Tétart F, Bouché J P
Centre de Recherche de Biochime et de Génétique Cellulaires du CNRS, Toulouse, France.
Mol Microbiol. 1992 Mar;6(5):615-20. doi: 10.1111/j.1365-2958.1992.tb01508.x.
We show that the 53-nucleotide RNA molecule encoded by gene dicF blocks cell division in Escherichia coli by inhibiting the translation of ftsZ mRNA. Such a role for dicF had been predicted on the basis of the complementarity of DicF RNA with the ribosome-binding region of the ftsZ mRNA. An analysis of ftsZ expression at its chromosomal locus, and of an ftsZ-lacZ translational fusion controlled by promoters ftsZ1p and ftsZ2p only, indicates that ftsZ is not autoregulated. Partial inhibition of FtsZ synthesis leads to increased cell size. However, the number of FtsZ molecules per cell can be reduced threefold without affecting the division rate significantly. Our results suggest that septation is not triggered by a fixed number of newly synthesized FtsZ molecules per cell.
我们发现,基因dicF编码的53个核苷酸的RNA分子通过抑制ftsZ mRNA的翻译来阻断大肠杆菌中的细胞分裂。基于DicF RNA与ftsZ mRNA核糖体结合区域的互补性,曾预测过dicF具有这样的作用。对ftsZ在其染色体位点的表达,以及仅由启动子ftsZ1p和ftsZ2p控制的ftsZ-lacZ翻译融合体的分析表明,ftsZ不受自身调控。对FtsZ合成的部分抑制会导致细胞尺寸增大。然而,每个细胞中FtsZ分子的数量可以减少三倍,而不会显著影响分裂速率。我们的结果表明,细胞分裂不是由每个细胞中固定数量的新合成FtsZ分子触发的。