期刊
PLANT CELL
卷 25, 期 5, 页码 1726-1739出版社
AMER SOC PLANT BIOLOGISTS
DOI: 10.1105/tpc.113.111898
关键词
-
资金
- U.S. Department of Energy, Office of Science (Biological and Environmental Research) [DE-SC0000797]
- University of Guelph Research Chairs Program
- Natural Sciences and Engineering Research Council of Canada [217291]
- USDA [5347-21000-005-00D, STELLAR 2007-38422-18084]
- National Science Foundation [DUE 0703118, 1126205]
- Direct For Biological Sciences
- Div Of Biological Infrastructure [1126205] Funding Source: National Science Foundation
- U.S. Department of Energy (DOE) [DE-SC0000797] Funding Source: U.S. Department of Energy (DOE)
COMPARATIVE GENE IDENTIFICATION-58 (CGI-58) is a key regulator of lipid metabolism and signaling in mammals, but its underlying mechanisms are unclear. Disruption of CGI-58 in either mammals or plants results in a significant increase in triacylglycerol (TAG), suggesting that CGI-58 activity is evolutionarily conserved. However, plants lack proteins that are important for CGI-58 activity in mammals. Here, we demonstrate that CGI-58 functions by interacting with the PEROXISOMAL ABC-TRANSPORTER1 (PXA1), a protein that transports a variety of substrates into peroxisomes for their subsequent metabolism by beta-oxidation, including fatty acids and lipophilic hormone precursors of the jasmonate and auxin biosynthetic pathways. We also show that mutant cgi-58 plants display changes in jasmonate biosynthesis, auxin signaling, and lipid metabolism consistent with reduced PXA1 activity in planta and that, based on the double mutant cgi-58 pxa1, PXA1 is epistatic to CGI-58 in all of these processes. However, CGI-58 was not required for the PXA1-dependent breakdown of TAG in germinated seeds. Collectively, the results reveal that CGI-58 positively regulates many aspects of PXA1 activity in plants and that these two proteins function to coregulate lipid metabolism and signaling, particularly in nonseed vegetative tissues. Similarities and differences of CGI-58 activity in plants versus animals are discussed.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据