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首页> 外文期刊>Molecular and Cellular Biology >Mds3 Regulates Morphogenesis in Candida albicans through the TOR Pathway
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Mds3 Regulates Morphogenesis in Candida albicans through the TOR Pathway

机译：Mds3通过TOR途径调节白色念珠菌的形态发生。

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The success of Candida albicans as a major human fungal pathogen is dependent on its ability to colonize and survive as a commensal on diverse mucosal surfaces. One trait required for survival and virulence in the host is the morphogenetic yeast-to-hypha transition. Mds3 was identified as a regulator of pH-dependent morphogenesis that functions in parallel with the classic Rim101 pH-sensing pathway. Microarray analyses revealed that mds3Δ/Δ cells had an expression profile indicative of a hyperactive TOR pathway, including the preferential expression of genes encoding ribosomal proteins and a decreased expression of genes involved in nitrogen source utilization. The transcriptional and morphological defects of the mds3Δ/Δ mutant were rescued by rapamycin, an inhibitor of TOR, and this rescue was lost in strains carrying the rapamycin-resistant TOR1-1 allele or an rbp1Δ/Δ deletion. Rapamycin also rescued the transcriptional and morphological defects associated with the loss of Sit4, a TOR pathway effector, but not the loss of Rim101 or Ras1. The sit4Δ/Δ and mds3Δ/Δ mutants had additional phenotypic similarities, suggesting that Sit4 and Mds3 function similarly in the TOR pathway. Finally, we found that Mds3 and Sit4 coimmunoprecipitate. Thus, Mds3 is a new member of the TOR pathway that contributes to morphogenesis in C. albicans as a regulator of this key morphogenetic pathway.
机译：白色念珠菌作为人类主要真菌病原体的成功取决于其在各种粘膜表面定殖和生存的能力。宿主中存活和毒力所需的一项特征是从酵母到菌丝的形态发生。 Mds3被确定为与经典Rim101 pH传感途径并行运行的pH依赖形态发生调节剂。芯片分析表明， mds3 Δ/Δ细胞的表达特征表明TOR通路活跃，包括核糖体蛋白编码基因的优先表达和氮源利用相关基因的表达减少。 mds3 Δ/Δ突变体的转录和形态缺陷被TOR抑制剂雷帕霉素挽救，这种挽救在携带雷帕霉素抗性 TOR1 -的菌株中消失了。 1 等位基因或 rbp1 Δ/Δ缺失。雷帕霉素还挽救了与TOR通路效应子Sit4缺失有关的转录和形态学缺陷，但没有挽救Rim101或Ras1的缺失。 sit4 Δ/Δ和 mds3 Δ/Δ突变体具有额外的表型相似性，表明Sit4和Mds3在TOR途径中的功能相似。最后，我们发现Mds3和Sit4共免疫沉淀。因此，Mds3是TOR途径的一个新成员，该途径有助于 C的形态发生。白色念珠菌作为该关键形态发生途径的调节剂。

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