@article {2021|2154,
	title = {Influences of ssDNA-RecA Filament Length on the Fidelity of Homologous Recombination},
	journal = {Journal of Molecular Biology},
	volume = {433},
	year = {2021},
	pages = {167143},
	abstract = {<p>Chromosomal double-strand breaks can be accurately repaired by homologous recombination, but genomic rearrangement can result if the repair joins different copies of a repeated sequence. Rearrangement can be advantageous or fatal. During repair, a broken double-stranded DNA (dsDNA) is digested by the RecBCD complex from the 5 {\"A} end, leaving a sequence gap that separates two 3{\"A} single-stranded DNA (ssDNA) tails. RecA binds to the 3 {\"A} tails forming helical nucleoprotein filaments.A three-strand intermediate is formed when a RecA-bound ssDNA with L nucleotides invades a homologous region of dsDNA and forms a heteroduplex product with a length \&le; L bp. The homology dependent stability of the heteroduplex determines how rapidly and accurately homologous recombination repairs double-strand breaks. If the heteroduplex is sufficiently sequence matched, repair progresses to irreversible DNA synthesis. Otherwise, the heteroduplex should rapidly reverse. In this work, we present in vitro measurements of the L dependent stability of heteroduplex products formed by filaments with 90 \&le; L \&le; 420 nt, which is within the range observed in vivo. We find that without ATP hydrolysis, products are irreversible when L \&gt; 50 nt. In contrast, with ATP hydrolysis when L \&lt; 160 nt, products reverse in \&lt; 30 seconds; however, with ATP hydrolysis when L \&gt;= 320 nt, some products reverse in \&lt; 30 seconds, while others last thousands of seconds. We consider why these two different filament length regimes show such distinct behaviors. We propose that the experimental results combined with theoretical insights suggest that filaments with 250 \&le; L \&le; 8500 nt optimize DSB repair.</p>
},
	keywords = {biased random walk, D-loop turnover, Double-strand break repair, genomic rearrangement, multiple reversible intermediates},
	issn = {0022-2836},
	doi = {https://doi.org/10.1016/j.jmb.2021.167143},
	url = {https://www.sciencedirect.com/science/article/pii/S0022283621003727},
	author = {Claudia Danilowicz and Evan Vietorisz and Veronica Godoy-Carter and Chantal Pr{\'e}vost and Mara Prentiss}
}
@article {2015|1641,
	title = {Structure/function relationships in RecA protein-mediated homology recognition and strand exchange},
	journal = {Crit. Rev. Biochem. Mol. Biol.},
	volume = {50},
	year = {2015},
	pages = {453{\textendash}76},
	abstract = {RecA family proteins include RecA, Rad51, and Dmc1. These recombinases are responsible for homology search and strand exchange. Homology search and strand exchange occur during double-strand break repair and in eukaryotes during meiotic recombination. In bacteria, homology search begins when RecA binds an initiating single-stranded DNA (ssDNA) in the primary DNA-binding site to form the presynaptic filament. The filament is a right-handed helix, where the initiating strand is bound deep within the filament. Once the presynaptic filament is formed, it interrogates nearby double-stranded DNA (dsDNA) to find a homologous sequence; therefore, we provide a detailed discussion of structural features of the presynaptic filament that play important functional roles. The discussion includes many diagrams showing multiple filament turns. These diagrams illustrate interactions that are not evident in single turn structures. The first dsDNA interactions with the presynaptic filament are insensitive to mismatches. The mismatch insensitive interactions lead to dsDNA deformation that triggers a homology testing process governed by kinetics. The first homology test involves {\^a}{\textonequarter}8 bases. Almost all interactions are rejected by this initial rapid test, leading to a new cycle of homology testing. Interactions that pass the initial rapid test proceed to a slower testing stage. That slower stage induces nonhomologous dsDNA to reverse strand exchange and begin a new cycle of homology testing. In contrast, homologous dsDNA continues to extend the heteroduplex strand-exchange product until ATP hydrolysis makes strand exchange irreversible.},
	keywords = {Double-strand break repair, meiosis, meiotic recombination, Rad51, recombinase},
	doi = {10.3109/10409238.2015.1092943},
	author = {Prentiss, Mara and Chantal Pr{\'e}vost and Danilowicz, Claudia}
}
