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渗透压可调控枯草芽孢杆菌基质基因表达。

Osmotic pressure can regulate matrix gene expression in Bacillus subtilis.

机构信息

Departments of Physics and Harvard School of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138, USA.

出版信息

Mol Microbiol. 2012 Oct;86(2):426-36. doi: 10.1111/j.1365-2958.2012.08201.x. Epub 2012 Sep 7.

DOI:10.1111/j.1365-2958.2012.08201.x
PMID:22882172
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3828655/
Abstract

Many bacteria organize themselves into structurally complex communities known as biofilms in which the cells are held together by an extracellular matrix. In general, the amount of extracellular matrix is related to the robustness of the biofilm. Yet, the specific signals that regulate the synthesis of matrix remain poorly understood. Here we show that the matrix itself can be a cue that regulates the expression of the genes involved in matrix synthesis in Bacillus subtilis. The presence of the exopolysaccharide component of the matrix causes an increase in osmotic pressure that leads to an inhibition of matrix gene expression. We further show that non-specific changes in osmotic pressure also inhibit matrix gene expression and do so by activating the histidine kinase KinD. KinD, in turn, directs the phosphorylation of the master regulatory protein Spo0A, which at high levels represses matrix gene expression. Sensing a physical cue such as osmotic pressure, in addition to chemical cues, could be a strategy to non-specifically co-ordinate the behaviour of cells in communities composed of many different species.

摘要

许多细菌会组织成结构复杂的群落,称为生物膜,其中细胞由细胞外基质结合在一起。通常,细胞外基质的数量与生物膜的坚固程度有关。然而,调节基质合成的特定信号仍然知之甚少。在这里,我们表明基质本身可以作为一种信号,调节枯草芽孢杆菌中参与基质合成的基因的表达。基质的胞外多糖成分的存在会导致渗透压增加,从而抑制基质基因的表达。我们进一步表明,渗透压的非特异性变化也会抑制基质基因的表达,其方式是激活组氨酸激酶 KinD。KinD 反过来又指导主调控蛋白 Spo0A 的磷酸化,高水平的 Spo0A 抑制基质基因的表达。除了化学信号外,感应物理信号(如渗透压)可能是一种策略,可以非特异性地协调由许多不同物种组成的群落中细胞的行为。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/450843269d60/nihms401672f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/a4392d23c32e/nihms401672f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/ec3be9fc0098/nihms401672f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/e08cb5ec7f91/nihms401672f6.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/ea429010d1f4/nihms401672f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/450843269d60/nihms401672f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/a4392d23c32e/nihms401672f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/6d8452673e71/nihms401672f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/df9c68c087d6/nihms401672f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/084968a5ed04/nihms401672f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/ec3be9fc0098/nihms401672f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/e08cb5ec7f91/nihms401672f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/778f94ca51d3/nihms401672f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/ea429010d1f4/nihms401672f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec4/3828655/450843269d60/nihms401672f9.jpg

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