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Meiosis is the central event of sexual reproduction, by which haploid gametes are formed from
diploid cells by two ensuing cell divisions that lack an intervening S-phase. This halving of
the chromosome number compensates for the genome doubling that occurs at fertilization.
Furthermore, meiosis represents the general source of genetic variation in the offspring of
sexually reproducing organisms: During the specialized prophase to the meiosis I division
parental chromosomes recombine and exchange genetic material by double stranded DNA break
repair. To this end, homologous chromosomes have to reorganize their structure and positioning
which leads to their synaptic pairing during mid prophase I. Chromosome pairing and/or
recombination fulfill the task of tethering parental chromosomes to each other, which allows
their faithful segregation at meiosis I.
Research in model systems has shown that genes which contribute to meiotic chromosome
structure and recombination are vital for meiotic differentiation and fertility. Some of
such genes have been found mutated in infertile humans. Telomeres are protein complexes at
the ends of linear chromosomes. They can mediate transcriptional repression and epigenetic
effects and contribute to genomic stability. Long-standing hypotheses predict that telomeres
carry out vital functions in the meiotic homologue pairing process and hence fertility. At
meiosis, specific protein additions to the telomere complex are associated with intranuclear
repositioning and a novel, nuclear envelope-associated dynamic mobility of telomeres.
We comparatively analyze the role of specific proteins for meiotic chromosome behavior
and dynamics with an emphasis on meiotic telomere clustering (bouquet formation). Molecular
cytology and live cell analysis is applied to study prophase I events in mutants of mammals,
budding yeast and in patients.
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