PAQR-2 regulates fatty acid desaturation during cold adaptation in C. elegans.
PAQR-2 regulates fatty acid desaturation during cold adaptation in C. elegans.
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DOI:
10.1371/journal.pgen.1003801
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发表时间:
2013
期刊:
影响因子:
4.5
通讯作者:
Pilon M
中科院分区:
文献类型:
--
作者:
Svensk E;Ståhlman M;Andersson CH;Johansson M;Borén J;Pilon M
C. elegans PAQR-2 is homologous to the insulin-sensitizing adiponectin receptors in mammals, and essential for adaptation to growth at 15°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 Δ9-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. Cold-blooded organisms such as insects, fish or worms must make physiological adjustments when the temperature in their environment decreases. One essential adaptive measure is to increase the fluidity of the cellular membranes that are made of fatty molecules and would tend to harden at low temperatures, just as butter would. In our study we identify genes that are regulated by PAQR-2, a membrane protein that we show to be essential for adjusting the membrane fluidity during cold adaptation in the nematode C. elegans. Interestingly, the genes influenced by PAQR-2 are all involved in fatty acid metabolism. We speculate that the human homologs of PAQR-2, which are receptors for the hormone adiponectin, may have similar functions.
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DOI:
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