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首页> 外文期刊>Molecular Microbiology >A Candida albicans cell wall-linked protein promotes invasive filamentation into semi-solid medium
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A Candida albicans cell wall-linked protein promotes invasive filamentation into semi-solid medium

机译:白色念珠菌细胞壁连接蛋白促进侵入性丝化成半固体培养基

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摘要

Growth of cells in contact with an abiotic or biological surface profoundly affects cellular physiology. In the opportunistic human pathogen, Candida alblcans, growth on a semi-solid matrix such as agar results in invasive filamentation, a process in which cells change their morphology to highly elongated filamentous hyphae that grow into the matrix. We hypothesized that a plasma membrane receptor-type protein would sense the presence of matrix and activate a signal transduction cascade, thus promoting invasive filamentation. In this communication, we demonstrate that during growth in contact with a semi-solid surface, activation of a MAP kinase, Cek1p, is promoted, in part, by a plasma membrane protein termed Dfi1p and results in invasive filamentation. A C. albi-cans mutant lacking Dfi1p showed reduced virulence in a murine model of disseminated candidiasis. Dfi1p is a relatively small, integral membrane protein that localizes to the plasma membrane. Some Dfi1p molecules become cross-linked to the carbohydrate polymers of the cell wall. Thus, Dfi1p is capable of linking the cell wall to the plasma membrane and cytoplasm.
机译:与非生物或生物表面接触的细胞生长深刻影响细胞生理。在机会性人类病原体,白色念珠菌中,在琼脂等半固体基质上生长会导致侵入性丝化,在此过程中,细胞会将其形态改变为高度伸长的丝状菌丝,然后长入基质。我们假设质膜受体型蛋白将感知基质的存在并激活信号转导级联反应,从而促进侵袭性丝化。在这种交流中,我们证明了在与半固体表面接触的生长过程中,MAP激酶Cek1p的激活部分被称为Dfi1p的质膜蛋白促进,并导致侵入性丝化。缺乏Dfi1p的C. albi-cans突变体在传播念珠菌病的鼠模型中显示出降低的毒力。 Dfi1p是定位在质膜上的相对较小的完整膜蛋白。一些Dfi1p分子与细胞壁的碳水化合物聚合物发生交联。因此,Dfi1p能够将细胞壁连接至质膜和细胞质。

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