Caenorhabditis elegans is a useful animal model to determine the underlying mechanism for the response to simulated microgravity. In this study, we employed C. elegans as an animal model to investigate the role of lipid metabolic sensors in regulating the response to simulated microgravity. Among the lipid metabolic sensors, simulated microgravity treatment could increase the expressions of sbp-1 and mdt-15. RNAi knockdown of sbp-1 or mdt-15 induced a susceptibility to toxicity of simulated microgravity, suggesting the alteration in SBP-1 and MDT-1 mediated a protective response to simulated microgravity. Tissue-specific activity analysis demonstrated that both MDT-15 and SBP-1 could act in the intestine to regulate the response to simulated microgravity. Genetic interaction analysis further indicated that intestinal MDT-15 acted upstream of SBP-1 to regulate the response to simulated microgravity. During the control of response to simulated microgravity, fatty acyl CoA desaturase FAT-6 was identified as the downstream target of intestinal SBP-1. Therefore, the identified signaling cascade of MDT-15-SBP-1-FAT-6 suggested the important function of lipid metabolic sensors in mediating a novel intestinal signaling pathway to regulate the response to simulated microgravity in nematodes.

中文翻译：

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MDT-15和SBP-1的脂质代谢传感器可调节秀丽隐杆线虫肠道中对模拟微重力的响应。

秀丽隐杆线虫是一种有用的动物模型，用于确定对模拟微重力的响应的潜在机制。在这项研究中，我们采用秀丽隐杆线虫作为动物模型，以研究脂质代谢传感器在调节对模拟微重力的响应中的作用。在脂质代谢传感器中，模拟微重力处理可以增加sbp-1和mdt-15的表达。RNAi敲低sbp-1或mdt-15诱导对模拟微重力的毒性敏感性，表明SBP-1和MDT-1的改变介导了对模拟微重力的保护反应。组织特异性活性分析表明，MDT-15和SBP-1均可在肠中调节对模拟微重力的反应。遗传相互作用分析进一步表明，肠道MDT-15在SBP-1的上游起作用，以调节对模拟微重力的反应。在控制对模拟微重力的响应过程中，脂肪酰基CoA去饱和酶FAT-6被确定为肠道SBP-1的下游靶标。因此，确定的MDT-15-SBP-1-FAT-6信号传导级联表明脂质代谢传感器在介导新的肠道信号传导途径以调节线虫对模拟微重力的反应中的重要功能。