Spermidine promotes Bacillus subtilis biofilm formation by activating expression of the matrix regulator slrR.
Spermidine promotes Bacillus subtilis biofilm formation by activating expression of the matrix regulator slrR.
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DOI：
10.1074/jbc.m117.789644
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发表时间：
2017-07-21
期刊：
影响因子：
--
通讯作者：
Michael AJ
中科院分区：
文献类型：
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作者：
Hobley L;Li B;Wood JL;Kim SH;Naidoo J;Ferreira AS;Khomutov M;Khomutov A;Stanley-Wall NR;Michael AJ
普遍存在的多胺亚精胺不是枯草芽孢杆菌正常生长所必需的，但对于生物膜的形成是必需的。然而，亚精胺所需的结构特征为B。枯草芽孢杆菌生物膜形成是未知的，所以是亚精胺刺激的生物膜发展的分子机制。我们在这里报告，在一个精胺缺乏B。枯草杆菌突变体，结构类似物去甲亚精胺，但不是homospermidine，恢复生物膜形成。细胞内生物合成的另一个亚精胺类似物，氨丙基尸胺，从外源性高胍丁胺也恢复生物膜的形成。C-甲基化的亚精胺类似物在生物膜形成中功能性地替代亚精胺的差异能力表明亚精胺的氨丙基部分对C-甲基化更敏感，这对于生物膜形成是必不可少的，但是分子的长度和对称性不是关键的。精脒缺失B的转录组学分析。枯草芽孢杆菌speD突变体揭示了氮，甲硫氨酸，和S-腺苷甲硫氨酸-充足的反应，导致抑制基因表达相关的嘌呤catenase，甲硫氨酸和S-腺苷甲硫氨酸生物合成和甲硫氨酸补救，和改变膜状态的迹象。与生物膜形成中的亚精胺需求一致，对该突变体的单细胞分析表明，用于产生外多糖和TasA蛋白生物膜基质成分以及SinR拮抗剂slrR的操纵子的表达减少。在亚精胺缺乏的ΔspeD背景下，sinR的缺失或slrR的异位表达恢复了生物膜的形成，表明亚精胺是生物膜调节因子slrR表达所必需的。我们的研究结果表明，亚精胺的功能，通过激活转录的生物膜基质胞外多糖和TasA操纵子通过调节slrR的生物膜的发展。
Ubiquitous polyamine spermidine is not required for normal planktonic growth of Bacillus subtilis but is essential for robust biofilm formation. However, the structural features of spermidine required for B. subtilis biofilm formation are unknown and so are the molecular mechanisms of spermidine-stimulated biofilm development. We report here that in a spermidine-deficient B. subtilis mutant, the structural analogue norspermidine, but not homospermidine, restored biofilm formation. Intracellular biosynthesis of another spermidine analogue, aminopropylcadaverine, from exogenously supplied homoagmatine also restored biofilm formation. The differential ability of C-methylated spermidine analogues to functionally replace spermidine in biofilm formation indicated that the aminopropyl moiety of spermidine is more sensitive to C-methylation, which it is essential for biofilm formation, but that the length and symmetry of the molecule is not critical. Transcriptomic analysis of a spermidine-depleted B. subtilis speD mutant uncovered a nitrogen-, methionine-, and S-adenosylmethionine-sufficiency response, resulting in repression of gene expression related to purine catabolism, methionine and S-adenosylmethionine biosynthesis and methionine salvage, and signs of altered membrane status. Consistent with the spermidine requirement in biofilm formation, single-cell analysis of this mutant indicated reduced expression of the operons for production of the exopolysaccharide and TasA protein biofilm matrix components and SinR antagonist slrR. Deletion of sinR or ectopic expression of slrR in the spermidine-deficient ΔspeD background restored biofilm formation, indicating that spermidine is required for expression of the biofilm regulator slrR. Our results indicate that spermidine functions in biofilm development by activating transcription of the biofilm matrix exopolysaccharide and TasA operons through the regulator slrR.