Shin Dongwoo, Cho Namwook, Kim You-Jin, Seok Yeong-Jae, Ryu Sangryeol
Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon 440-746, Republic of Korea.
Biochem Biophys Res Commun. 2008 Jun 13;370(4):609-12. doi: 10.1016/j.bbrc.2008.03.145. Epub 2008 Apr 8.
When Escherichia coli cells were grown with limited levels of oxygen, the glucose-induced transcription of ptsG was decreased whereas deletion of the arcA gene partially restored it, which was consistent with the previous report that the ArcA protein represses ptsG transcription. However, under this circumstance, we found that the level of EIICB(Glc) protein encoded by the ptsG gene was rather increased. This paradoxical phenomenon can be explained by the delayed turnover of ptsG mRNA in cells anaerobically grown in the presence of glucose. Finally, our data showed that anaerobic expression of the ptsHIcrr operon is also enhanced by increasing the longevity of the reduced mRNA levels.
当大肠杆菌细胞在有限的氧气水平下生长时,葡萄糖诱导的ptsG转录会降低,而arcA基因的缺失会部分恢复这种转录,这与之前关于ArcA蛋白抑制ptsG转录的报道一致。然而,在这种情况下,我们发现ptsG基因编码的EIICB(Glc)蛋白水平反而增加了。这种矛盾的现象可以通过在葡萄糖存在下厌氧生长的细胞中ptsG mRNA周转延迟来解释。最后,我们的数据表明,通过延长还原mRNA水平的寿命,ptsHIcrr操纵子的厌氧表达也会增强。