Biomedical subjects

E Bi

Publications and source records attributed to E Bi.

21 records · Page 2Linked to original sources

PubMed1990

FtsZ regulates frequency of cell division in Escherichia coli.

Cell division is regulated so that it occurs only once per cell cycle. In Escherichia coli, a rod-shaped bacterium, division normally takes place at the center of the long axis of the cell; however, in the minicell mutant, division can also take place at the cell pole. Such divisions take place at the expense of normal divisions, resulting in an overall increase in nucleated cell length. We report here that increasing the level of FtsZ can completely suppress the cell length of the minicell mutant by increasing the frequency at which cell division events take place. This result suggests that the level of FtsZ controls the frequency of cell division in E. coli.

Bacterial Proteins↗

PubMedDate not supplied

FtsZ and cell division.

The ftsZ gene in Escherichia coli is thought to be an essential gene and to play a pivotal role in cell division. Gene disruption experiments confirmed that ftsZ is an essential gene. Examination of cellular responses to FtsZ depletion indicated that FtsZ was required for division but not for nucleoid segregation. Analysis of mutations within the ftsZ, gene, selected for resistance to the cell division inhibitor SulA, revealed that they also conferred resistance to MinCD. This raises the possibility that ftsZ is the target of these two cell division inhibitors. Analysis of the ftsZ gene from Bacillus subtilis revealed that the gene was required for both septation during vegetative growth and asymmetric septation during sporulation.

Bacillus subtilis↗

PubMedDate not supplied

Cyk3, a novel SH3-domain protein, affects cytokinesis in yeast.

Cytokinesis requires the wholesale reorganization of the cytoskeleton and secretion to complete the division of one cell into two. In the budding yeast Saccharomyces cerevisiae, the IQGAP-related protein Iqg1 (Cyk1) promotes cytokinetic actin ring formation and is required for cytokinesis and viability [1-3]. As the actin ring is not essential for cytokinesis or viability, Iqg1 must act by another mechanism [4]. To uncover this mechanism, a screen for high-copy suppressors of the iqg1 lethal phenotype was performed. CYK3 suppressed the requirement for IQG1 in viability and cytokinesis without restoration of the actin ring, demonstrating that CYK3 promotes cytokinesis through an actomyosin-ring-independent pathway. CYK3 encodes a novel SH3-domain protein that was found in association with the actin ring and the mother-bud neck. cyk3 null cells had misshapen mother-bud necks and were deficient in cytokinesis. In the cyk3 null strain, actin rearrangements associated with cytokinesis appeared normal, suggesting that the phenotype reflects a defect in secretory targeting or septal synthesis. Deletion of either cyk3 or hof1 alone results in a mild cytokinetic phenotype [5-7], but deletion of both genes resulted in lethality and a complete cytokinetic block, suggesting overlapping function. Thus, Cyk3 appears to be important for cytokinesis and acts potentially downstream of Iqg1.

Amino Acid Sequence↗