NDLI: A Saccharomyces cerevisiae mutant defective in the kinesin-like protein Kar3 is sensitive to NaCl-stress

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A Saccharomyces cerevisiae mutant defective in the kinesin-like protein Kar3 is sensitive to NaCl-stress

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Current Genetics : Volume 32, Issue 4, October 1997

Current Genetics : Volume 32, Issue 3, September 1997

Current Genetics : Volume 32, Issue 2, September 1997

Current Genetics : Volume 32, Issue 1, August 1997

Current Genetics : Volume 31

A Saccharomyces cerevisiae mutant defective in the kinesin-like protein Kar3 is sensitive to NaCl-stress

Content Provider	Springer Nature Link
Author	Schoch, Conrad L. Brüning, Adrian R. N. E. Entian, Karl Dieter Pretorius, Gert H. J. Prior, B. A.
Copyright Year	1997
Abstract	Several mutants of Saccharomyces cerevisiae showing poor growth in the presence of elevated concentrations of NaCl were isolated to identify genes involved in the osmo-stress response. One of these mutants (WAY.5-4A-11; osr11) which showed a clear 2:2 segregation of the salt-stress phenotype upon tetrad analysis when crossed to a wild-type strain has been characterised. The mutation responsible for poor growth under salt-stress was recessive. The corresponding gene was cloned by complementation of the mutant phenotype and a 3.5-kb fragment was isolated. The sequence of this fragment matched that of KAR3, a gene previously identified to be involved in karyogamy and mitosis. Allelism of OSR11 to KAR3 was confirmed by tetrad analysis, and disruption mutants showed the same NaCl-phenotype as the original osr11 mutation. The disruption mutant was more sensitive to high sucrose concentrations than the original mutant was to high glucose concentrations. In a different genetic background (W303-1A), the kar3 disruptants were less sensitive to osmo-stress than the WAY.5-4A strain. Heat-stress, nitrogen-starvation and cultivation on ethanol failed to affect the growth of osr11 and kar3 mutants, pointing to a possible specific involvement of KAR3 in the osmotic-stress response. Microscopic studies showed that cell division of the kar3 mutants was impaired and NaCl-stress conditions aggravated the phenotype.
Starting Page	315
Ending Page	322
Page Count	8
File Format	PDF
ISSN	01728083
Journal	Current Genetics
Volume Number	32
Issue Number	5
e-ISSN	14320983
Language	English
Publisher	Springer-Verlag
Publisher Date	1997-11-28
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Genetics Medicine

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