Regulation of cell wall synthesis by the clathrin light chain is essential for viability in Schizosaccharomyces pombe.

Regulation of cell wall synthesis by the clathrin light chain is essential for viability in Schizosaccharomyces pombe.
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DOI:
10.1371/journal.pone.0071510
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Valdivieso MH
Valdivieso MH
中科院分区:
综合性期刊3区
文献类型:
--
作者:
de León N;Sharifmoghadam MR;Hoya M;Curto MÁ;Doncel C;Valdivieso MH

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细胞壁合成的调控已被阐明。在渗透压不稳定的情况下,裂殖酵母CLc1Δ突变体不能存活;在添加山梨醇的培养基中生长,Δ细胞生长缓慢,形成聚集体,形态上有明显的缺陷。此外,CLc1Δ细胞的细胞壁成分也发生了变化。创造了一个允许调节Clc1p数量的突变体,以更详细地分析细胞壁合成对clathrin的依赖。减少40%的Clc1p量并不影响酸性磷酸酶的分泌和大量脂质的内化。在此条件下,β(1,3)葡聚糖合成酶活性和细胞壁合成均降低。此外,葡聚糖合成酶向细胞表面的传递和Eng1p葡聚糖酶的分泌也存在缺陷。这些结果表明,在条件突变体中观察到的细胞壁缺陷是由于参与该结构合成/重塑的酶的分泌缺陷,而不是由于它们的内吞作用。我们的结果表明,减少对一般囊泡运输影响较小的笼状蛋白对细胞壁的合成有很大的影响,这表明这是CLc1Δ细胞在没有渗透稳定的情况下致死的原因。
The regulation of cell wall synthesis by the clathrin light chain has been addressed. Schizosaccharomyces pombe clc1Δ mutant was inviable in the absence of osmotic stabilization; when grown in sorbitol-supplemented medium clc1Δ cells grew slowly, formed aggregates, and had strong defects in morphology. Additionally, clc1Δ cells exhibited an altered cell wall composition. A mutant that allowed modulating the amount of Clc1p was created to analyze in more detail the dependence of cell wall synthesis on clathrin. A 40% reduction in the amount of Clc1p did not affect acid phosphatase secretion and bulk lipid internalization. Under these conditions, β(1,3)glucan synthase activity and cell wall synthesis were reduced. Also, the delivery of glucan synthases to the cell surface, and the secretion of the Eng1p glucanase were defective. These results suggest that the defects in the cell wall observed in the conditional mutant were due to a defective secretion of enzymes involved in the synthesis/remodelling of this structure, rather than to their endocytosis. Our results show that a reduction in the amount of clathrin that has minor effects on general vesicle trafficking has a strong impact on cell wall synthesis, and suggest that this is the reason for the lethality of clc1Δ cells in the absence of osmotic stabilization.
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