Vossen J H, Müller W H, Lipke P N, Klis F M
Institute for Molecular Cell Biology, University of Amsterdam, The Netherlands.
J Bacteriol. 1997 Apr;179(7):2202-9. doi: 10.1128/jb.179.7.2202-2209.1997.
We previously reported that the defects in the Saccharomyces cerevisiae cwh6 Calcofluor white-hypersensitive cell wall mutant are caused by a mutation in SPT14/GPI3, a gene involved in glycosylphosphatidylinositol (GPI) anchor biosynthesis. Here we describe the effect of cwh6/spt14/gpi3 on the biogenesis of cell wall proteins. It was found that the release of precursors of cell wall proteins from the endoplasmic reticulum (ER) was retarded. This was accompanied by proliferation of ER structures. The majority of the cell wall protein precursors that eventually left the ER were not covalently incorporated into the cell wall but were secreted into the growth medium. Despite the inefficient incorporation of cell wall proteins, there was no net effect on the protein level in the cell wall. It is postulated that the availability of GPI-dependent cell wall proteins determines the rate of cell wall construction and limits growth rate.
我们之前报道过，酿酒酵母cwh6（对荧光增白剂超敏感的细胞壁突变体）中的缺陷是由SPT14/GPI3基因突变引起的，该基因参与糖基磷脂酰肌醇（GPI）锚的生物合成。在此我们描述了cwh6/spt14/gpi3对细胞壁蛋白生物合成的影响。结果发现，细胞壁蛋白前体从内质网（ER）的释放受到阻碍。这伴随着内质网结构的增殖。最终离开内质网的大多数细胞壁蛋白前体并未共价结合到细胞壁中，而是分泌到生长培养基中。尽管细胞壁蛋白的掺入效率低下，但对细胞壁中的蛋白质水平没有净影响。据推测，GPI依赖性细胞壁蛋白的可用性决定了细胞壁构建的速率并限制了生长速率。
