Yu X C, Margolin W
Department of Microbiology and Molecular Genetics, University of Texas-Houston Medical School, Houston, Texas 77030, USA.
J Bacteriol. 2000 Nov;182(21):6203-13. doi: 10.1128/JB.182.21.6203-6213.2000.
To investigate the interaction between FtsZ and the Min system during cell division of Escherichia coli, we examined the effects of combining a well-known thermosensitive mutation of ftsZ, ftsZ84, with DeltaminCDE, a deletion of the entire min locus. Because the Min system is thought to down-regulate Z-ring assembly, the prediction was that removing minCDE might at least partially suppress the thermosensitivity of ftsZ84, which can form colonies below 42 degrees C but not at or above 42 degrees C. Contrary to expectations, the double mutant was significantly more thermosensitive than the ftsZ84 single mutant. When shifted to the new lower nonpermissive temperature, the double mutant formed long filaments mostly devoid of Z rings, suggesting a likely cause of the increased thermosensitivity. Interestingly, even at 22 degrees C, many Z rings were missing in the double mutant, and the rings that were present were predominantly at the cell poles. Of these, a large number were present only at one pole. These cells exhibited a higher than expected incidence of polar divisions, with a bias toward the newest pole. Moreover, some cells exhibited dramatically elongated septa that stained for FtsZ, suggesting that the double mutant is defective in Z-ring disassembly, and providing a possible mechanism for the polar bias. Thermoresistant suppressors of the double mutant arose that had modestly increased levels of FtsZ84. These cells also exhibited elongated septa and, in addition, produced a high frequency of branched cells. A thermoresistant suppressor of the ftsZ84 single mutant also synthesized more FtsZ84 and produced branched cells. The evidence from this study indicates that removing the Min system exposes and exacerbates the inherent defects of the FtsZ84 protein, resulting in clear septation phenotypes even at low growth temperatures. Increasing levels of FtsZ84 can suppress some, but not all, of these phenotypes.
为了研究大肠杆菌细胞分裂过程中FtsZ与Min系统之间的相互作用，我们检测了ftsZ一个著名的温度敏感突变体ftsZ84与整个min基因座缺失的ΔminCDE相结合的效果。由于Min系统被认为会下调Z环组装，因此预测是去除minCDE可能至少部分抑制ftsZ84的温度敏感性，ftsZ84在42℃以下能形成菌落，但在42℃及以上则不能。与预期相反，双突变体比ftsZ84单突变体对温度更敏感。当转移到新的更低的非允许温度时，双突变体形成了大多没有Z环的长丝，这表明温度敏感性增加的一个可能原因。有趣的是，即使在22℃时，双突变体中也有许多Z环缺失，并且存在的环主要位于细胞两极。其中，大量环仅存在于一个极。这些细胞表现出比预期更高的极向分裂发生率，且偏向于最新的极。此外，一些细胞表现出显著伸长的、被FtsZ染色的隔膜，这表明双突变体在Z环解体方面存在缺陷，并为极向偏向提供了一种可能的机制。双突变体产生了耐热抑制子，其FtsZ84水平适度增加。这些细胞也表现出伸长的隔膜，此外，还产生了高频率的分支细胞。ftsZ84单突变体的一个耐热抑制子也合成了更多的FtsZ84并产生了分支细胞。这项研究的证据表明，去除Min系统会暴露并加剧FtsZ84蛋白的固有缺陷，即使在低生长温度下也会导致明显的隔膜形成表型。增加FtsZ84的水平可以抑制其中一些但不是所有这些表型。
