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拟南芥酰基-ACP甘油-3-磷酸酰基转移酶缺陷型突变体叶绿体中的磷脂酰甘油生物合成

Phosphatidylglycerol biosynthesis in chloroplasts of Arabidopsis mutants deficient in acyl-ACP glycerol-3- phosphate acyltransferase.

作者信息

Xu Changcheng, Yu Bin, Cornish Adam J, Froehlich John E, Benning Christoph

机构信息

Department of Biochemistry, Michigan State University, East Lansing, MI 48824, USA.

出版信息

Plant J. 2006 Jul;47(2):296-309. doi: 10.1111/j.1365-313X.2006.02790.x. Epub 2006 Jun 15.

DOI:10.1111/j.1365-313X.2006.02790.x
PMID:16774646
Abstract

The biosynthesis of phosphatidylglycerol represents a central pathway in lipid metabolism in all organisms. The enzyme catalyzing the first reaction of the pathway in the plastid, glycerol-3-phosphate acyl-acyl carrier protein acyltransferase, is thought to be encoded in Arabidopsis by the ATS1 locus. A number of genetic mutants deficient in this activity have been described. However, the corresponding mutant alleles have not yet been analyzed at the molecular level and a causal relationship between the mutant phenotypes and a deficiency at the ATS1 locus has not been established. The presence in all known ats1 mutants of near wild-type amounts of phosphatidylglycerol raised the question of whether an alternative pathway of phosphatidylglycerol assembly in the plastid exists. However, detailed analysis of several independent ats1 mutant alleles revealed that all are leaky. Reduction by RNAi of ats1-1 RNA levels in the ats1-1 mutant background led to a more severe growth phenotype (small green plants and reduced seed set), but did not decrease the relative amount of phosphatidylglycerol. In contrast, when the amount of ATS2 mRNA encoding the plastidic lysophosphatidic acid acyltransferase catalyzing the second reaction of the pathway was reduced by RNAi in the ats1-1 mutant background, phosphatidylglycerol amounts decreased, leading to a growth phenotype (small pale-yellow plants) that is reminiscent of the pgp1-1 mutant deficient in a late step of plastidic phosphatidylglycerol biosynthesis. These observations indicate coordinated regulation of plastid lipid metabolism and plant development.

摘要

磷脂酰甘油的生物合成是所有生物体脂质代谢的核心途径。催化该途径在质体中第一步反应的酶,即甘油-3-磷酸酰基-酰基载体蛋白酰基转移酶,被认为在拟南芥中由ATS1位点编码。已经描述了许多缺乏这种活性的遗传突变体。然而,相应的突变等位基因尚未在分子水平上进行分析,并且突变表型与ATS1位点缺陷之间的因果关系尚未确立。所有已知的ats1突变体中磷脂酰甘油含量接近野生型,这引发了一个问题,即质体中是否存在磷脂酰甘油组装的替代途径。然而,对几个独立的ats1突变等位基因的详细分析表明,所有这些都是渗漏突变体。在ats1-1突变背景下,通过RNA干扰降低ats1-1 RNA水平会导致更严重的生长表型(矮小的绿色植株和结实率降低),但并未降低磷脂酰甘油的相对含量。相反,在ats1-1突变背景下,当通过RNA干扰降低编码催化该途径第二步反应的质体溶血磷脂酸酰基转移酶的ATS2 mRNA量时,磷脂酰甘油含量下降,导致一种生长表型(矮小的浅黄色植株),这让人联想到在质体磷脂酰甘油生物合成后期步骤中存在缺陷的pgp1-1突变体。这些观察结果表明质体脂质代谢与植物发育之间存在协同调控。

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