Lamin regulates the dietary restriction response via the mTOR pathway in Caenorhabditis elegans

被引:4
|
作者
Charar, Chayki [1 ,2 ]
Metsuyanim-Cohen, Sally [1 ]
Bar, Daniel Z. [1 ]
机构
[1] Tel Aviv Univ, Fac Med, Sch Dent Med, IL-69978 Tel Aviv, Israel
[2] Hebrew Univ Jerusalem, Alexander Silberman Inst Life Sci, IL-9190401 Jerusalem, Israel
关键词
Caenorhabditis elegans; Lamin; Dietary restriction; mTOR; GILFORD PROGERIA SYNDROME; C; ELEGANS; NUCLEAR LAMINA; LIFE-SPAN; LOCALIZATION; ACCUMULATION; ARCHITECTURE; LONGEVITY; GROWTH; ACID;
D O I
10.1242/jcs.258428
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Animals subjected to dietary restriction (DR) have reduced body size, low fecundity, slower development, lower fat content and longer life span. We identified lamin as a regulator of multiple dietary restriction phenotypes. Downregulation of lmn-1, the single Caenorhabditis elegans lamin gene, increased animal size and fat content specifically in DR animals. The LMN-1 protein acts in the mTOR pathway, upstream of RAPTOR and S6 kinase beta 1 (S6K), a key component of and target of the mechanistic target of rapamycin (mTOR) complex 1 (mTORC1), respectively. DR excludes the mTORC1 activator RAGC-1 from the nucleus. Downregulation of lmn-1 restores RAGC-1 to the nucleus, a necessary step for the activation of the mTOR pathway. These findings further link lamin to metabolic regulation.
引用
收藏
页数:12
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