A cilia-independent function of BBSome mediated by DLK-MAPK signaling in C. elegans photosensation.
A cilia-independent function of BBSome mediated by DLK-MAPK signaling in C. elegans photosensation.
复制标题
DOI:
10.1016/j.devcel.2022.05.005
复制
发表时间:
2022-06-20
影响因子:
11.8
通讯作者:
Xu, X. Z. Shawn
中科院分区:
文献类型:
--
作者:
Zhang, Xinxing;Liu, Jinzhi;Pan, Tong;Ward, Alex;Liu, Jianfeng;Xu, X. Z. Shawn
Bardet-Biedl Syndrome (BBS) is a genetic disorder affecting primary cilia. BBSome, a protein complex composed of eight BBS proteins, regulates the structure and function of cilia, and its malfunction causes BBS in humans. Here, we report a cilia-indepedent function of BBSome. To identify genes regulating the C. elegans photoreceptor protein LITE-1 in ciliated ASH photosensory neurons, we performed a genetic screen and isolated bbs mutants. Functional analysis revealed that BBSome regulates LITE-1 protein stability independently of cilia. Through another round of genetic screen, we found that this cilia-independent function of BBSome is mediated by DLK MAPK signaling, which acts downstream of BBSome to control LITE-1 stability via Rab5-mediated endocytosis. BBSome exerts its function by regulating the expression of DLK. BBSome also regulates the expression of LZK, a mammalian DLK in human cells. These studies identify a cilia-independent function of BBSome and uncover DLK as an evolutionarily conserved BBSome effector. The BBSome complex is best known for its role in maintaining the function and structure of cilia. Zhang, Liu et al. report a cilia-independent role for the BBSome. They show that the BBSome regulates the stability of the C. elegans photoreceptor protein LITE-1 through DLK MAPK signaling.
登录
查看更多内容
影响因子:
9.8
作者:
Lee BH;Liu J;Wong D;Srinivasan S;Ashrafi K
通讯作者:
Ashrafi K
影响因子:
4.5
作者:
Cornils A;Maurya AK;Tereshko L;Kennedy J;Brear AG;Prahlad V;Blacque OE;Sengupta P
通讯作者:
Sengupta P
影响因子:
--
作者:
Ghanta KS;Ishidate T;Mello CC
通讯作者:
Mello CC
影响因子:
3.7
作者:
Doitsidou M;Poole RJ;Sarin S;Bigelow H;Hobert O
通讯作者:
Hobert O
影响因子:
16.2
作者:
Coburn, CM;Bargmann, CI
通讯作者:
Bargmann, CI