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GRD-1/PTR-11,C. elegans的刺/补丁类形态原体受体对,调节了发育速度

Sinclair W Emans^1,2, Armen Yerevanian^1,3, Fasih M Ahsan^1,2

¹Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.

Development (Cambridge, England)

|November 20, 2023

概括

刺 (Hh) 途径组件grd-1和ptr-11在拉巴胺素复合体2 (TORC2) 突变的目标中拯救发育延迟. 这些发现揭示了Hh信号在调节生物体生长和发育中的新角色.

科学领域:

发展生物学发展生物学
分子信号通路分子信号通路
遗传学是一个遗传学.

背景情况:

刺 (Hh) 和拉巴胺素复合体2 (TORC2) 的标是进化保存的信号通路,对发育和新陈代谢至关重要.
在C. elegans (rict-1突变体) 中,TORC2功能丧失导致发育延迟,寿命缩短,体型缩小和脂肪积累增加.

研究的目的:

研究Hh和TORC2信号通路在调节发育速度中的相互作用.
为了确定参与TORC2-介导的生物生长控制的分子参与者.

主要方法:

基因淘汰的RNA干扰 (RNAi) (grd-1, ptr-11). 基因淘汰的RNA干扰 (RNAi) 在基因淘汰 (grd-1, ptr-11).
对Hh通路组件的过度表达研究 (grd-1, ptr-11).
对C. elegans的发育时间和生物体生长的分析.
使用遗传方法识别转录效应因子.

主要成果:

镇压与刺相关的形态原体grd-1及其受体ptr-11拯救了TORC2功能丧失突变体的延迟发育.
过度表达grd-1和ptr-11显著延迟了野生类型的发展,反映了TORC2功能丧失的表型.
转录因子pqm-1被确定为一个关键的效应因子,它调解了grd-1和ptr-11的增长减缓效应.

结论:

刺路径的grd-1和ptr-11组成部分在减缓发育速度方面发挥着意想不到的作用,可能是营养感应路径的下游.
TORC2,grd-1和ptr-11信号汇聚在转录因子pqm-1上,以调节生物体的发育和生长.
这项研究揭示了Hh信号和营养感应途径之间在控制发育时间方面的新联系.

关键词:

发展发展发展发展发展刺是一只刺.代谢过程中的代谢.修补补丁补丁补丁补丁在TOR复合体2 (TORC2) 中.拉帕米辛的目标 (TOR)

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