Direct homologous dsDNA-dsDNA pairing: how, where and why?

TL;DR

This paper explores the mechanisms of homologous dsDNA pairing in eukaryotes, highlighting DNA recognition processes that occur independently of recombination proteins, with implications for understanding chromosome behavior.

Contribution

It provides evidence for direct homologous dsDNA pairing mechanisms in vivo, independent of traditional recombination proteins, through analysis of fungal silencing phenomena.

Findings

Homologous dsDNA pairing can occur without RecA/Rad51/Dmc1 proteins.

RIP and MSUD rely on interspersed base-pair triplet matching.

DNA recognition is efficient and occurs without DNA breakage.

Abstract

The ability of homologous chromosomes (or selected chromosomal loci) to pair specifically in the apparent absence of DNA breakage and recombination represents a prominent feature of eukaryotic biology. The mechanism of homology recognition at the basis of such recombination-independent pairing has remained elusive. A number of studies have supported the idea that sequence homology can be sensed between intact DNA double helices in vivo. In particular, recent analyses of the two silencing phenomena in fungi, known as repeat-induced point mutation (RIP) and meiotic silencing by unpaired DNA (MSUD), have provided genetic evidence for the existence of the direct homologous dsDNA-dsDNA pairing. Both RIP and MSUD likely rely on the same search strategy, by which dsDNA segments are matched as arrays of interspersed base-pair triplets. This process is general and very efficient, yet it proceeds normally without the RecA/Rad51/Dmc1 proteins. Further studies of RIP and MSUD may yield surprising insights into the function of DNA in the cell.