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Eukaryotic Cell doi:10.1128/EC.00310-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The MOS1 osmosensor of Metarhizium anisopliae is required for adaptation to insect host hemolymph

Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200032, China, and Department of Entomology, University of Maryland, College Park, Maryland, 20742

^* To whom correspondence should be addressed. Email: cswang{at}sibs.ac.cn. stleger{at}umd.edu.

	Abstract

Entomopathogenic fungi such as Metarhizium anisopliae infect insects by direct penetration of the cuticle, after which the fungus adapts to the high osmotic pressure of the hemolymph and multiplies. Here we characterize the M. anisopliae Mos1 gene, and demonstrate that it encodes the osmosensor required for this process. MOS1 contains transmembrane regions and a C-terminal SH3 domain similar to those of yeast osmotic adaptor proteins and homologs of MOS1 are widely distributed in the fungal kingdom. RT-PCR demonstrated that Mos1 is up-regulated in insect hemolymph as well as artificial media with high osmotic pressure. Transformants containing an antisense vector directed to the Mos1 mRNA depleted transcript levels by 80 %. This produced selective alterations in regulation of genes involved in hyphal body formation, cell membrane stiffness and generation of intracellular turgor pressure, suggesting these processes are mediated by MOS1. Consistent with a role in stress responses, transcript depletion of Mos1 increased sensitivity to osmotic and oxidative stresses and to compounds that interfere with cell wall biosynthesis. It also disrupted developmental processes including formation of appressoria and hyphal bodies. Insect bioassays confirmed that Mos1 knockdown significantly reduces virulence. Overall, our data shows that M. anisopliae MOS1 mediates cellular responses to high osmotic pressure and subsequent adaptations to colonize host hemolymph.