resulted in multiple developmental defects, including reduced hyphal growth, abnormal formation of conidia and appressoria, and impaired appressorium function. The reduction in appressorial turgor pressure also contributed to an attenuation of pathogenicity. The ΔMoswi6 mutant also displayed a defect in cell wall integrity, was hypersensitive to oxidative stress, and showed a significant reduction in transcription and activity of extracellular enzymes, including peroxidases and laccases. Collectively, these roles are similar to those of MoMps1, confirming that MoSwi6 functions in the MoMps1 pathway to govern growth, development and full pathogenicity.

PMID:
22321443
PMCID:
PMC3355222
DOI:
10.1111/j.1364-3703.2011.00779.x
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley Icon for PubMed Central
    Loading ...
    Support Center