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Onset of sporulation – (Stage I - II) |
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3.Onset of sporulation – (Stage I - II)
During growth and proliferation, bacterial rod-shaped cells divide by a process called medial cell division. In general this encompasses the formation of a central ring composed of the filamentous FtsZ protein (also referred to as a Z-ring). This ring marks the division site that is essential for the recruitment of other proteins that are involved in septum formation. The septum will eventually divide the cell into two similar-sized daughter cells. Two inhibitory systems have been identified that play a key role in ensuring medial Z-ring formation (extensively reviewed in 65). One of these, the MinCDE complex, localizes to the cell poles and prevents polar Z-ring formation. When cells accumulate the required threshold level of Spo0A~P, this protein together with σH initiates a commitment to sporulation by activating or enhancing transcription of genes that promote chromosome elongation and asymmetric cell division. Furthermore, transcription of the spoIIA operon results in the appearance of sporulation-specific sigma factor σF and its regulators, which are essential for further successful development of the forespore 66.
Axial filamentation
At the onset of sporulation, two chromosomes elongate along the long axis of the cell. This structure, the axial filament 67, allows for movement of both chromosomes to the poles of the cell at their origin of replication region68. In contrast to equal separation during medial cell division, the formation of an asymmetric septum upon sporulation crosses one of the two chromosomes. This leads to an uneven distribution of DNA between the two cellular parts that are formed. For more extensive information about chromosome segregation and important factors involved, see a recent review by Jeff Errington 69.
Asymmetric cell division – the roles of RacA and SpoIIE
One of the earliest visible signs of the cell's commitment to sporulation, is the formation of an asymmetric septum dividing the cell into two unequal parts. This deviant form of cell division is mediated by the competitive action of RacA that displaces MinCD from the cell poles 70. This eliminates the inhibitory effect of MinCD and allows for the formation of two polar Z-rings caused by increased levels of FtsZ and another protein called SpoIIE 71. SpoIIE plays two essential roles in the sporulation process, one of which being interaction with FtsZ and subsequent shifting of the central Z-ring formation towards the poles. The other role involves activation of pro-σF, which is discussed in the COMMITMENT state.
For yet unknown reasons, the formation of an asymmetric septum at the two polar division sites by accumulation of peptidoglycan layers is temporally unequal between both sites. This results in only one of the Z-rings to eventually form the asymmetric septum (reviewed in 72). Bipolar septum formation is later prevented by the expression of a set of mother cell-specific genes including spoIID, spoIIM, and spoIIP. Their protein products are involved in the degradation of the peptidoglycan layer of the developing septum at the forespore-distal pole 73 and furthermore play an important role during the sporulation stage of commitment 74. Interestingly, the expression of these genes depends on the activation of mother cell-specific σE, which in turn depends on the activity of forespore-specific σF. However, release of σF does not occur until after the asymmetric septum is formed (also see the COMMITMENT state) as it depends on the localization of SpoIIE to this division site. This tightly regulated system ensures the completion of asymmetric septum formation before sporulation can proceed, which lays the basis for compartmental gene expression and prevents the formation of another septum.