A proteolytic pathway coordinates cell division and heterocyst differentiation in the cyanobacterium Anabaena sp. PCC 7120.
A proteolytic pathway coordinates cell division and heterocyst differentiation in the cyanobacterium Anabaena sp. PCC 7120.
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DOI:
10.1073/pnas.2207963119
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发表时间:
2022-09-06
影响因子:
11.1
通讯作者:
中科院分区:
文献类型:
--
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Protein degradation is an important regulation mechanism in biology. Although HetF has long been predicted to be a putative protease in the filamentous cyanobacterium Anabaena sp. PCC 7120, its activity or substrate has never been demonstrated. In this study, we provided in vitro and in vivo evidence for the protease activity of HetF acting on PatU3 as a specific substrate. The degradation of PatU3 by HetF relieves the inhibitory effects of PatU3 on cell division and heterocyst development, thus providing a mechanism for the coordination of the two biological processes. The proteolytic system reported here enriched our understanding on the control mechanism for cell division and development in cyanobacteria. The filamentous, multicellular cyanobacterium Anabaena sp. PCC 7120 (Anabaena) is a prokaryotic model for the study of cell differentiation and cell-cell interactions. Upon combined-nitrogen deprivation, Anabaena forms a particular cell type, heterocyst, for aerobic nitrogen fixation. Heterocysts are semiregularly spaced among vegetative cells. Heterocyst differentiation is coupled to cell division, but the underlying mechanism remains unclear. This mechanism could be mediated by the putative protease HetF, which is a divisome component and is necessary for heterocyst differentiation. In this study, by suppressor screening, we identified PatU3, as a negative regulator acting downstream of HetF for cell division and heterocyst development. The inactivation of patU3 restored the capacity of cell division and heterocyst differentiation in the ΔhetF mutant, and overexpression of patU3 inhibited both processes in the wild-type background. We demonstrated that PatU3 was a specific substrate of the protease activity of HetF. Consequently, PatU3 accumulated in the hetF-deficient mutant, which was responsible for the resultant mutant phenotype. The cleavage site of PatU3 by HetF was mapped after the Arg117 residue, whose mutation made PatU3 resistant to HetF processing, and mimicked the effect of hetF deletion. Our results provided evidence that HetF regulated cell division and heterocyst differentiation by controlling the inhibitory effects of PatU3. This proteolytic pathway constituted a mechanism for the coordination between cell division and differentiation in a prokaryotic model used for studies on developmental biology and multicellularity.
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影响因子:
2.9
作者:
Gorelova, O. A.;Baulina, O. I.;Koksharova, O. A.
通讯作者:
Koksharova, O. A.
DOI:
10.1073/pnas.1207530109
发表时间:
2012-09-18
影响因子:
11.1
作者:
Risser, Douglas D.;Wong, Francis C. Y.;Meeks, John C.
通讯作者:
Meeks, John C.
影响因子:
3.2
作者:
Du, Ye;Cai, Yan;Xu, Xudong
通讯作者:
Xu, Xudong
影响因子:
4.7
作者:
Niu, Tian-Cai;Lin, Gui-Ming;Zhang, Cheng-Cai
通讯作者:
Zhang, Cheng-Cai
影响因子:
4.2
作者:
Flaherty BL;Johnson DB;Golden JW
通讯作者:
Golden JW