The defects in cell wall integrity and G2-M transition of the ∆htl1 mutant are interconnected.

The Saccharomyces cerevisiae RSC (remodel the structure of chromatin) complex is involved in functions associated with the transcriptional regulation, cell cycle progression, DNA damage repair and cell wall integrity. Here we investigate the cellular functioning of HTL1, which encodes a non-essential subunit of the RSC complex. The results show that the ∆htl1 mutant displays a characteristic defect in cell wall integrity, and the phenotype of the ∆htl1 cells, which include the cell wall defect, temperature sensitivity and ploidy increase, are rescued by the osmotic stabilizer sorbitol but not by overexpression of the signalling kinase important for the cell wall biogenesis and stress response. In addition, the expression level of Slt2p, the MAP kinase downstream of the cell wall integrity pathway, is upregulated in ∆htl1 cells. Furthermore, the mitotic arrest of the ∆htl1 mutant is moderated by 1 m sorbitol and deletion of SLT2. The present findings suggest that HTL1 may play a role that is different from other RSC components in terms of cell wall integrity and the G(2)-M transition. The results also suggest that the defects in cell wall integrity and the G(2)-M transition of the ∆htl1 mutant are interconnected.

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