Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.653966
Title: A study of the Escherichia coli cell cycle
Author: Liu, Guowen
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 2000
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Abstract:
The ftsK gene of Escherichia coli encodes a 147kDa peptide, which consists of three distinct domains; namely a conserved N-terminal domain, a proline and glutamine rich region, and a C-terminal domain with consensus nucleotide-binding pocket (Begg et al., 1995). The N-terminus is essential for cell division (Begg et al., 1995; Draper et al 1998; Wang and Lutkenhaus 1998) and targets the whole protein to the septum (Yu et al., 1998 and Wang and Lutkenhaus, 1998). It was found in this thesis that depletion of the C-terminal domain resulted in the appearance of cells with abnormally located chromosomes and also in cell division-dependent SOS induction. Further study in this thesis showed that it was required only for chromosomal dimer resolution. The phenomenon of cell division-dependent SOS induction in FtsK-depleted GLC600 cells suggested that chromosome partition mutants should have continuous SOS induction. A study of the mutants obtained in this way showed that the RuvABC proteins, which are required for the resolution of recombination intermediates, are involved in chromosome partition. Over-expression of RuvAB could cause inhibition of cell division even in recA- cells, slow down the elongation of chromosome replication and cause the repression of transcription of cell division genes in the 2min region of the E. coli chromosome. To confirm that cell division and chromosome replication are coupled, nalidixic acid treatment and thymine starvation were used to block chromosome replication and it was found that cell division was coupled with chromosome replication at the level of transcription. It was also found that over-expression of DsbB, a protein required for protein disulfide bond formation in E. coli (Bardwell et al., 1993), resulted in the loss of the rod shape of E. coli cells. Over-expression of another gene named friL caused inhibition of cell division at a very early stage. It is proposed that FriL might be a regulator of cell division.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.653966  DOI: Not available
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