The Mammalian Synaptonemal Complex: A Scaffold and Beyond

Yang, Fan; Wang, P J

doi:10.1159/000166620

Cited by 70 publications

(57 citation statements)

References 68 publications

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“…Here we show that the level of oocyte cAMP regulates the dissolution of SYCP1 from the SC. SYCP1 is a core component of the SC (Yang and Wang, 2009;Fraune et al, 2012) and the disassembly of SYCP1 is a key step to entering the diplotene stage in rat oocytes (Paredes et al, 2005). Thus, we hypothesize that the level of cAMP in oocytes potentially controls the progress of meiotic prophase I by regulating SC separation in the perinatal ovary.…”

Section: Discussionmentioning

confidence: 93%

Cyclic AMP in oocytes controls meiotic prophase I and primordial folliculogenesis in the perinatal mouse ovary

Wang

Teng

et al. 2015

Development

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In mammalian ovaries, a fixed population of primordial follicles forms during the perinatal stage and the oocytes contained within are arrested at the dictyate stage of meiotic prophase I. In the current study, we provide evidence that the level of cyclic AMP (cAMP) in oocytes regulates oocyte meiotic prophase I and primordial folliculogenesis in the perinatal mouse ovary. Our results show that the early meiotic development of oocytes is closely correlated with increased levels of intra-oocyte cAMP. Inhibiting cAMP synthesis in fetal ovaries delayed oocyte meiotic progression and inhibited the disassembly and degradation of synaptonemal complex protein 1. In addition, inhibiting cAMP synthesis in in vitro cultured fetal ovaries prevented primordial follicle formation. Finally, using an in situ oocyte chromosome analysis approach, we found that the dictyate arrest of oocytes is essential for primordial follicle formation under physiological conditions. Taken together, these results suggest a role for cAMP in early meiotic development and primordial follicle formation in the mouse ovary.

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Section: Discussionmentioning

confidence: 93%

Cyclic AMP in oocytes controls meiotic prophase I and primordial folliculogenesis in the perinatal mouse ovary

Wang

Teng

et al. 2015

Development

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“…First, we stained meiotic chromosome spreads with SYCP1 and SYCP3 to examine synaptonemal complex (SC) formation, which normally begins during leptonema and is completed by pachynema (Cohen et al, 2006;Fraune et al, 2012;Yang and Wang, 2009). The SC formed in mutant spermatocytes but frequently was incomplete: 37/50 mutant pachytene spermatocytes had incomplete synapsis compared with 4/50 in wild type (Fig.…”

Section: Dmrt6mentioning

confidence: 99%

The mammalian Doublesex homolog DMRT6 coordinates the transition between mitotic and meiotic developmental programs during spermatogenesis

et al. 2014

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In mammals, a key transition in spermatogenesis is the exit from spermatogonial differentiation and mitotic proliferation and the entry into spermatocyte differentiation and meiosis. Although several genes that regulate this transition have been identified, how it is controlled and coordinated remains poorly understood. Here, we examine the role in male gametogenesis of the Doublesex-related gene Dmrt6 (Dmrtb1) in mice and find that Dmrt6 plays a crucial role in directing germ cells through the mitotic-to-meiotic germ cell transition. DMRT6 protein is expressed in late mitotic spermatogonia. In mice of the C57BL/6J strain, a null mutation in Dmrt6 disrupts spermatogonial differentiation, causing inappropriate expression of spermatogonial differentiation factors, including SOHLH1, SOHLH2 and DMRT1 as well as the meiotic initiation factor STRA8, and causing most late spermatogonia to undergo apoptosis. In mice of the 129Sv background, most Dmrt6 mutant germ cells can complete spermatogonial differentiation and enter meiosis, but they show defects in meiotic chromosome pairing, establishment of the XY body and processing of recombination foci, and they mainly arrest in midpachynema. mRNA profiling of Dmrt6 mutant testes together with DMRT6 chromatin immunoprecipitation sequencing suggest that DMRT6 represses genes involved in spermatogonial differentiation and activates genes required for meiotic prophase. Our results indicate that Dmrt6 plays a key role in coordinating the transition in gametogenic programs from spermatogonial differentiation and mitosis to spermatocyte development and meiosis.

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“…1A, reviewed in ref. 7). Knockout of each of these genes leads to very similar synaptic defects; the chromosomes align but fail to synapse, and meiotic DSB repair is stalled.…”

Section: -6mentioning

confidence: 99%

DNA double strand break repair, chromosome synapsis and transcriptional silencing in meiosis

Inagaki

Schoenmakers²,

Baarends³

2010

Epigenetics

105

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C hromosome pairing and synapsis during meiotic prophase requires the formation and repair of DNA double-strand breaks (DSBs) by the topoisomerase-like enzyme SPO11. Chromosomes, or chromosomal regions, that lack a pairing partner, such as the largely heterologous X and Y chromosomes, show delayed meiotic DSB repair and are transcriptionally silenced. Herein, we review meiosis-specific aspects of DSB repair in relation to homology recognition and meiotic silencing of heterologous regions. We propose a dynamic interplay between progression of synapsis and persistent meiotic DSBs. Signaling from these persistent breaks could inhibit heterologous synapsis and stimulate meiotic silencing of the X and Y chromosomes.

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The Mammalian Synaptonemal Complex: A Scaffold and Beyond

Cited by 70 publications

References 68 publications

Cyclic AMP in oocytes controls meiotic prophase I and primordial folliculogenesis in the perinatal mouse ovary

Cyclic AMP in oocytes controls meiotic prophase I and primordial folliculogenesis in the perinatal mouse ovary

The mammalian Doublesex homolog DMRT6 coordinates the transition between mitotic and meiotic developmental programs during spermatogenesis

DNA double strand break repair, chromosome synapsis and transcriptional silencing in meiosis

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