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Meiotic recombination protein Dmc1 is a homolog of the bacterial strand exchange protein RecA. Dmc1 plays the central role in homologous recombination in meiosis by assembling at the sites of programmed DNA double strand breaks and carrying out a search for allelic DNA sequences located on homologous chromatids. The name "Dmc" stands for ...
The RecA/Rad51/DMC1 gene family plays a central role in homologous recombination during bacterial transformation as it does during eukaryotic meiosis and mitosis. For instance, the RecA protein is essential for transformation in Bacillus subtilis and Streptococcus pneumoniae , [ 85 ] and expression of the RecA gene is induced during the ...
The RecA protein catalyzes unidirectional branch migration and by doing so makes it possible to complete recombination, producing a region of heteroduplex DNA that is thousands of base pairs long. Since it is a DNA-dependent ATPase , RecA contains an additional site for binding and hydrolyzing ATP .
During meiosis Rad51 interacts with another recombinase, Dmc1, to form a presynaptic filament that is an intermediate in homologous recombination. [9] Dmc1 function appears to be limited to meiotic recombination. Like Rad51, Dmc1 is homologous to bacterial RecA.
Genetic recombination is catalyzed by many different enzymes. Recombinases are key enzymes that catalyse the strand transfer step during recombination. RecA, the chief recombinase found in Escherichia coli, is responsible for the repair of DNA double strand breaks (DSBs).
It repairs breaks that occur on only one of DNA's two strands, known as single-strand gaps. The RecF pathway can also repair double-strand breaks in DNA when the RecBCD pathway, another pathway of homologous recombination in bacteria, is inactivated by mutations. [1] Like the RecBCD pathway, the RecF pathway requires RecA for strand
Recombination between non-sister chromosomes at meiosis is known to be a recombinational repair process that can repair double-strand breaks and other types of double-strand damage. [2] In contrast, recombination between sister chromosomes cannot repair double-strand damages arising prior to the replication which produced them.
Because recombination is initiated by double stranded breaks (DSBs) at certain regions of the genome, entry into Meiosis 1 must be delayed until the DSBs are repaired. [30] The meiosis-specific kinase Mek1 plays an important role in this and recently, it has been discovered that Mek1 is able to phosphorylate Ndt80 independently of IME2.