Snf1 kinases with different β-subunit isoforms play distinct roles in regulating haploid invasive growth
Snf1 kinases with different β-subunit isoforms play distinct roles in regulating haploid invasive growth
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DOI：
10.1128/mcb.23.4.1341-1348.2003
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发表时间：
2003-02-01
影响因子：
5.3
通讯作者：
Carlson, M
中科院分区：
文献类型：
--
作者：
Vyas, VK;Kuchin, S;Carlson, M
酿酒酵母的 Snf1 蛋白激酶已被证明在响应葡萄糖消耗而调节单倍体侵入性生长中发挥作用。细胞含有三种形式的 Snf1 激酶，每种形式都有不同的 P 亚基亚型，即 Gal83、Sip1 或 Sip2。我们提供的证据表明，不同的 Snf1 激酶在侵袭性生长的两个方面发挥着不同的作用，即粘附于琼脂基质和丝状化。 Snf1-Gal83 形式的激酶是粘附所必需的，而 Snf1-Gal83 或 Snf1-Sip2 足以形成丝状。遗传证据表明 Snf1-Gal83 通过拮抗 Nrg1 和 Nrg2 介导的 FLO11 絮蛋白和粘附素基因抑制来影响粘附。相反，Snf1-Gal83 和 Snf1-Sip2 影响丝状化的机制与 FLO11 无关。因此，Snf1 激酶通过至少两种不同的机制调节侵袭性生长。
The Snf1 protein kinase of Saccharomyces cerevisiae has been shown to have a role in regulating haploid invasive growth in response to glucose depletion. Cells contain three forms of the Snf1 kinase, each with a different P-subunit isoform, either GaI83, Sip1, or Sip2. We present evidence that different Snf1 kinases play distinct roles in two aspects of invasive growth, namely, adherence to the agar substrate and filamentation. The Snf1-GaI83 form of the kinase is required for adherence, whereas either Snf1-GaI83 or Snf1-Sip2 is sufficient for filamentation. Genetic evidence indicates that Snf1-GaI83 affects adherence by antagonizing Nrg1- and Nrg2-mediated repression of the FLO11 flocculin and adhesin gene. In contrast, the mechanism(s) by which Snf1-GaI83 and Snf1-Sip2 affect filamentation is independent of FLO11. Thus, the Snf1 kinase regulates invasive growth by at least two distinct mechanisms.