Saccharomyces cerevisiae cho2 mutants are deficient in phospholipid methylation and cross-pathway regulation of inositol synthesis.
Saccharomyces cerevisiae cho2 mutants are deficient in phospholipid methylation and cross-pathway regulation of inositol synthesis.
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酿酒酵母 cho2 突变体缺乏磷脂甲基化和肌醇合成的跨途径调节。
DOI：
10.1093/genetics/120.4.909
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发表时间：
1988
期刊：
影响因子：
3.3
通讯作者：
Henry,SA
中科院分区：
文献类型：
--
作者：
Summers,EF;Letts,VA;McGraw,P;Henry,SA
利用两种不同的筛选技术，分离出了5个磷脂酰乙醇胺（PE）甲基化缺陷的等位基因酿酒酵母突变体。生化分析表明，这些突变体定义一个位点，命名为CHO 2，可能编码甲基转移酶。与40- 45%PC和15- 20%PE的野生型水平相比，在限定培养基中生长的cho 2突变细胞的膜含有约10%的磷脂酰胆碱（PC）和40- 50%PE。尽管磷脂组成发生了很大变化，cho 2突变细胞在成分确定的培养基中仍能存活，并且对胆碱或其他磷脂前体（如单甲基乙醇胺（MME））没有营养缺陷。然而，对携带一个以上影响磷脂生物合成的突变的酵母菌株的分析表明，一定水平的甲基化磷脂对生存力是必不可少的。四分体分析表明cho 2位点与其他影响磷脂合成的位点不连锁。有趣的是，cho 2突变体和其他突变株，产生甲基化磷脂的水平降低，不能适当地抑制合成的细胞质酶肌醇-1-磷酸合酶。这种酶先前被证明是在mRNA丰度水平上响应于生长培养基中的肌醇和胆碱而被调节。我们克隆了CHO 2基因的3.6 kb的基因组DNA片段，并通过破坏CHO 2基因在体内产生了一个无效的等位基因。cho 2破坏剂，像所有其他cho 2突变体，是可行的，表现出改变调节肌醇生物合成和不是胆碱或MME营养缺陷型。
Five allelic Saccharomyces cerevisiae mutants deficient in the methylation of phosphatidylethanolamine (PE) have been isolated, using two different screening techniques. Biochemical analysis suggested that these mutants define a locus, designated CHO2, that may encode a methyltransferase. Membranes of cho2 mutant cells grown in defined medium contain approximately 10% phosphatidylcholine (PC) and 40-50% PE as compared to wild-type levels of 40-45% PC and 15-20% PE. In spite of this greatly altered phospholipid composition, cho2 mutant cells are viable in defined medium and are not auxotrophic for choline or other phospholipid precursors such as monomethylethanolamine (MME). However, analysis of yeast strains carrying more than one mutation affecting phospholipid biosynthesis indicated that some level of methylated phospholipid is essential for viability. The cho2 locus was shown by tetrad analysis to be unlinked to other loci affecting phospholipid synthesis. Interestingly, cho2 mutants and other mutant strains that produce reduced levels of methylated phospholipids are unable to properly repress synthesis of the cytoplasmic enzyme inositol-1-phosphate synthase. This enzyme was previously shown to be regulated at the level of mRNA abundance in response to inositol and choline in the growth medium. We cloned the CHO2 gene on a 3.6-kb genomic DNA fragment and created a null allele of cho2 by disrupting the CHO2 gene in vivo. The cho2 disruptant, like all other cho2 mutants, is viable, exhibits altered regulation of inositol biosynthesis and is not auxotrophic for choline or MME.
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酵母磷脂酰乙醇胺甲基化途径。
影响因子：
4.8
作者：
Tsutomu Kodaki;S. Yamashita
通讯作者：
S. Yamashita
影响因子：
4.8
作者：
F. Audubert;D. Vance
通讯作者：
D. Vance
DOI：
10.1016/s0021-9258(19)69102-7
发表时间：
1981-07
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
T. Donahue;S. Henry
通讯作者：
T. Donahue;S. Henry
DOI：
10.1073/pnas.78.1.238
发表时间：
1981-01-01
期刊：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES
影响因子：
--
作者：
FRIED, HM;WARNER, JR
通讯作者：
WARNER, JR
从大鼠肝脏中纯化磷脂酰乙醇胺 N-甲基转移酶。
影响因子：
4.8
作者：
N. Ridgway;D. Vance
通讯作者：
D. Vance