Journal
FEBS JOURNAL
Volume 285, Issue 13, Pages 2405-2427Publisher
WILEY
DOI: 10.1111/febs.14509
Keywords
cell wall; complex sphingolipids; ergosterol; Saccharomyces cerevisiae; sphingolipids
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Funding
- Ministry of Education, Culture, Sports, Science, and Technology, Japan [26450127, 18H02139]
- Grants-in-Aid for Scientific Research [26450127, 18H02139] Funding Source: KAKEN
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In the yeast Saccharomyces cerevisiae, complex sphingolipids have three types of polar head group, and breakdown of their normal composition causes several cellular dysfunctions. Previously we found that loss of biosynthesis of mannosylinositol phosphorylceramide (MIPC) causes a defect in cell wall integrity (CWI). In this study, we screened for multicopy suppressor genes that rescue the defect in CWI in cells lacking MIPC synthases (Sur1 and Csh1), and found that the defect is partly suppressed by upregulation of ergosterol biosynthesis. In addition, repression of expression of ERG9, which encodes squalene synthase in the ergosterol biosynthesis pathway, in sur1 csh1 cells caused a strong growth defect and enhancement of the defect in CWI. The repression of ERG9 and/or the deletion of SUR1 and CSH1 caused an increase in the phosphorylated form of Slt2, a mitogen-activated protein kinase activated through impairment of CWI. Moreover, the deletion of SLT2 or WSC1/2, encoding a sensor protein recognizing CWI, enhanced the growth defect in the ERG9-repressed sur1 csh1 cells. On the other hand, the ERG9-repressed sur1 csh1 cells also exhibited an increase in the cell wall chitin level in a Slt2- and Wsc1/2-independent manner. These results suggested that MIPC and ergosterol are coordinately involved in maintenance of CWI, and the activation of Slt2 suppressed the CWI defect caused by these metabolic defects.
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