Untitled

In marsupials, dosage compensation involves silencing of the father's X-chromosome. Because no XIST orthologue has been found, how imprinted X-inactivation occurs is unknown. In eutherians, the X is subject to meiotic sex chromosome inactivation (MSCI) in the paternal germ line and persists thereafter as postmeiotic sex chromatin (PMSC). One hypothesis proposes that the paternal X is inherited by the eutherian zygote as a preinactive X and raises the possibility of a similar process in the marsupial germ line. Here we demonstrate that MSCI and PMSC occur in the opossum. Surprisingly, silencing occurs before X-Y association. After MSCI, the X and Y fuse through a dense plate without obvious synapsis. Significantly, sex chromosome silencing continues after meiosis, with the opossum PMSC sharing features of eutherian PMSC. These results reveal a common gametogenic program in two diverse clades of mammals and support the idea that male germ-line silencing may have provided an ancestral form of mammalian dosage compensation.meiosis ͉ X-inactivation

Section: Resultsmentioning

confidence: 99%

Sex chromosome silencing in the marsupial male germ line

Namekawa

VandeBerg

McCarrey

et al. 2007

“…For immunostaining, meiotic cell spreads were prepared by the drying-down technique (46) and stained according to standard protocols (2). Primary antibodies used for immunofluorescence were rabbit anti-Sycp1 (1:500), rabbit anti-Sycp3 Diego, CA).…”

Section: Methodsmentioning

confidence: 99%

Poly(ADP-ribose) polymerase-2 contributes to the fidelity of male meiosis I and spermiogenesis

Dantzer

Mark

Quénet

et al. 2006

113

103

Besides the established central role of poly(ADP-ribose) polymerase-1 (Parp-1) and Parp-2 in the maintenance of genomic integrity, accumulating evidence indicates that poly(ADP-ribosyl)ation may modulate epigenetic modifications under physiological conditions. Here, we provide in vivo evidence for the pleiotropic involvement of Parp-2 in both meiotic and postmeiotic processes. We show that Parp-2-deficient mice exhibit severely impaired spermatogenesis, with a defect in prophase of meiosis I characterized by massive apoptosis at pachytene and metaphase I stages. Although Parp-2 ؊/؊ spermatocytes exhibit normal telomere dynamics and normal chromosome synapsis, they display defective meiotic sex chromosome inactivation associated with derailed regulation of histone acetylation and methylation and up-regulated X-and Y-linked gene expression. Furthermore, a drastically reduced number of crossover-associated Mlh1 foci are associated with chromosome missegregation at metaphase I. Moreover, Parp-2 ؊/؊ spermatids are severely compromised in differentiation and exhibit a marked delay in nuclear elongation. Altogether, our findings indicate that, in addition to its well known role in DNA repair, Parp-2 exerts essential functions during meiosis I and haploid gamete differentiation.

“…Surface spreading of meiocytes was prepared by a drying-down technique and stained for synaptonemal complexes, according to the procedure described (19,25,26). In brief, dissected ovaries or testes were placed in hypoextraction buffer, fixed in 1% paraformaldehyde, washed in PhotoFlo, air-dried, and stored at Ϫ20°C.…”

Section: Immunostaining and Fluorescence Microscopy Of Meiocyte Spreadsmentioning

confidence: 99%

Irregular telomeres impair meiotic synapsis and recombination in mice

Liu

Franco

Spyropoulos

et al. 2004

154

106

Telomere shortening can lead to chromosome instability, replicative senescence, and apoptosis in both somatic and male germ cells. To study roles for mammalian telomeres in homologous pairing and recombination, we characterized effects of telomere shortening on spermatogenesis and oogenesis in late-generation telomerase-deficient mice. We show that shortened telomeres of late-generation telomerase-deficient mice impair meiotic synapsis and decrease recombination, in particular, in females. In response to telomere shortening, male germ cells mostly undergo apoptosis, whereas female germ cells preferentially arrest in early meiosis, suggesting sexually dimorphic surveillance mechanisms for telomere dysfunction during meiosis in mice. Further, meiocytes of late-generation telomerase-deficient females with shortened telomeres, bred with early-generation males harboring relatively long telomeres, exhibit severely impaired chromosome pairing and synapsis and reduced meiotic recombination. These findings imply that functional telomeres are important in mammalian meiotic synapsis and recombination. meiosis ͉ mouse ͉ oocytes