Meiosis
Meiosis
Meiosis is a differentiation pathway common to sexually developing eukaryotes thatproduces four haploid gametes from a single diploid cell. Importantly, it shuffles thegenetic material by random segregation of paternal and maternal chromosomes, and, in mostcases, by physical recombination between homologous chromosomes [1].
During the meiotic division each chromosome consists of two identical sisterchromatids following DNA replication. Accurate segregation of homologouschromosomes in the first meiotic division requires a physical connection betweenhomologs. In order to accomplish such an interaction homologous chromosomes must firstfind each other and subsequently form an interhomolog connection by crossing overnon-sister chromatids. A reductional division segregates the homologous chromosomes, eachof which still consists of two sister chromatids. However, as a consequence of the crossover these sister chromatids are no longer genetically identical. The second division issimilar to the mitotic division and separates the sister chromatids and results in theformation of four haploid gametes [1].
Replication origins are bound throughout the cell cycle by the origin recognitioncomplex ( ORC ). During the G1 phase of the cell cycle, ORC is sequentiallybound first by the Cell division cycle 6 homolog ( CDC18L (CDC6) ) and Chromatinlicensing and DNA replication factor 1 ( Cdt1 ) proteins and then by theMinichromosome maintenance complex ( MCM4/6/7 complex ) to form a prereplicativecomplex. This complex is poised for activation by Cyclin-dependent kinases 1 and 2 (CDK1 and CDK2 ) and Cell division cycle 7 homolog ( CDC7 ), whichresults in the loading of additional replication factors and actual DNA synthesis[1].
The molecular basis for sister chromatid cohesion in meiosis is a chromosomal proteincomplex called Meiotic cohesin complex. It consists of at least six subunits thattogether form a large proteinaceous ring [2], [3].
Homologous recombination is essential during meiosis in most sexually reproducingorganisms. There are intimate links between replication and recombination. S phaseprogression is accompanied by stalls and starts that require intact recombination systemsto repair them. There is an additional source of double-strand breaks (DSBs) in meiosisthat requires active recombination for their resolution. These DSBs are deliberatelyinduced throughout the genome by the conserved, meiosis-specific SPO11 meiotic proteincovalently bound to DSB homolog ( SPO11 ) endonuclease. SPO11 -inducedbreaks are processed somewhat differently than other breaks, leading to delayed timing inresection and repair [4]. In consequence, the cell may be driven to use thehomologous chromosome as a template. These changes may reflect recruitment of newcomponents to the recombination machinery at SPO11 -induced breaks. For example,DMC1 dosage suppressor of mck1 homolog, meiosis-specific homologous recombination (DMC1 ), a Rad51 relative that acts after DSBs occur in meiosis, promotesrecombination between homologs rather than sisters [5].
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