National Laboratory of Biomacromolecules, Cas Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
University of Chinese Academy of Sciences, Beijing, China.
Gut Microbes. 2022 Jan-Dec;14(1):2013762. doi: 10.1080/19490976.2021.2013762.
Dietary and symbiotic bacteria can exert powerful influence on metazoan lipid metabolism. Recent studies have emerged that microbiota have a role in animal obesity and related health disorders, but the mechanisms by which bacteria influence lipid storage in their host are unknown. To reduce the complexity of the relationship between gut microbiota and the host, () has been chosen as a model organism to study interspecies interaction. Here, we demonstrate that feeding with an opportunistic pathogenic bacterium () retards growth and promotes excessive neutral lipid storage. Gene expression analysis reveals that dietary induces a lipogenic transcriptional response that includes the SREBP ortholog SBP-1, and fatty acid desaturases FAT-6 and FAT-7. Live imaging and ultrastructural analysis suggest that excess neutral lipid is stored in greatly expanded lipid droplets (LDs), as a result of enhanced endoplasmic reticulum (ER)-LD interaction. We also report that loss of function mutations in in confers resistance to . Dietary induces supersized LDs by enhancing lipogenesis and ER-LD contacts in . This work delineates a new model for understanding microbial regulation of metazoan physiology.
饮食和共生细菌可以对后生动物的脂质代谢产生强大的影响。最近的研究表明，微生物群在动物肥胖和相关健康障碍中起作用，但细菌影响宿主脂质储存的机制尚不清楚。为了降低肠道微生物群与宿主之间关系的复杂性，（秀丽隐杆线虫）已被选为研究种间相互作用的模式生物。在这里，我们证明，用机会性病原体（）喂养会减缓生长并促进过多的中性脂质储存。基因表达分析表明，饮食（）诱导了一种生脂转录反应，包括 SREBP 同源物 SBP-1，以及脂肪酸去饱和酶 FAT-6 和 FAT-7。活体成像和超微结构分析表明，过量的中性脂质储存在大大扩展的脂滴（LDs）中，这是由于内质网（ER）-LD 相互作用增强的结果。我们还报告说，（）中 SBP-1 的功能丧失突变赋予了对（）的抗性。饮食（）通过增强脂生成和 ER-LD 接触来诱导（）中的超大脂滴。这项工作描绘了一个理解微生物对后生动物生理学调节的新模式。
