Germ-cell loss extends C-elegans life span through regulation of DAF-16 by kri-1 and lipophilic-hormone signaling
Germ-cell loss extends C-elegans life span through regulation of DAF-16 by kri-1 and lipophilic-hormone signaling
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DOI：
10.1016/j.cell.2006.01.039
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发表时间：
2006-03-10
期刊：
影响因子：
64.5
通讯作者：
Kenyon, C
中科院分区：
文献类型：
--
作者：
Berman, JR;Kenyon, C
In C.在线虫中，去除生殖细胞通过触发肠中的转录因子的核定位和激活来延长寿命。在这项研究中，我们确定并分析了生殖细胞去除所需的基因，以延长寿命。我们发现，生殖系统通过亲脂激素信号与肠道进行交流，一种名为kri-1的基因可能在肠道中起作用，以响应这种信号，促进nitro-16的核定位。在胰岛素/IGF-1信号转导减少的动物中，这种亲脂信号通路和kri-1对于α-16的核定位和寿命延长并不是必需的。因此，这种途径特别能够整合来自生殖系统的线索与中枢β-16激活途径，以影响动物的衰老。
In C. elegans, removing the germ cells extends life span by triggering the nuclear localization and activation of the DAF-16/FOXO transcription factor in the intestine. In this study, we identify and analyze genes required for germline removal to extend life span. We find that the reproductive system communicates with the intestine through lipophilic-hormone signaling and that a gene called kri-1 is likely to act in the intestine to promote DAF-16 nuclear localization in response to this signal. This lipophilic-signaling pathway and kri-1 are not required for DAF-16's nuclear localization and life-span extension in animals with decreased insulin/IGF-1 signaling. Thus, this pathway specifically enables the integration of cues from the reproductive system with central DAF-16-activation pathways to influence the aging of the animal.