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KCS1编码一种脂肪酸延长酶3-酮酰基辅酶A合酶,影响拟南芥中的蜡质生物合成。

KCS1 encodes a fatty acid elongase 3-ketoacyl-CoA synthase affecting wax biosynthesis in Arabidopsis thaliana.

作者信息

Todd J, Post-Beittenmiller D, Jaworski J G

机构信息

Department of Chemistry and Biochemistry, Miami University, Oxford, OH 45056, USA.

出版信息

Plant J. 1999 Jan;17(2):119-30. doi: 10.1046/j.1365-313x.1999.00352.x.

DOI:10.1046/j.1365-313x.1999.00352.x
PMID:10074711
Abstract

An Arabidopsis fatty acid elongase gene, KCS1, with a high degree of sequence identity to FAE1, encodes a 3-ketoacyl-CoA synthase which is involved in very long chain fatty acid synthesis in vegetative tissues, and which also plays a role in wax biosynthesis. Sequence analysis of KCS1 predicted that this synthase was anchored to a membrane by two adjacent N-terminal, membrane-spanning domains. Analysis of a T-DNA tagged kcs1-1 mutant demonstrated the involvement of the KCS1 in wax biosynthesis. Phenotypic changes in the kcs1-1 mutant included thinner stems and less resistance to low humidity stress at a young age. Complete loss of KCS1 expression resulted in decreases of up to 80% in the levels of C26 to C30 wax alcohols and aldehydes, but much smaller effects were observed on the major wax components, i.e. the C29 alkanes and C29 ketones on leaves, stems and siliques. In no case did the loss of KCS1 expression result in complete loss of any individual wax component or significantly decrease the total wax load. This indicated that there was redundancy in the elongase KCS activities involved in wax synthesis. Furthermore, since alcohol, aldehyde, alkane and ketone levels were affected to varying degrees, involvement of the KCS1 synthase in both the decarbonylation and acyl-reduction wax synthesis pathways was demonstrated.

摘要

一种拟南芥脂肪酸延长酶基因KCS1,与FAE1具有高度的序列同一性,编码一种3-酮脂酰辅酶A合酶,该酶参与营养组织中极长链脂肪酸的合成,并且在蜡质生物合成中也发挥作用。KCS1的序列分析预测,这种合酶通过两个相邻的N端跨膜结构域锚定在膜上。对一个T-DNA标签的kcs1-1突变体的分析表明KCS1参与了蜡质生物合成。kcs1-1突变体的表型变化包括茎变细以及在幼龄时对低湿度胁迫的抗性降低。KCS1表达的完全丧失导致C26至C30蜡醇和醛水平下降高达80%,但对主要蜡质成分,即叶片、茎和角果上的C29烷烃和C29酮的影响要小得多。在任何情况下,KCS1表达的丧失都不会导致任何单一蜡质成分的完全丧失或显著降低总蜡质含量。这表明蜡质合成中涉及的延长酶KCS活性存在冗余。此外,由于醇、醛、烷烃和酮水平受到不同程度的影响,证明了KCS1合酶参与了脱羰和酰基还原蜡质合成途径。

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