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粟酒裂殖酵母硫胺素焦磷酸激酶由tnr3基因编码,是硫胺素代谢、磷酸盐代谢、交配和生长的调节因子。

Schizosaccharomyces pombe thiamine pyrophosphokinase is encoded by gene tnr3 and is a regulator of thiamine metabolism, phosphate metabolism, mating, and growth.

作者信息

Fankhauser H, Zurlinden A, Schweingruber A M, Edenharter E, Schweingruber M E

机构信息

Institute of General Microbiology, University of Bern, Switzerland.

出版信息

J Biol Chem. 1995 Nov 24;270(47):28457-62. doi: 10.1074/jbc.270.47.28457.

Abstract

The Schizosaccharomyces pombe gene tnr3 has been genetically defined as a negative regulator of genes involved in thiamine metabolism (Schweingruber, A. M., Frankhauser, H., Dlugonski, J., Steinmann-Loss, C., and Schweingruber, M. E. (1992) Genetics 130, 445-449). We have isolated and sequenced the gene and show that it codes for a putative protein of 569 amino acids which exhibits, in its carboxyl-terminal half, good homology to Saccharomyces cerevisiae thiamine pyrophosphokinase (TPK). tnr3 mutants have reduced levels of intracellular thiamine diphosphate, show impaired TPK activity, which is enhanced by introducing the tnr3 wild type gene on a plasmid, and can be complemented by the S. cerevisiae TPK-encoding gene TH180. These data strongly suggest that tnr3 encodes S. pombe TPK. We present evidence that TPK also acts as a negative regulator for gene pho1, which is derepressed when cells are starved for phosphate and show that in contrast to wild type cells, tnr3 mutants mate constitutively in response to thiamine, indicating that TPK is also involved in regulation of mating. Disruption of the tnr3 gene is lethal, and a tnr3 mutant expressing only residual TPK activity grows slowly and shows aberrant morphology.

摘要

粟酒裂殖酵母基因tnr3在遗传学上被定义为参与硫胺素代谢的基因的负调节因子(施温格鲁伯,A.M.,弗兰克豪泽,H.,德鲁戈尼斯基,J.,施泰因曼-洛斯,C.,以及施温格鲁伯,M.E.(1992年)《遗传学》130卷,445 - 449页)。我们已经分离并测序了该基因,结果表明它编码一种含有569个氨基酸的假定蛋白质,该蛋白质在其羧基末端部分与酿酒酵母硫胺素焦磷酸激酶(TPK)具有高度同源性。tnr3突变体的细胞内硫胺素二磷酸水平降低,TPK活性受损,将tnr3野生型基因导入质粒可增强该活性,并且可以用酿酒酵母TPK编码基因TH180进行互补。这些数据有力地表明tnr3编码粟酒裂殖酵母TPK。我们提供证据表明TPK也是基因pho1的负调节因子,当细胞缺乏磷酸盐时该基因会去抑制,并且表明与野生型细胞不同,tnr3突变体在硫胺素存在时组成型交配,这表明TPK也参与交配调节。tnr3基因的破坏是致死的,一个仅表达残余TPK活性的tnr3突变体生长缓慢且形态异常。

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