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MADS盒转录因子Mbx2/Pvg4通过诱导裂殖酵母中gsf2+的表达来调控侵袭性生长和絮凝。

MADS box transcription factor Mbx2/Pvg4 regulates invasive growth and flocculation by inducing gsf2+ expression in fission yeast.

作者信息

Matsuzawa Tomohiko, Yoritsune Ken-ichi, Takegawa Kaoru

机构信息

Department of Bioscience & Biotechnology, Faculty of Agriculture, Kyushu University, Hakozaki 6-10-1, Fukuoka, Japan.

出版信息

Eukaryot Cell. 2012 Feb;11(2):151-8. doi: 10.1128/EC.05276-11. Epub 2011 Dec 16.

Abstract

The fission yeast Schizosaccharomyces pombe exhibits invasive growth and nonsexual flocculation in response to nitrogen limitation. Gsf2, a flocculin of fission yeast, is required not only for nonsexual flocculation but also for invasive growth through the recognition of galactose residues on cell surface glycoconjugates. We found that pyruvylation negatively regulates nonsexual flocculation by capping the galactose residues of N-linked galactomannan. We investigated whether pyruvylation also regulates invasive growth. The pvg4(+) gene originally was isolated as a multicopy suppressor of a pvg4 mutant defective in the pyruvylation of N-linked oligosaccharides. However, we did not detect a defect in cell surface pyruvylation in the pvg4/mbx2 deletion mutant, as assessed by alcian blue staining and a Q-Sepharose binding assay. Instead, the deletion prevented invasive growth under conditions of low nitrogen and high glucose, and it reduced the adhesion and flocculation of otherwise flocculent mutants by reducing gsf2(+) expression. mbx2(+)-overexpressing strains exhibited nonsexual and calcium-dependent aggregation, which was inhibited in the presence of galactose but mediated by the induction of gsf2(+). These findings indicate that Mbx2 mediates invasive growth and flocculation via the transcriptional activation of gsf2(+) in fission yeast. In addition, we found that fission yeast Mbx2 induces the nonsexual flocculation of budding yeast by the activation of FLO1.

摘要

裂殖酵母粟酒裂殖酵母在氮限制条件下会表现出侵袭性生长和无性絮凝。Gsf2是裂殖酵母的一种絮凝素,不仅对于无性絮凝是必需的,而且对于通过识别细胞表面糖缀合物上的半乳糖残基进行的侵袭性生长也是必需的。我们发现丙酮酸化通过封闭N-连接的半乳甘露聚糖的半乳糖残基来负向调节无性絮凝。我们研究了丙酮酸化是否也调节侵袭性生长。pvg4(+)基因最初是作为N-连接寡糖丙酮酸化缺陷的pvg4突变体的多拷贝抑制子被分离出来的。然而,通过阿尔新蓝染色和Q-琼脂糖凝胶结合试验评估,我们在pvg4/mbx2缺失突变体中未检测到细胞表面丙酮酸化缺陷。相反,该缺失在低氮和高葡萄糖条件下阻止了侵袭性生长,并且通过降低gsf2(+)的表达减少了原本絮凝突变体的黏附与絮凝。过表达mbx2(+)的菌株表现出无性和钙依赖性聚集,在半乳糖存在时受到抑制,但由gsf2(+)的诱导介导。这些发现表明,Mbx2通过转录激活裂殖酵母中的gsf2(+)来介导侵袭性生长和絮凝。此外,我们发现裂殖酵母Mbx2通过激活FLO1诱导出芽酵母的无性絮凝。

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