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The Rex system of bacteriophage lambda: tolerance and altruistic cell death
D H Parma1, M Snyder, S Sobolevski
1Department of Molecular, Cellular, and Development Biology, University of Colorado, Boulder 80309-0347.
Genes & Development
|March 1, 1992
Summary
Bacteriophage lambda's Rex system uses RexA and RexB proteins to halt viral growth by depolarizing the cell membrane. Overexpression of RexB prevents self-exclusion, ensuring lambda's survival during lytic cycles.
Area of Science:
- Microbiology
- Molecular Biology
- Virology
Background:
- Bacteriophage lambda possesses a two-component Rex system (RexA and RexB) that inhibits the lytic development of other bacterial viruses.
- This Rex exclusion mechanism leads to the cessation of macromolecular synthesis, impaired active transport, ATP hydrolysis, and ultimately cell death.
Purpose of the Study:
- To investigate the intracellular localization and membrane topology of the RexB protein.
- To elucidate the mechanism by which the Rex system causes cell death and how bacteriophage lambda avoids self-exclusion.
Main Methods:
- Cell fractionation was employed to determine the location of the RexB protein within the cell.
- RexB-alkaline phosphatase fusions were constructed to analyze the membrane topology of RexB.
- Experiments involving overexpression of RexB in lambda lysogens were conducted to assess its role in preventing self-exclusion.
Main Results:
- The RexB protein was identified as a polytopic transmembrane protein, suggesting it forms ion channels.
- These channels likely depolarize the cytoplasmic membrane, leading to the observed effects of Rex exclusion.
- Overexpression of RexB in lambda lysogens successfully prevented the exclusion of T4 rII mutants and lambda ren mutants.
Conclusions:
- The RexB protein functions as an ion channel, mediating membrane depolarization during bacteriophage lambda's lytic cycle.
- Overexpression of RexB is proposed as the mechanism by which lambda prevents its own exclusion, likely through transcriptional regulation.