<P> The specific causes of non-homologous crossover events are unknown, but several influential factors are known to increase the likelihood of an unequal crossover . One common vector leading to unbalanced recombination is the repair of double - strand breaks (DSBs). DSBs are often repaired using non-homologous end joining, a process which involves invasion of a template strand by the DSB strand (see figure below). Nearby homologous regions of the template strand are often used for repair, which can give rise to either insertions or deletions in the genome if a non-homologous but complementary part of the template strand is used . Sequence similarity is a major player in crossover--crossover events are more likely to occur in long regions of close identity on a gene . This means that any section of the genome with long sections of repetitive DNA is prone to crossover events . </P> <P> The presence of transposable elements is another influential element of non-homologous crossover . Repetitive regions of code characterize transposable elements; complementary but non-homologous regions are ubiquitous within transposons . Because chromosomal regions composed of transposons have large quantities of identical, repetitious code in a condensed space, it is thought that transposon regions undergoing a crossover event are more prone to erroneous complementary match - up; that is to say, a section of a chromosome containing a lot of identical sequences, should it undergo a crossover event, is less certain to match up with a perfectly homologous section of complementary code and more prone to binding with a section of code on a slightly different part of the chromosome . This results in unbalanced recombination, as genetic information may be either inserted or deleted into the new chromosome, depending on where the recombination occurred . </P> <P> While the motivating factors behind unequal recombination remain obscure, elements of the physical mechanism have been elucidated . Mismatch repair (MMR) proteins, for instance, are a well - known regulatory family of proteins, responsible for regulating mismatched sequences of DNA during replication and escape regulation . The operative goal of MMRs is the restoration of the parental genotype . One class of MMR in particular, MutSβ, is known to initiate the correction of insertion - deletion mismatches of up to 16 nucleotides . Little is known about the excision process in eukaryotes, but E. coli excisions involve the cleaving of a nick on either the 5' or 3' strand, after which DNA helicase and DNA polymerase III bind and generate single - stranded proteins, which are digested by exonucleases and attached to the strand by ligase . Multiple MMR pathways have been implicated in the maintenance of complex organism genome stability, and any of many possible malfunctions in the MMR pathway result in DNA editing and correction errors . Therefore, while it is not certain precisely what mechanisms lead to errors of non-homologous crossover, it is extremely likely that the MMR pathway is involved . </P>

Where does crossing over and independent assortment occur