EAT-2 attenuates C. elegans development via metabolic remodeling in a chemically defined food environment

doi:10.1007/s00018-023-04849-x

IOCAS-IR > 实验海洋生物学重点实验室

	EAT-2 attenuates C. elegans development via metabolic remodeling in a chemically defined food environment
	Cao, Xuwen1,2,3,4,6 ; Xie, Yusu 1,2,3; Yang, Hanwen 1,2,3; Sun, Peiqi 1,2,3,4; Xue, Beining 1,2,3,4; Garcia, L. Rene 5; Zhang, Liusuo 1,2,3
	2023-08-01
发表期刊	CELLULAR AND MOLECULAR LIFE SCIENCES
ISSN	1420-682X
卷号	80 期号:8 页码:18
通讯作者	Zhang, Liusuo(lzhang@qdio.ac.cn)
摘要	Dietary intake and nutrient composition regulate animal growth and development; however, the underlying mechanisms remain elusive. Our previous study has shown that either the mammalian deafness homolog gene tmc-1 or its downstream acetylcholine receptor gene eat-2 attenuates Caenorhabditis elegans development in a chemically defined food CeMM (C. elegans maintenance medium) environment, but the underpinning mechanisms are not well-understood. Here, we found that, in CeMM food environment, for both eat-2 and tmc-1 fast-growing mutants, several fatty acid synthesis and elongation genes were highly expressed, while many fatty acid beta-oxidation genes were repressed. Accordingly, dietary supplementation of individual fatty acids, such as monomethyl branch chain fatty acid C17ISO, palmitic acid and stearic acid significantly promoted wild-type animal development on CeMM, and mutations in either C17ISO synthesis gene elo-5 or elo-6 slowed the rapid growth of eat-2 mutant. Tissue-specific rescue experiments showed that elo-6 promoted animal development mainly in the intestine. Furthermore, transcriptome and metabolome analyses revealed that elo-6/C17ISO regulation of C. elegans development may be correlated with up-regulating expression of cuticle synthetic and hedgehog signaling genes, as well as promoting biosynthesis of amino acids, amino acid derivatives and vitamins. Correspondingly, we found that amino acid derivative S-adenosylmethionine and its upstream metabolite methionine sulfoxide significantly promoted C. elegans development on CeMM. This study demonstrated that C17ISO, palmitic acid, stearic acid, S-adenosylmethionine and methionine sulfoxide inhibited or bypassed the TMC-1 and EAT-2-mediated attenuation of development via metabolic remodeling, and allowed the animals to adapt to the new nutritional niche.
关键词	C. elegans maintenance medium CeMM Development Acetylcholine receptor Fatty acid C17ISO S-adenosylmethionine SAM
DOI	10.1007/s00018-023-04849-x
收录类别	SCI
语种	英语
WOS研究方向	Biochemistry & Molecular Biology ; Cell Biology
WOS类目	Biochemistry & Molecular Biology ; Cell Biology
WOS记录号	WOS:001030563000003
出版者	SPRINGER BASEL AG
WOS关键词	CHAIN FATTY-ACID ; CAENORHABDITIS-ELEGANS ; DIET ; INSULIN ; IDENTIFICATION ; BIOSYNTHESIS ; LONGEVITY ; EXTENSION ; PATHWAYS ; CIRCUIT
引用统计
文献类型	期刊论文
条目标识符	http://ir.qdio.ac.cn/handle/337002/182635
专题	实验海洋生物学重点实验室
通讯作者	Zhang, Liusuo
作者单位	1.Chinese Acad Sci, Inst Oceanol, CAS & Shandong Prov Key Lab Expt Marine Biol, Qingdao 266071, Peoples R China 2.Qingdao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao 266237, Peoples R China 3.Chinese Acad Sci, Ctr Ocean Mega Sci, 7 Nanhai Rd, Qingdao 266071, Peoples R China 4.Univ Chinese Acad Sci, Beijing 100049, Peoples R China 5.Texas A&M Univ, Dept Biol, College Stn, TX 77843 USA 6.Shandong Univ, Inst Marine Sci & Technol, 72 Binhai Rd, Qingdao 266237, Peoples R China
第一作者单位	中国科学院海洋研究所
通讯作者单位	中国科学院海洋研究所
推荐引用方式 GB/T 7714	Cao, Xuwen,Xie, Yusu,Yang, Hanwen,et al. EAT-2 attenuates C. elegans development via metabolic remodeling in a chemically defined food environment[J]. CELLULAR AND MOLECULAR LIFE SCIENCES,2023,80(8):18.
APA	Cao, Xuwen.,Xie, Yusu.,Yang, Hanwen.,Sun, Peiqi.,Xue, Beining.,...&Zhang, Liusuo.(2023).EAT-2 attenuates C. elegans development via metabolic remodeling in a chemically defined food environment.CELLULAR AND MOLECULAR LIFE SCIENCES,80(8),18.
MLA	Cao, Xuwen,et al."EAT-2 attenuates C. elegans development via metabolic remodeling in a chemically defined food environment".CELLULAR AND MOLECULAR LIFE SCIENCES 80.8(2023):18.