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BMC Res Notes. 2009 May 9;2:87. doi: 10.1186/1756-0500-2-87.

Differential gene expression signatures for cell wall integrity found in chitin synthase II (chs2Delta) and myosin II (myo1Delta) deficient cytokinesis mutants of Saccharomyces cerevisiae.

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Department of Biochemistry, School of Medicine, University of Puerto Rico, Medical Sciences Campus, San Juan, Puerto Rico.



Myosin II-dependent contraction of the cytokinetic ring and primary septum formation by chitin synthase II are interdependent processes during cytokinesis in Saccharomyces cerevisiae. Hence, null mutants of myosin II (myo1Delta) and chitin synthase II (chs2Delta) share multiple morphological and molecular phenotypes. To understand the nature of their interdependent functions, we will seek to identify genes undergoing transcriptional regulation in chs2Delta strains and to establish a transcription signature profile for comparison with myo1Delta strains.


A total of 467 genes were commonly regulated between myo1Delta and chs2Delta mutant strains (p <or= 0.01). Common regulated biological process categories identified by Gene Set Enrichment Analysis (GSEA) in both gene expression profiles were: protein biosynthesis, RNA processing, and stress response. Expression of 17/20 genes in the main transcriptional fingerprint for cell wall stress was confirmed in the chs2Delta strain versus 5/20 for the myo1Delta strain. One of these genes, SLT2/MPK1, was up-regulated in both strains and both strains accumulated the hyperphosphorylated form of Slt2p thereby confirming that the PKC1 cell wall integrity pathway (CWIP) was activated by both mutations. The SLT2/MPK1 gene, essential for myo1Delta strains, was not required in the chs2Delta strain.


Comparison of the chs2Delta and myo1Delta gene expression profiles revealed similarities in the biological process categories that respond to the chs2Delta and myo1Delta gene mutations. This supports the view that these mutations affect a common function in cytokinesis. Despite their similarities, these mutants exhibited significant differences in expression of the main transcriptional fingerprint for cell wall stress and their requirement of the CWIP for survival.

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