Gap-Filling by Homologous Recombination Repair in E. coli and in Mammalian Cells

Replication gaps caused by DNA lesions can be filled-in at least in theory, by a process of homologous recombination, depending on the presence of an intact homologous DNA, e.g., a sister chromatid in a replicating genome. Indeed, it was suggested in the late Sixties that replication gaps may be filled-in by homologous replication. We are investigating this process of gap-filling homologous recombination repair (HRR) in E. coli and in mammalian cells.

We developed a bi-plasmidic assay system, in which both TLR and HRR can be assayed simultaneously. Using this system we provided evidence, for the first time, that gaps are repaired in E. coli by HRR, in a process that is dependent on RecA, and the presence of a homologous DNA partner. Moreover, in this system HRR predominated over TLR, and was responsible for at least 85% of the gap-filling events. A similar system is currently used to examine whether HRR repairs gaps in mammalian cells.

Relevant publications
Berdichevsky, A., Izhar, L. and Livneh, Z. (2002) Error-Free Recombinational Repair Predominates over Mutagenic Translesion Replication in E. coli.
Mol. Cell 10, 917-924.
*Editorial Preview in: McGlynn, P. & Lloyd, R. G. (2002) Mol. Cell 10, 700-701.