Osmotic stress‐coupled maintenance of polar growth in Aspergillus nidulans

Summary Free‐living cells monitor extracellular ‘osmotic strength’ and respond metabolically to offset unfavourable osmotic intracellular solute concentrations. Here, we report the reconstruction of the Aspergillus nidulans salt stress‐controlling MAP kinase pathway, based on homology analysis with...

Full description

Saved in:
Bibliographic Details
Published inMolecular microbiology Vol. 43; no. 5; pp. 1065 - 1078
Main Authors Han, Kap‐Hoon, Prade, Rolf A.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Science Ltd 01.03.2002
Blackwell Publishing Ltd
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Summary Free‐living cells monitor extracellular ‘osmotic strength’ and respond metabolically to offset unfavourable osmotic intracellular solute concentrations. Here, we report the reconstruction of the Aspergillus nidulans salt stress‐controlling MAP kinase pathway, based on homology analysis with known yeast genes. In A. nidulans, salt stress HOG genes, such as pbsA, hogA, ptpA and msnA, are upregulated when exposed to high concentrations of salt and, in a hogA deletion mutant (SIK1), the accumulation of pbsA is strongly reduced, suggesting a salt‐specific feedback induction mechanism. Growth of SIK1 appears to be unchanged in unstressed cells, but hyphal extension rates are reduced by as much as 60% in the presence of salt. Microscopic observation revealed abnormal hyperbranched hyphal tips, disproportionate accumulation of nuclei and absence of septa. Thus, the inability to maintain turgor pressure depresses cell expansion and results in slower volume increases. In addition, SIK1 fails to partition the apical cell; thus, nuclei are not likely to arrest mitosis in interphase as in normal cells, but continue to divide, accumulating to high levels.
Bibliography:Present address: Department of Microbiology and Toxicology, University of Wisconsin‐Madison, Madison, WI 53706, USA.
ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Article-1
ObjectType-Feature-2
ISSN:0950-382X
1365-2958
DOI:10.1046/j.1365-2958.2002.02774.x