Overexpression of the transcription factor Rst2 in <i>Schizosaccharomyces pombe</i> indicates growth defect, mitotic defects, and microtubule disorder

In Schizosaccharomyces pombe, the transcription factor Rst2 regulates ste11 in meiosis and fbp1 in glucogenesis downstream of the cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA) pathway. Here, we demonstrate that Rst2 regulates additional cellular events. Overexpressed Rst2 elevated the frequency of oval, bent, branched, septated, and multi-septated cells. Cells showed normal nuclear divisions but exhibited abnormal nuclear organization at low frequency. In oval cells, microtubules were curved but they were rescued by the deletion of mal3. Since growth defect was not rescued by mal3 deletion, we argue that it is regulated independently. Loss of functional Pka1 exaggerated growth defect upon Rst2 overexpression because its downregulation by Pka1 was lost. Overexpression of Rst2 also caused sensitivity to KCl and CaCl2. These findings suggest that, in addition to meiosis and glucogenesis, Rst2 is involved in cellular events such as regulation of cell growth, cell morphology, mitosis progression, microtubules structure, nuclear structure, and stress response. Overexpression of Rst2 enhances growth defect, sensitive to salt stresses, abnormal morphology, abnormal nucleus, curved microtubule, and sporulation.在粟酒裂殖酵母（Schizosaccharomyces pombe）中，转录因子Rst2在环腺苷单磷酸（cyclic adenosine monophosphate，cAMP）依赖型蛋白激酶（PKA，protein kinase A）通路的下游调控减数分裂中的ste11基因以及糖异生途径中的fbp1基因。本研究证实，Rst2还可调控其他细胞事件。过表达Rst2会提升卵形、弯曲、分枝、具隔膜及多隔膜细胞的出现频率。细胞的核分裂过程正常，但少数情况下会出现异常的核组织结构。在卵形细胞中，微管呈弯曲状态，而mal3基因的缺失可挽救该表型。由于mal3基因缺失无法挽救生长缺陷，我们认为该生长缺陷的调控通路独立于微管弯曲的调控通路。功能缺失型Pka1会加剧Rst2过表达引发的生长缺陷，因为此时Pka1对Rst2的下调作用消失。过表达Rst2还会使细胞对KCl和CaCl2产生敏感性。上述研究结果表明，除减数分裂和糖异生过程外，Rst2还参与调控细胞生长、细胞形态、有丝分裂进程、微管结构、核结构以及应激反应等多种细胞事件。 过表达Rst2可加剧生长缺陷、引发盐胁迫敏感性、导致细胞形态异常、核结构异常、微管弯曲以及孢子形成异常。