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:
影响因子:
--
通讯作者:
and Hiroshi Hara
中科院分区:
文献类型:
--
作者:
Satoshi Matsuoka;Takahiro Seki;Kouji Matsumoto;and Hiroshi Hara
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.