PAQR-2 Regulates Fatty Acid Desaturation during Cold Adaptation in C. elegans

被引:93
作者
Svensk, Emma [1 ]
Stahlman, Marcus [2 ]
Andersson, Carl-Henrik [1 ]
Johansson, Maja [1 ]
Boren, Jan [2 ]
Pilon, Marc [1 ]
机构
[1] Univ Gothenburg, Dept Chem & Mol Biol, Gothenburg, Sweden
[2] Univ Gothenburg, Inst Med, Dept Mol & Clin Med, Wallenberg Lab, Gothenburg, Sweden
基金
瑞典研究理事会;
关键词
CAENORHABDITIS-ELEGANS; BIOLOGICAL-MEMBRANES; IDENTIFICATION; TEMPERATURE; MECHANISMS; HYPOTHESIS; TOLERANCE; PATHWAYS; EXPOSURE; SUBUNIT;
D O I
10.1371/journal.pgen.1003801
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
C. elegans PAQR-2 is homologous to the insulin-sensitizing adiponectin receptors in mammals, and essential for adaptation to growth at 15 degrees C, a low but usually acceptable temperature for this organism. By screening for novel paqr-2 suppressors, we identified mutations in genes involved in phosphatidylcholine synthesis (cept-1, pcyt-1 and sams-1) and fatty acid metabolism (ech-7, hacd-1, mdt-15, nhr-49 and sbp-1). We then show genetic evidence that paqr-2, phosphatidylcholines, sbp-1 and Delta 9-desaturases form a cold adaptation pathway that regulates the increase in unsaturated fatty acids necessary to retain membrane fluidity at low temperatures. This model is supported by the observations that the paqr-2 suppressors normalize the levels of saturated fatty acids, and that low concentrations of detergents that increase membrane fluidity can rescue the paqr-2 mutant.
引用
收藏
页数:15
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