![]() Over such short distances there is a positive correlation (negative interference) of recombinational events. High negative interference (HNI), in contrast to positive interference, refers to the association of recombination events ordinarily measured over short genomic distances, usually within a gene. High negative interference Bacteriophage T4 Furthermore, placement of female recombination events appears to become increasingly deregulated with maternal age, with a larger fraction of events occurring within closer proximity to each other than would be expected under simple models of crossover interference. In humans, recombination rate increases with maternal age. RTEL-1 appears to enforce meiotic crossover interference by directing the repair of some DSBs towards NCOs rather than COs. Normally, about half of all DSBs are converted into NCOs. RTEL1 likely acts by promoting synthesis-dependent strand annealing which results in non-crossover (NCO) recombinants instead of COs (see diagram). In rtel-1 mutants meiotic CO recombination is significantly increased and crossover interference appears to be absent. The RTEL-1 protein is required to prevent excess meiotic COs. Thus not all DSBs are repaired by a recombination process(es) leading to COs. ![]() In the nematode worm Caenorhabditis elegans, meiotic double-strand breaks (DSBs) outnumber COs. Meiotic crossovers (COs) appear to be regulated to ensure that COs on the same chromosome are distributed far apart (crossover interference). Most recombination events appear to be the SDSA type. NCO recombinants are thought to occur primarily by the Synthesis Dependent Strand Annealing (SDSA) model, illustrated on the left, above. CO recombination is thought to occur by the Double Holliday Junction (DHJ) model, illustrated on the right, above. ![]() 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 an homologous chromosome and strand invasion to initiate the recombinational repair process.
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