Turnover of phosphatidylcholine in Saccharomyces cerevisiae -: The role of the CDP-choline pathway

被引:101
作者
Dowd, SR
Bier, ME
Patton-Vogt, JL
机构
[1] Carnegie Mellon Univ, Dept Biol Sci, Pittsburgh, PA 15213 USA
[2] Carnegie Mellon Univ, Dept Chem, Pittsburgh, PA 15213 USA
关键词
D O I
10.1074/jbc.M003694200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The regulation of phosphatidylcholine degradation as a function of the route of phosphatidylcholine (PC) synthesis and changing environmental conditions has been investigated in the yeast Saccharomyces cerevisiae. In the wild-type strains studied, deacylation of phosphatidylcholine to glycerophosphocholine is induced when choline is supplied to the culture medium and, also, when the culture temperature is raised from 30 to 37 degreesC. In strains bearing mutations in any of the genes encoding enzymes of the GDP-choline pathway for phosphatidylcholine biosynthesis (CKI1, choline kinase; CPT1, 1, 2-diacylglycerol choline phosphotransferase; PCT1, CTP:phosphocholine cytidylyltransferase), no induction of phosphatidylcholine turnover and glycerophosphocholine production is seen in response to choline availability or elevated temperature. In contrast, the induction of phosphatidylcholine deacylation does occur in a strain bearing mutations in genes encoding enzymes of the methylation pathway for phosphatidylcholine biosynthesis (i.e. CHO2/PEM1 and OPI3/PEM2). Whereas the synthesis of PC via CDP-choline is accelerated when shifted from 30 to 37 degreesC, synthesis of PC via the methylation pathway is largely unaffected by the temperature shift. These results suggest that the deacylation of PC to GroPC requires an active CDP-choline pathway for PC biosynthesis but not an active methylation pathway. Furthermore, the data indicate that the synthesis and turnover of CDP-choline-derived PC, but not methylation pathway-derived PC, are accelerated by the stress of elevated temperature.
引用
收藏
页码:3756 / 3763
页数:8
相关论文
共 51 条
[1]  
Aboagye EO, 1999, CANCER RES, V59, P80
[3]   Inhibition of phosphatidylcholine biosynthesis following induction of apoptosis in HL-60 cells [J].
Anthony, ML ;
Zhao, M ;
Brindle, KM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (28) :19686-19692
[4]   SECRETION CAN PROCEED UNCOUPLED FROM NET PLASMA-MEMBRANE EXPANSION IN INOSITOL-STARVED SACCHAROMYCES-CEREVISIAE [J].
ATKINSON, KD ;
RAMIREZ, RM .
JOURNAL OF BACTERIOLOGY, 1984, 160 (01) :80-86
[5]   Cellular responses to excess phospholipid [J].
Baburina, I ;
Jackowski, S .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (14) :9400-9408
[6]   Regulation of phosphatidylcholine homeostasis by calcium-independent phospholipase A2 [J].
Barbour, SE ;
Kapur, A ;
Deal, CL .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS, 1999, 1439 (01) :77-88
[7]   MUTATIONS IN THE CDP CHOLINE PATHWAY FOR PHOSPHOLIPID BIOSYNTHESIS BYPASS THE REQUIREMENT FOR AN ESSENTIAL PHOSPHOLIPID TRANSFER PROTEIN [J].
CLEVES, AE ;
MCGEE, TP ;
WHITTERS, EA ;
CHAMPION, KM ;
AITKEN, JR ;
DOWHAN, W ;
GOEBL, M ;
BANKAITIS, VA .
CELL, 1991, 64 (04) :789-800
[9]   A genetic defect in phosphatidylcholine biosynthesis triggers apoptosis in Chinese hamster ovary cells [J].
Cui, Z ;
Houweling, M ;
Chen, MH ;
Record, M ;
Chap, H ;
Vance, DE ;
Terce, F .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (25) :14668-14671
[10]  
Daum G, 1999, YEAST, V15, P601, DOI 10.1002/(SICI)1097-0061(199905)15:7<601::AID-YEA390>3.0.CO