Essential role of the endocytic site-associated protein Ecm25 in stress-induced cell elongation.
Essential role of the endocytic site-associated protein Ecm25 in stress-induced cell elongation.
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内吞位点相关蛋白 Ecm25 在应激诱导的细胞伸长中的重要作用
DOI:
10.1016/j.celrep.2021.109122
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发表时间:
2021-05-18
期刊:
影响因子:
8.8
通讯作者:
Bi E
中科院分区:
文献类型:
--
作者:
Duan X;Chen X;Wang K;Chen L;Glomb O;Johnsson N;Feng L;Zhou XQ;Bi E
How cells adopt a different morphology to cope with stress is not well understood. Here, we show that budding yeast Ecm25 associates with polarized endocytic sites and interacts with the polarity regulator Cdc42 and several late-stage endocytic proteins via distinct regions, including an actin filament-binding motif. Deletion of ECM25 does not affect Cdc42 activity or cause any strong defects in fluid-phase and clathrin-mediated endocytosis but completely abolishes hydroxyurea-induced cell elongation. This phenotype is accompanied by depolarization of the spatiotemporally coupled exo-endocytosis in the bud cortex while maintaining the overall mother-bud polarity. These data suggest that Ecm25 provides an essential link between the polarization signal and the endocytic machinery to enable adaptive morphogenesis under stress conditions. How cells adopt a different morphology to cope with stress is not well understood. Duan et al. report that the budding yeast protein Ecm25 plays an essential role in stress-induced cell elongation by linking the polarity regulator Cdc42 to the late-stage endocytic machinery.
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DOI:
10.1083/jcb.143.3.709
发表时间:
1998-11-02
期刊:
The Journal of cell biology
影响因子:
--
作者:
Carroll CW;Altman R;Schieltz D;Yates JR;Kellogg D
通讯作者:
Kellogg D
影响因子:
3.3
作者:
Dewar, H;Warren, DT;Ayscough, KR
通讯作者:
Ayscough, KR
影响因子:
10.5
作者:
Chen, GC;Kim, YJ;Chan, CSM
通讯作者:
Chan, CSM
DOI:
10.1083/jcb.200605080
发表时间:
2006-12-04
期刊:
The Journal of cell biology
影响因子:
--
作者:
Enserink JM;Smolka MB;Zhou H;Kolodner RD
通讯作者:
Kolodner RD
DOI:
10.1099/13500872-142-6-1391
发表时间:
1996-06-01
期刊:
MICROBIOLOGY-UK
影响因子:
--
作者:
Dickinson, JR
通讯作者:
Dickinson, JR