New insights into the regulation of plant metabolism by O-acetylserine: sulfate and beyond

被引:11
|
作者
Apodiakou, Anastasia [1 ]
Hoefgen, Rainer [1 ]
机构
[1] Max Planck Inst Mol Plant Physiol, Muhlenberg 1, D-14476 Potsdam, Germany
关键词
APR; ATTED-II; BGLU28; gene regulation; network; O-acetylserine; oxidative stress; ROS; SDIs; sulfur; sulfur deficiency; SLIM1; ACETYLTRANSFERASE GENE FAMILY; INDOLIC GLUCOSINOLATE BIOSYNTHESIS; SULFUR-DEFICIENCY RESPONSE; ARABIDOPSIS-THALIANA; TRANSCRIPTION FACTORS; SUBCELLULAR-LOCALIZATION; FUNCTIONAL-ANALYSIS; STRESS RESPONSES; SALT STRESS; EXPRESSION;
D O I
10.1093/jxb/erad124
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
O-Acetylserine (OAS), a sulfate deprivation marker, accumulates under stress conditions. We provide information about the function and regulation of OAS cluster genes and an OAS cluster co-expression network. Under conditions of sulfur deprivation, O-acetylserine (OAS) accumulates, which leads to the induction of a common set of six genes, called OAS cluster genes. These genes are induced not only under sulfur deprivation, but also under other conditions where OAS accumulates, such as shift to darkness and stress conditions leading to reactive oxygen species (ROS) or methyl-jasmonate accumulation. Using the OAS cluster genes as a query in ATTED-II, a co-expression network is derived stably spanning several hundred conditions. This allowed us not only to describe the downstream function of the OAS cluster genes but also to score for functions of the members of the co-regulated co-expression network and hence the effects of the OAS signal on the sulfate assimilation pathway and co-regulated pathways. Further, we summarized existing knowledge on the regulation of the OAS cluster and the co-expressed genes. We revealed that the known sulfate deprivation-related transcription factor EIL3/SLIM1 exhibits a prominent role, as most genes are subject to regulation by this transcription factor. The role of other transcription factors in response to OAS awaits further investigation.
引用
收藏
页码:3361 / 3378
页数:18
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