Abstract

Introduction: cell deaths programmed by selfish genetic elements

Post-segregational cell killing by restriction modification systems

Competition between restriction modification systems

Homologous recombination as adaptation

References

Discussion
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Restriction modification gene complexes attack invading unmodified DNAs, but they also attack host bacterial chromosome when they were displaced by a competitor genetic element --- an incompatible plasmid or a homologous stretch of DNA. Such post-segregational host killing would help persistence of their copies in the neighboring, clonal cells in nature. The host RecABCD exonuclease/ recombinase machinery recognizing a specific sequence, chi (= 5' GCTGGTGG), helps the host survive such attacks by repairing chromosomal cleavage. Presumably, this enzyme starts exonucleolytic degradation from a restriction break, whether on an invader or on the chromosome, but switches to recombinational repair at chi, which serves as an identification marker of the enteric chromosome. Such conflict and cooperation among three groups of self-recognizing genetic elements may underlie the maintenance of homologous recombination, reproductive isolation and genome evolution in bacteria.

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Poster Number PAkobayashi0812
Keywords: restriction, epigenetics, recombination, phage exclusion, plasmid