Читать книгу Snyder and Champness Molecular Genetics of Bacteria - Tina M. Henkin - Страница 97

In E. coli, three proteins called MinC, MinD, and MinE are known to be involved in localizing the division septum at the center of the cell. The min genes of E. coli were found because mutations in these genes can cause division septa to form in the wrong places, sometimes pinching off smaller cells called minicells. Apparently, in the absence of the Min proteins, division septa can form in places other than the middle of the cell. When this happens, smaller minicells that lack a chromosome are pinched off, hence the name Min proteins, for minicell-producing. It was predicted that the Min proteins would be localized in the ends of the E. coli cell, where they could prevent FtsZ from forming a division septum anywhere but the middle of the cell. However, when the localization of the Min proteins was studied using GFP fusions to the Min proteins, a very surprising result was revealed: the Min proteins oscillate from one pole of the cell to the other during the cell cycle. A model used to account for this finding held that oscillations of MinD and MinE drive the oscillation of MinC, which interacts with MinD (see MinCD in Figure 1.22) and is ultimately responsible for preventing FtsZ ring formation at the cell poles and enforcing the formation of a single FtsZ ring at mid-cell. The molecular mechanism that drives the redistribution of the proteins within the cell stems from the interaction of MinD (an ATPase) and MinE, which stimulates ATPase activity in MinD. MinD interacts with the membrane only in the ATP-bound state. More recent work with the system suggests that changes in the nature of MinD and MinE membrane-bound complexes and the states found in the cytoplasm are important for setting a distribution of these proteins (see Vecchiarelli et al., Suggested Reading). Ultimately, the concentration gradient set by the dynamic behavior of MinE and MinD sets a low concentration of MinCD at the center of the cell, allowing FtsZ to form a ring at the center of the cell.

Regulation of septum formation in B. subtilis differs from that found in E. coli. In B. subtilis, MinE is lacking and MinC and MinD do not oscillate. Instead, MinCD appears to tether directly to the cell poles by binding to another protein at the cell poles, called DivIVA. This binding creates a gradient of concentration of MinCD in the cell and similarly only allows formation of a single FtsZ ring at the center of the cell. Therefore, these two model bacteria use somewhat different mechanisms to establish a gradient of MinCD concentration and thereby restrict FtsZ ring formation to the center of the cell (Figure 1.22).