Eukaryotic Cell IAI Online 2003
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
EC.00310-07v1
7/2/302    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Wang, C.
Right arrow Articles by St. Leger, R. J.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wang, C.
Right arrow Articles by St. Leger, R. J.
Eukaryotic Cell, February 2008, p. 302-309, Vol. 7, No. 2
1535-9778/08/$08.00+0     doi:10.1128/EC.00310-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

MOS1 Osmosensor of Metarhizium anisopliae Is Required for Adaptation to Insect Host Hemolymph{triangledown}

Chengshu Wang,1* Zhibing Duan,1 and Raymond J. St. Leger2*

Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200032, China,1 Department of Entomology, University of Maryland, College Park, Maryland 207422

Received 23 August 2007/ Accepted 19 November 2007

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 Src homology 3 domain similar to those of yeast osmotic adaptor proteins, and homologs of MOS1 are widely distributed in the fungal kingdom. Reverse transcription-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 that 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 show that M. anisopliae MOS1 mediates cellular responses to high osmotic pressure and subsequent adaptations to colonize host hemolymph.

* Corresponding author. Mailing address for Chengshu Wang: Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 300 Fenglin Road, Shanghai 200032, China. Phone: 86-21-54924157. Fax: 86-54924015. E-mail: cswang{at}sibs.ac.cn. Mailing address for Raymond J. St. Leger: Department of Entomology, University of Maryland, 4112 Plant Sciences Building, College Park, MD 20742. Phone: (301) 405-5402. Fax: (301) 314-9290. E-mail: stleger{at}umd.edu

{triangledown} Published ahead of print on 30 November 2007.

Eukaryotic Cell, February 2008, p. 302-309, Vol. 7, No. 2
1535-9778/08/$08.00+0     doi:10.1128/EC.00310-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Appl. Environ. Microbiol. Infect. Immun. J. Bacteriol.
Mol. Cell Biol. Microbiol. Mol. Biol. Rev. ALL ASM JOURNALS
Copyright © 2008 by the American Society for Microbiology.