The C. elegans lipase-like 5 (lipl-5) gene is predicted to code for a lipase homologous to the human gastric acid lipase. Its expression was previously shown to be modulated by nutritional or immune cues, but nothing is known about its impact on the lipid landscape and ensuing functional consequences. In the present work, we used mutants lacking LIPL-5 protein and found that lipl-5 is important for normal lipidome composition as well as its remodeling in response to food deprivation. Particularly, lipids with signaling functions such as ceramides and mitochondrial lipids were affected by lipl-5 silencing. In comparison with wild type worms, animals lacking LIPL-5 were enriched in cardiolipins linked to polyunsaturated C20 fatty acids and coenzyme Q-9. Differences in mitochondrial lipid composition were accompanied by differences in mitochondrial activity as mitochondria from well-fed lipl-5 mutants were significantly more able to oxidize respiratory substrates when compared with mitochondria from well-fed wild type worms. Strikingly, starvation elicited important changes in mitochondrial activity in wild type worms, but not in lipl-5 worms. This indicates that this lipase is a determinant of mitochondrial functional remodeling in response to food withdrawal.

中文翻译：

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脂肪酶样5酶响应线虫的饥饿而控制线粒体的活性。

秀丽隐杆线虫脂肪酶样5（lipl-5）基因预计编码与人胃酸脂肪酶同源的脂肪酶。先前已证明其表达受营养或免疫提示的调节，但对其对脂质结构的影响和随之而来的功能后果一无所知。在目前的工作中，我们使用了缺少LIPL-5蛋白的突变体，发现lipl-5对于正常脂质组组成及其对食物缺乏的重塑具有重要意义。尤其是，具有信号传导功能的脂质（例如神经酰胺和线粒体脂质）受到lipl-5沉默的影响。与野生型蠕虫相比，缺少LIPL-5的动物富含与多不饱和C20脂肪酸和辅酶Q-9连接的心磷脂。线粒体脂质组成的差异伴随着线粒体活性的差异，因为与进食野生型蠕虫的线粒体相比，进食lipl-5突变体的线粒体更能氧化呼吸底物。令人惊讶的是，饥饿导致野生型蠕虫的线粒体活性发生了重要变化，而lipl-5蠕虫却没有。这表明该脂肪酶是响应食物戒断的线粒体功能重塑的决定因素。