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Saccharomyces cerevisiae MPT5 and SSD1 function in parallel pathways to promote cell wall integrity.

机译:酿酒酵母MPT5和SSD1在平行途径中发挥作用以促进细胞壁完整性。

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摘要

Yeast MPT5 (UTH4) is a limiting component for longevity. We show here that MPT5 also functions to promote cell wall integrity. Loss of Mpt5p results in phenotypes associated with a weakened cell wall, including sorbitol-remedial temperature sensitivity and sensitivities to calcofluor white and sodium dodecyl sulfate. Additionally, we find that mutation of MPT5, in the absence of SSD1-V, is lethal in combination with loss of either Ccr4p or Swi4p. These synthetic lethal interactions are suppressed by the SSD1-V allele. Furthermore, we have provided evidence that the short life span caused by loss of Mpt5p is due to a weakened cell wall. This cell wall defect may be the result of abnormal chitin biosynthesis or accumulation. These analyses have defined three genetic pathways that function in parallel to promote cell integrity: an Mpt5p-containing pathway, an Ssd1p-containing pathway, and a Pkc1p-dependent pathway. This work also provides evidence that post-transcriptional regulation is likely to be important both for maintaining cell integrity and for promoting longevity.
机译:酵母MPT5(UTH4)是延长寿命的限制因素。我们在这里显示MPT5还可以促进细胞壁完整性。 Mpt5p的丧失会导致与细胞壁变弱相关的表型,包括山梨糖醇对温度的敏感性以及对钙氟荧光白和十二烷基硫酸钠的敏感性。此外,我们发现在缺少SSD1-V的情况下,MPT5的突变与Ccr4p或Swi4p的丧失结合在一起,具有致命性。这些合成的致命相互作用被SSD1-V等位基因抑制。此外,我们已经提供了证据,表明Mpt5p丢失导致的寿命短是由于细胞壁变弱所致。这种细胞壁缺陷可能是几丁质生物合成或积累异常的结果。这些分析已定义了三个平行发挥功能以促进细胞完整性的遗传途径:一个包含Mpt5p的途径,一个包含Ssd1p的途径和一个依赖Pkc1p的途径。这项工作还提供了证据,证明转录后调控对于维持细胞完整性和促进寿命很重要。

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