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首页> 外文期刊>Cell metabolism >Regulation of C. elegans fat uptake and storage by acyl-CoA synthase-3 is dependent on NR5A family nuclear hormone receptor nhr-25.
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Regulation of C. elegans fat uptake and storage by acyl-CoA synthase-3 is dependent on NR5A family nuclear hormone receptor nhr-25.

机译：酰基辅酶A合酶-3对秀丽隐杆线虫脂肪摄取和储存的调节取决于NR5A家族核激素受体nhr-25。

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摘要

Acyl-CoA synthases are important for lipid synthesis and breakdown, generation of signaling molecules, and lipid modification of proteins, highlighting the challenge of understanding metabolic pathways within intact organisms. From a C. elegans mutagenesis screen, we found that loss of ACS-3, a long-chain acyl-CoA synthase, causes enhanced intestinal lipid uptake, de novo fat synthesis, and accumulation of enlarged, neutral lipid-rich intestinal depots. Here, we show that ACS-3 functions in seam cells, epidermal cells anatomically distinct from sites of fat uptake and storage, and that acs-3 mutant phenotypes require the nuclear hormone receptor NHR-25, a key regulator of C. elegans molting. Our findings suggest that ACS-3-derived long-chain fatty acyl-CoAs, perhaps incorporated into complex ligands such as phosphoinositides, modulate NHR-25 function, which in turn regulates an endocrine program of lipid uptake and synthesis. These results reveal a link between acyl-CoA synthase function and an NR5A family nuclear receptor in C. elegans.
机译：酰基辅酶A合成酶对于脂质的合成和分解，信号分子的产生以及蛋白质的脂质修饰非常重要，突显了理解完整生物体内代谢途径的挑战。从秀丽隐杆线虫诱变筛选中，我们发现长链酰基辅酶A合成酶ACS-3的丢失会引起肠道脂质的吸收增加，从头脂肪合成以及堆积的，中性的富含脂质的肠道贮库的积累。在这里，我们显示ACS-3在接缝细胞，解剖学上不同于脂肪摄取和储存部位的表皮细胞中起作用，并且acs-3突变表型需要核激素受体NHR-25（秀丽隐杆线虫蜕皮的关键调节剂）。我们的发现表明，可能结合到复杂配体（如磷酸肌醇）中的ACS-3-衍生的长链脂肪酰基辅酶A调节NHR-25的功能，进而调节脂质吸收和合成的内分泌程序。这些结果揭示了秀丽隐杆线虫中酰基辅酶A合酶功能与NR5A家族核受体之间的联系。

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