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HetL、HetR 和 PatS 形成一个反应扩散系统,以控制蓝藻 PCC 7120 中的模式形成。

HetL, HetR and PatS form a reaction-diffusion system to control pattern formation in the cyanobacterium PCC 7120.

机构信息

Aix Marseille Univ, CNRS, LCB, Laboratoire de Chimie Bactérienne, Marseille, France.

Aix Marseille Univ, CNRS, Protein Expression Facility, Institut de Microbiologie de la Méditerranée, Marseille, France.

出版信息

Elife. 2020 Aug 7;9:e59190. doi: 10.7554/eLife.59190.

DOI:10.7554/eLife.59190
PMID:32762845
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7476756/
Abstract

Local activation and long-range inhibition are mechanisms conserved in self-organizing systems leading to biological patterns. A number of them involve the production by the developing cell of an inhibitory morphogen, but how this cell becomes immune to self-inhibition is rather unknown. Under combined nitrogen starvation, the multicellular cyanobacterium PCC 7120 develops nitrogen-fixing heterocysts with a pattern of one heterocyst every 10-12 vegetative cells. Cell differentiation is regulated by HetR which activates the synthesis of its own inhibitory morphogens, diffusion of which establishes the differentiation pattern. Here, we show that HetR interacts with HetL at the same interface as PatS, and that this interaction is necessary to suppress inhibition and to differentiate heterocysts. expression is induced under nitrogen-starvation and is activated by HetR, suggesting that HetL provides immunity to the heterocyst. This protective mechanism might be conserved in other differentiating cyanobacteria as HetL homologues are spread across the phylum.

摘要

局部激活和远程抑制是自组织系统中保守的机制,导致生物模式的形成。其中有一些涉及到发育细胞产生抑制性形态发生因子,但细胞如何对自身抑制产生免疫仍不得而知。在氮饥饿条件下,多细胞蓝藻 PCC 7120 形成具有每 10-12 个营养细胞一个异形胞的模式的固氮异形胞。细胞分化受 HetR 调控,HetR 激活其自身抑制性形态发生因子的合成,其扩散建立了分化模式。在这里,我们表明 HetR 在与 PatS 相同的界面上与 HetL 相互作用,并且这种相互作用对于抑制和分化异形胞是必要的。在氮饥饿下诱导表达,并被 HetR 激活,表明 HetL 提供了异形胞的免疫。这种保护机制可能在其他分化蓝藻中保守,因为 HetL 同源物在门内广泛存在。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1545/7476756/9e405aca8fc4/elife-59190-fig7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1545/7476756/9e405aca8fc4/elife-59190-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1545/7476756/7bfcaa184822/elife-59190-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1545/7476756/df86a03fb46e/elife-59190-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1545/7476756/2e4433f67f35/elife-59190-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1545/7476756/5e615336057c/elife-59190-fig2-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1545/7476756/0f1a3579a77a/elife-59190-fig2-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1545/7476756/86c23ae6ed5e/elife-59190-fig2-figsupp3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1545/7476756/171d01b6568a/elife-59190-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1545/7476756/9e633b62a067/elife-59190-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1545/7476756/70f753a40259/elife-59190-fig4-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1545/7476756/c3a26ce3408b/elife-59190-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1545/7476756/071ac76801c4/elife-59190-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1545/7476756/9e405aca8fc4/elife-59190-fig7.jpg

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