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E.coli cell-cycle regulation by bacteriophage lambda.
Kirill Sergueev1, Donald Court, Lucretia Reaves
1Gene Regulation and Chromosome Biology Laboratory, National Cancer Institute, NCI-FCRDC, PO Box B, Building 539, Frederick, MD 21702-1201, USA.
Journal of Molecular Biology
|November 21, 2002
Summary
Transient expression of bacteriophage lambda genes causes temporary cell cycle blocks in Escherichia coli, leading to partial cell division synchrony. This phenomenon involves distinct blocks in cell division and DNA replication initiation.
Area of Science:
- Molecular Biology
- Microbiology
- Genetics
Background:
- Bacteriophage lambda's p(L) promoter is known to influence gene expression.
- Previous studies suggested lambda gene expression could induce cell-cycle synchrony in Escherichia coli.
Purpose of the Study:
- To re-examine the claim that bacteriophage lambda gene expression induces cell-cycle synchrony in Escherichia coli.
- To identify the genetic elements responsible for observed cell cycle modifications.
Main Methods:
- Re-examination of Kourilsky and Knapp's claim.
- Deletion-substitution mutagenesis to analyze genetic regions.
- Observation of cell division and DNA replication initiation in Escherichia coli.
Main Results:
- Lasting cell-cycle synchrony was not reproduced, but a temporary cessation of division followed by synchronous divisions was observed.
- Two genetically separable events were identified: a transient cell division block and a block to DNA replication initiation.
- The cell division block is mediated by the lambda kil gene, while the DNA replication initiation block involves the 'bin' region upstream of the xis gene, including four open reading frames (ORFs).
Conclusions:
- Bacteriophage lambda possesses mechanisms to transiently block host cell division and DNA replication initiation.
- These blocks likely serve as a phage strategy to enhance lysogeny or lytic growth.
- The 'bin' region, comprising ea22, ea8.5, and two flanking ORFs, is crucial for blocking DNA replication initiation.