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

机译:Het1Hetr和PATS形成反应扩散系统以控制蓝蓝杆菌PCC 7120的图案形成

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摘要

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 Nostoc 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. hetL 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.
机译:局部激活和远程抑制是在导致生物模式的自组织系统中保守的机制。其中许多涉及通过抑制形态学的显影细胞的产生,但这种细胞如何对自我抑制的影响是相当熟知的。在组合氮饥饿下,多细胞骨杆菌PCC 7120通过每10-12个营养细胞的一种杂环的图案显影氮固定杂物。细胞分化由HETH调节,其激活其自身抑制变形的合成,其扩散建立了分化模式。在这里,我们表明HETL在与PATS相同的界面处与HETL相互作用,并且该相互作用是抑制抑制和分化杂物的必要条件。在氮饥饿下诱导Het1表达,并通过HetR激活,表明Het1为杂环提供免疫。这种保护机制可能在其他区分的蓝细菌中保存,因为Het1同源物涂抹在门外。

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