Fidelity of Genetic Recombination
Fidelity of Genetic recombination represents the fidelity DNA of transgenic and stabilize the cell genome by blocking recombination events in DNA sequences between different. If you are responsible for the direction of specific adjustments of mispaired bases, reaction and evolution of Mutl and MutS of bacteria that play an important role in the initiation and repair recognition of mismatches have been identified in mammalian cells and yeast well It is held between the cognate. It is a variation voluntarily increased significantly in the case of the mouse and human, inactivation of the gene encoding a result of these activities, predisposition to tumor development.
In budding yeast, suggesting an important role in the alignment of Hop2 proper homologous chromosomes during meiotic prophase, lack of Hop2 protein is formed extensive Shinaputonema non-homologous chromosomes between (SC). Hop2 act in the same way, and gene analysis, shows the two homologs of RecA RAD51 DMC1 protein, the EE. Therefore, hop2 mutant phenotype shows the importance of recombination mechanism to facilitate proper chromosome pairing. Dmc1/Rad51 recombinase Hop2 provided need to distinguish homologous sequences from heterologous in the process of homology search we. In this way, Hop2 absence non-homologous sequences between interaction is inappropriate stable, I will start the formation SC. Overexpression of RAD51 suppresses the defects in meiosis of hop2 mutant and DMC1 mainly. We, whereas require additional elements DMC1 such as Hop2, RAD51 concluded that to be able to perform homology search independently.
That the two modes of mismatch repair operates in patch mismatch repair and very short patch mismatch repair long bacteria are known. In order to protect the single base pair, patch mismatch repair system is very short, operated at a particular disorder. Thus, recombination of the hyper-specific marker patch mismatch repair action in a very short recombinant hetero intermediate, creating patchwork sequence, ie events, field repair of apparent multiple for the exchange. Disassemble the apparent heteroduplex DNA, recognizes a gap to be formed by strand exchange between the non-identical parent sequence sufficiently by preventing their formation, long patch mismatch repair is antirecombinagenic. In order to ensure the high fidelity of homologous recombination, this discrepancy stimulation antirecombination long patch mismatch repair, it is assumed that the “correction” system it. In suggesting a role of non-coding sequence or other error repeatedly as an element antirecombination of the chromosome, which, mitosis and chromosomal abnormalities compared to the high frequency of sister chromatid exchange (accurate chromosome stability in eukaryotes because it represents a rare event) that is recombinant and differentiate without the need for a geographically separated to provide a molecular mechanism.
Molecular mechanisms of meiotic recombination has been studied in budding yeast well. Double-strand break formed from SPO11, II topoisomerase homolog protein (the DSB), the process begins. DSB is completed, an end portion 5 thereof ‘is decomposed therefrom leading to DNA strand. It is thought to be used in the homology search (recombinase) enzyme strand exchange single-stranded DNA thereof. , Single-stranded DNA sequence homologous intrusion staining nonsister finally, this is, of double Holiday junction the crossovers are leading double Holiday junction and aggression to one end or middle / it was assumed that by resolution, and is formed mainly.
In budding yeast, the genetic research, it has the ability meiotic recombination mechanism detects the sequence homology between the location of the ectopic effective as the site of the allele are shown. I indicates that this observation has been made recombinant mediated homology search, throughout the genome. Meanwhile, fluorescence in situ hybridization (FISH), the binding of several homologs occurs even in the absence of recombination has been shown. In this way, it looks coupling mechanism that does not depend on recombination and meiotic recombination to work with homolog of the redundant circuit. However, it remains ratio of each mechanism homologs scheme is unknown.
In this study, we provide evidence that Hop2 is involved in meiotic recombination. Hop2 act, and epistasis analysis indicates the RAD51 DMC1 as that. Thus, heterologous synapses were observed to show the importance of recombination in the plant homologue method hop2 mutation. We are offering to run a new step downstream of meiotic recombination and RAD51 Hop2 DMC1, in this step, I guarantee the homology search efficient and accurate. In addition, I found that overproduction of RAD51 suppresses the meiotic recombination defect in DMC1, this suppression is not required to Hop2 protein. We suggest that the pathway of homologous recombination-mediated pairs is present. Not once RAD51, DMC1-dependent applications of other, more complex and Hop2/Mnd1 Hop2/Mnd1, or DMC1