Stolz L E, Kuo W J, Longchamps J, Sekhon M K, York J D
Departments of Pharmacology and Cancer Biology and of Biochemistry, Duke Medical Center, Durham, North Carolina 27710, USA.
J Biol Chem. 1998 May 8;273(19):11852-61. doi: 10.1074/jbc.273.19.11852.
Sequence analysis of Saccharomyces cerevisiae chromosome IX identified a 946 amino acid open reading frame (YIL002C), designated here as INP51, that has carboxyl- and amino-terminal regions similar to mammalian inositol polyphosphate 5-phosphatases and to yeast SAC1. This two-domain primary structure resembles the mammalian 5-phosphatase, synaptojanin. We report that Inp51p is associated with a particulate fraction and that recombinant Inp51p exhibits intrinsic phosphatidylinositol 4,5-bisphosphate 5-phosphatase activity. Deletion of INP51 (inp51) results in a "cold-tolerant" phenotype, enabling significantly faster growth at temperatures below 15 degreesC as compared with a parental strain. Complementation analysis of an inp51 mutant strain demonstrates that the cold tolerance is strictly due to loss of 5-phosphatase catalytic activity. Furthermore, deletion of PLC1 in an inp51 mutant does not abrogate cold tolerance, indicating that Plc1p-mediated production of soluble inositol phosphates is not required. Cells lacking INP51 have a 2-4-fold increase in levels of phosphatidylinositol 4,5-bisphosphate and inositol 1,4, 5-trisphosphate, whereas cells overexpressing Inp51p exhibit a 35% decrease in levels of phosphatidylinositol 4,5-bisphosphate. We conclude that INP51 function is critical for proper phosphatidylinositol 4,5-bisphosphate homeostasis. In addition, we define a novel role for a 5-phosphatase loss of function mutant that improves the growth of cells at colder temperatures without alteration of growth at normal temperatures, which may have useful commercial applications.
对酿酒酵母IX号染色体的序列分析鉴定出一个946个氨基酸的开放阅读框(YIL002C),在此命名为INP51,其羧基末端和氨基末端区域与哺乳动物的肌醇多磷酸5-磷酸酶以及酵母SAC1相似。这种双结构域一级结构类似于哺乳动物的5-磷酸酶突触素。我们报道Inp51p与微粒部分相关,并且重组Inp51p表现出内在的磷脂酰肌醇4,5-二磷酸5-磷酸酶活性。INP51缺失(inp51)导致“耐冷”表型,与亲本菌株相比,在低于15摄氏度的温度下生长明显更快。对inp51突变菌株的互补分析表明,耐冷性严格归因于5-磷酸酶催化活性的丧失。此外,在inp51突变体中删除PLC1并不会消除耐冷性,这表明不需要Plc1p介导的可溶性肌醇磷酸的产生。缺乏INP51的细胞中磷脂酰肌醇4,5-二磷酸和肌醇1,4,5-三磷酸的水平增加2-4倍,而过度表达Inp51p的细胞中磷脂酰肌醇4,5-二磷酸的水平降低35%。我们得出结论,INP51的功能对于维持适当的磷脂酰肌醇4,5-二磷酸稳态至关重要。此外,我们定义了一种5-磷酸酶功能丧失突变体的新作用,该突变体可改善细胞在较低温度下的生长,而不会改变正常温度下的生长,这可能具有有用的商业应用价值。