A role for the Swe1 checkpoint kinase during filamentous growth of Saccharomyces cerevisiae.
A role for the Swe1 checkpoint kinase during filamentous growth of Saccharomyces cerevisiae.
复制标题
Swe1 检查点激酶在酿酒酵母丝状生长过程中的作用。
DOI：
10.1093/genetics/158.2.549
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发表时间：
2001
期刊：
影响因子：
3.3
通讯作者：
Wittenberg,C
中科院分区：
文献类型：
--
作者：
LaValle,R;Wittenberg,C
在这项研究中，我们发现Hsl1或Hsl7 （Swe1激酶的负调节因子）失活可增强单倍体和二倍体细胞的侵袭行为。这两种基因的失活导致丝状生长的增强是通过Swe1蛋白激酶介导的。尽管在所有测试条件下，Swe1对单倍体侵袭性生长的有效性都有显著贡献，但它对假菌丝生长的贡献仅限于标准测试条件下的形态响应。然而，在一些非标准分析条件下，包括改变温度和增加氮，Swe1是假菌丝分化所必需的。在缺乏Tec1的情况下，假菌丝的生长和丁醇诱导成丝（一种相关现象）也需要Swe1。虽然Hsl1的失活足以抑制Tec1或Flo8失活导致的丝状生长缺陷，但在缺乏这两种因素的情况下，Hsl1的失活不足以促进丝状生长。此外，Hsl1的失活不会绕过假菌丝分化对氮饥饿或在固体培养基上生长的要求。我们得出结论，Swe1激酶在广泛的条件下调节丝状发育，其作用与Tec1和Flo8转录因子部分冗余。
In this study we show that inactivation of Hsl1 or Hsl7, negative regulators of the Swe1 kinase, enhances the invasive behavior of haploid and diploid cells. The enhancement of filamentous growth caused by inactivation of both genes is mediated via the Swe1 protein kinase. Whereas Swe1 contributes noticeably to the effectiveness of haploid invasive growth under all conditions tested, its contribution to pseudohyphal growth is limited to the morphological response under standard assay conditions. However, Swe1 is essential for pseudohyphal differentiation under a number of nonstandard assay conditions including altered temperature and increased nitrogen. Swe1 is also required for pseudohyphal growth in the absence of Tec1 and for the induction of filamentation by butanol, a related phenomenon. Although inactivation of Hsl1 is sufficient to suppress the defect in filamentous growth caused by inactivation of Tec1 or Flo8, it is insufficient to promote filamentous growth in the absence of both factors. Moreover, inactivation of Hsl1 will not bypass the requirement for nitrogen starvation or growth on solid medium for pseudohyphal differentiation. We conclude that the Swe1 kinase modulates filamentous development under a broad spectrum of conditions and that its role is partially redundant with the Tec1 and Flo8 transcription factors.