Suppression of abnormal morphology and extracytoplasmic function sigma activity in Bacillus subtilis ugtP mutant cells by expression of heterologous glucolipid synthases from Acholeplasma laidlawii.

Suppression of abnormal morphology and extracytoplasmic function sigma activity in Bacillus subtilis ugtP mutant cells by expression of heterologous glucolipid synthases from Acholeplasma laidlawii.
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通过表达莱氏无胆原体异源糖脂合酶来抑制枯草芽孢杆菌 ugtP 突变细胞中的异常形态和胞质外功能 sigma 活性。

DOI:
10.1080/09168451.2016.1217147
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发表时间:
2016
期刊:
Bioscience, Biotechnology, and Biochemistry
影响因子:
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通讯作者:
and Hiroshi Hara
and Hiroshi Hara
中科院分区:
--
文献类型:
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作者:
Satoshi Matsuoka;Takahiro Seki;Kouji Matsumoto;and Hiroshi Hara

文献摘要

相似文献

枯草杆菌中的糖脂是通过UgtP将葡萄糖从UDP-葡萄糖过程性地转移到二酰基甘油而合成的。在这里,我们得出结论,augtPmutant的异常形态是由缺乏糖脂引起的,因为同样的形态出现后,废除糖脂生产中断ofpgcA和gtaB,这是参与UDP-葡萄糖合成。相反,由来自莱氏无胆甾原体的1,2-二酰基甘油3-葡糖基转移酶(alMGS)产生的单葡糖基二酰基甘油(MGlcDG)的表达几乎完全抑制了ugtP破坏物表型。在ugtP突变体中,细胞质外功能(ECF)σ(SigM、SigV和SigX)的激活被alMGS表达降低,并且被MgSO4添加抑制到低水平。当alMGS和alDGS(A. Laidlawii 1,2-二酰基甘油-3-葡萄糖(1 - 2)-葡糖基转移酶产生二葡糖基二酰基甘油(DGlcDG))同时表达,SigX活化被抑制至野生型水平。这些观察结果表明,MGlcDG分子是维持B所必需的。枯草杆菌细胞形状和ECF σ的调节,DGlcDG调节SigX活性。
Glucolipids inBacillus subtilisare synthesized by UgtP processively transferring glucose from UDP-glucose to diacylglycerol. Here we conclude that the abnormal morphology of augtPmutant is caused by lack of glucolipids, since the same morphology arises after abolition of glucolipid production by disruption ofpgcAandgtaB,which are involved in UDP-glucose synthesis. Conversely, expression of a monoglucosyldiacylglycerol (MGlcDG) produced by 1,2-diacylglycerol 3-glucosyltransferase fromAcholeplasma laidlawii(alMGS) almost completely suppressed theugtPdisruptant phenotype. Activation of extracytoplasmic function (ECF) sigmas (SigM, SigV, and SigX) in theugtPmutant was decreased by alMGS expression, and was suppressed to low levels by MgSO4addition. When alMGS and alDGS (A. laidlawii1,2-diacylglycerol-3-glucose (1-2)-glucosyltransferase producing diglucosyldiacylglycerol (DGlcDG)) were simultaneously expressed, SigX activation was repressed to wild type level. These observations suggest that MGlcDG molecules are required for maintenance ofB. subtiliscell shape and regulation of ECF sigmas, and DGlcDG regulates SigX activity.