S-adenosyl methionine synthetase SAMS-5 mediates dietary restriction-induced longevity in Caenorhabditis elegans.

S-adenosyl methionine synthetase SAMS-5 mediates dietary restriction-induced longevity in Caenorhabditis elegans.
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DOI:
10.1371/journal.pone.0241455
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发表时间:
2020
期刊:
影响因子:
3.7
通讯作者:
Ching TT
Ching TT
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Chen CC;Lim CY;Lee PJ;Hsu AL;Ching TT

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s -腺苷甲硫氨酸合成酶(SAMS)催化s -腺苷甲硫氨酸(SAM)的生物合成,SAM是许多生化反应的通用甲基供体。先前的研究已经清楚地表明,与哺乳动物SAMS同源的秀丽隐杆线虫SAMS-1对饮食限制(DR)诱导的秀丽隐杆线虫长寿至关重要。除了SAMS-1外,在秀丽隐杆线虫中还发现了另外三个SAMS类似物。然而,它们在长寿调节中的作用从未被探索过。在这里,我们证明了sams-5的消耗,而不是sams-3或sams-4,可以延长蠕虫的寿命。然而,sams-5的表型和表达模式与sams-1不同,这表明这两种sams可能通过不同的机制调节dr诱导的长寿。通过遗传上位分析,我们已经确定了sams-5以pha-4/FOXA依赖的方式是dr诱导的长寿所必需的。
S-adenosyl methionine synthetase (SAMS) catalyzes the biosynthesis of S-adenosyl methionine (SAM), which serves as a universal methyl group donor for numerous biochemical reactions. Previous studies have clearly demonstrated that SAMS-1, a C. elegans homolog of mammalian SAMS, is critical for dietary restriction (DR)-induced longevity in Caenorhabditis elegans. In addition to SAMS-1, three other SAMS paralogs have been identified in C. elegans. However, their roles in longevity regulation have never been explored. Here, we show that depletion of sams-5, but not sams-3 or sams-4, can extend lifespan in worms. However, the phenotypes and expression pattern of sams-5 are distinct from sams-1, suggesting that these two SAMSs might regulate DR-induced longevity via different mechanisms. Through the genetic epistasis analysis, we have identified that sams-5 is required for DR-induced longevity in a pha-4/FOXA dependent manner.
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