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Double-strand break repair models that act via homologous recombination. Two primary models for how homologous recombination repairs double-strand breaks in DNA are the double-strand break repair (DSBR) pathway (sometimes called the double Holliday junction model) and the synthesis-dependent strand annealing (SDSA) pathway. [43]
Three possible sub-pathways for a double-strand break to repair via homologous recombination: Gene conversion, BIR and SDSA. The gene conversion is referring to the double-strand break repair model. The other sub-pathway is the synthesis-dependent strain annealing. SSA is the fourth sub-pathway and it is not shown in this diagram.
The most common form of HDR is homologous recombination. The HDR mechanism can only be used by the cell when there is a homologous piece of DNA present in the nucleus, mostly in G2 and S phase of the cell cycle. Other examples of homology-directed repair include single-strand annealing and breakage-induced replication.
The two pathways for homologous recombination in eukaryotes, showing the formation and resolution of Holliday junctions. The Holliday junction is a key intermediate in homologous recombination, a biological process that increases genetic diversity by shifting genes between two chromosomes, as well as site-specific recombination events involving integrases.
Homologous recombination is the exchange of genes between two DNA strands that include extensive regions of base sequences that are identical to one another. In eukaryotic species, bacteria, and some viruses, homologous recombination happens spontaneously and is a useful tool in genetic engineering.
A model of meiotic recombination, initiated by a double-strand break or gap, followed by pairing with an homologous chromosome and strand invasion to initiate the recombinational repair process. Repair of the gap can lead to crossover (CO) or non-crossover (NCO) of the flanking regions.
A current model of meiotic recombination, initiated by a double-strand break or gap, followed by pairing with a homologous chromosome and strand invasion to initiate the recombinational repair process. Repair of the gap can lead to crossover (CO) or non-crossover (NCO) of the flanking regions.
A disordered DNA loop in RecA, Loop 2, contains the residues responsible for DNA homologous recombination. [10] In some bacteria, RecA posttranslational modification via phosphorylation of a serine residue on Loop 2 can interfere with homologous recombination. [11] There are multiple proposed models for how RecA finds complementary DNA. [9]