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Updated: Aug 1, 2026
Aip1p Dynamics Are Altered by the R256H Mutation in Actin
Published on: July 30, 2014
A defect in a fatty acyl-CoA synthetase gene, lcf1+, results in a decrease in viability after entry into the
1Laboratory of Molecular Microbiology, School of Agriculture, Nagoya University, Chikusa-ku, 464-8601 Nagoya, Japan.
Abstract:
An intriguing mutant was isolated in Schizosaccharomyces pombe, which is defective in the maintenance of viability after entry into the stationary phase. In the logarithmic growth phase, the mutant cells grow at the same rate as the parental cells. Upon the onset of the stationary phase, however, the mutant cells lose viability very rapidly. It was found that this phenotype was due to a mutational lesion in the lcf1+ gene, which encodes a long-chain fatty acyl-CoA synthetase. The lcf1Deltamutant shows pleiotropic phenotypes, in that they are also sensitive to high temperature (37 degrees C) and to high salt concentrations (0.9 M KCl) in the medium. Based on the fact that Lcf1 is highly homologous to Faa1 and Faa4 of Saccharomyces cerevisiae, both of which have previously been suggested to play roles in the maintenance of endogenous acyl-CoA pools, the possible function of Lcf1 in S. pombe is discussed.
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