Shin Sang-Min, Song Sung-Hyun, Lee Jin-Woo, Kwak Min-Kyu, Kang Sa-Ouk
Laboratory of Biophysics, School of Biological Sciences, and Institute of Microbiology, Seoul National University, Seoul 151-742, Republic of Korea.
Laboratory of Biophysics, School of Biological Sciences, and Institute of Microbiology, Seoul National University, Seoul 151-742, Republic of Korea.
Int J Biochem Cell Biol. 2017 Oct;91(Pt A):14-28. doi: 10.1016/j.biocel.2017.08.005. Epub 2017 Aug 12.
Methylglyoxal regulates cell division and differentiation through its interaction with polyamines. Loss of their biosynthesizing enzyme causes physiological impairment and cell elongation in eukaryotes. However, the reciprocal effects of methylglyoxal and polyamine production and its regulatory metabolic switches on morphological changes in prokaryotes have not been addressed. Here, Bacillus subtilis methylglyoxal synthase (mgsA) and polyamine biosynthesizing genes encoding arginine decarboxylase (SpeA), agmatinase (SpeB), and spermidine synthase (SpeE), were disrupted or overexpressed. Treatment of 0.2mM methylglyoxal and 1mM spermidine led to the elongation and shortening of B. subtilis wild-type cells to 12.38±3.21μm (P<0.05) and 3.24±0.73μm (P<0.01), respectively, compared to untreated cells (5.72±0.68μm). mgsA-deficient (mgsA) and -overexpressing (mgsA) mutants also demonstrated cell shortening and elongation, similar to speB- and speE-deficient (speB and speE) and -overexpressing (speB and speE) mutants. Importantly, both mgsA-depleted speB and speE mutants (speB/mgsA and speE/mgsA) were drastically shortened to 24.5% and 23.8% of parental speB and speE mutants, respectively. These phenotypes were associated with reciprocal alterations of mgsA and polyamine transcripts governed by the contents of methylglyoxal and spermidine, which are involved in enzymatic or genetic metabolite-control mechanisms. Additionally, biophysically detected methylglyoxal-spermidine Schiff bases did not affect morphogenesis. Taken together, the findings indicate that methylglyoxal triggers cell elongation. Furthermore, cells with methylglyoxal accumulation commonly exhibit an elongated rod-shaped morphology through upregulation of mgsA, polyamine genes, and the global regulator spx, as well as repression of the cell division and shape regulator, FtsZ.
甲基乙二醛通过与多胺相互作用来调节细胞分裂和分化。其生物合成酶的缺失会导致真核生物出现生理损伤和细胞伸长。然而，甲基乙二醛和多胺产生的相互作用及其调节性代谢开关对原核生物形态变化的影响尚未得到研究。在此，枯草芽孢杆菌的甲基乙二醛合酶（mgsA）以及编码精氨酸脱羧酶（SpeA）、胍丁胺酶（SpeB）和亚精胺合酶（SpeE）的多胺生物合成基因被破坏或过表达。与未处理的细胞（5.72±0.68μm）相比，用0.2mM甲基乙二醛和1mM亚精胺处理导致枯草芽孢杆菌野生型细胞分别伸长至12.38±3.21μm（P<0.05）和缩短至3.24±0.73μm（P<0.01）。mgsA缺陷型（mgsA）和过表达型（mgsA）突变体也表现出细胞缩短和伸长，类似于speB和speE缺陷型（speB和speE）以及过表达型（speB和speE）突变体。重要的是，mgsA缺失的speB和speE突变体（speB/mgsA和speE/mgsA）分别大幅缩短至亲本speB和speE突变体的24.5%和23.8%。这些表型与受甲基乙二醛和亚精胺含量控制的mgsA和多胺转录本的相互改变有关，这些改变涉及酶促或遗传代谢物控制机制。此外，生物物理检测到的甲基乙二醛 - 亚精胺席夫碱不影响形态发生。综上所述，这些发现表明甲基乙二醛会引发细胞伸长。此外，甲基乙二醛积累的细胞通常通过上调mgsA、多胺基因和全局调节因子spx，以及抑制细胞分裂和形状调节因子FtsZ，呈现出细长的杆状形态。
