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Title: Role of MinD and related proteins in chromosome partitioning in Bacillus subtilis during sporulation
Author: Lenarcic, Rok
Awarding Body: Newcastle University
Current Institution: University of Newcastle upon Tyne
Date of Award: 2011
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Abstract:
When conditions for growth are unfavourable, cells of Bacillus subtilis are able to enter sporulation cycle which leads to formation of highly resistant spores; dormant form of the organism that is able to survive harsh conditions and can germinate when environmental conditions are favourable for growth again. Asymmetric division in the early stages of sporulation divides the sporulating cell into 2 unequal compartments; the bigger mother cell and the smaller prespore. Asymmetric septation also results in asymmetric chromosome distribution, with the prespore containing only about 30% of one chromosome at completion of septation, and the mother cell containing the rest of this chromosome plus one intact one. Although the programs of gene expression in the two compartments are different, each compartment contains one intact chromosome. This is crucial for the development of the spore and the viability of its progeny. Therefore dedicated systems are employed to ensure that one intact copy of the chromosome ends in the prespore, including conformational change of the chromosomes and attachment of the chromosomes to the cell poles, In this work the cell division protein MinD (part of the ‘Min’ system) is shown to play an important role during the trapping of initial part of the chromosome into the prespore. Absence of MinD causes a trapping defect such that the chromosomal region surround the origin of replication (oriC) is excluded from the prespore, but the flanking regions to the left and right of oriC are segregated into the prespore. Further analysis showed that this defect of the MinD mutants is not due to the loss of the Min function per se, or to possible over-replication of the chromosomes during sporulation in the absence of MinD. We also show that absence of DNA binding protein Soj can suppress this trapping defect of MinD, although the exact mechanism of the suppression is still unclear. We propose that during spore development Soj imposes some topological control over the oriC region of the chromosome to prevent its release from the quarter positions or/and its migration to the cell poles, and that this activity is counteracted by MinD.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.556001  DOI: Not available
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