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Journal articles on the topic 'Female meiotic prophase'
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Fan, Xueying, Ioannis Moustakas, Vanessa Torrens-Juaneda, Qijing Lei, Geert Hamer, Leoni A. Louwe, Gonneke S. K. Pilgram, et al. "Transcriptional progression during meiotic prophase I reveals sex-specific features and X chromosome dynamics in human fetal female germline." PLOS Genetics 17, no. 9 (September 9, 2021): e1009773. http://dx.doi.org/10.1371/journal.pgen.1009773.
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During gametogenesis in mammals, meiosis ensures the production of haploid gametes. The timing and length of meiosis to produce female and male gametes differ considerably. In contrast to males, meiotic prophase I in females initiates during development. Hence, the knowledge regarding progression through meiotic prophase I is mainly focused on human male spermatogenesis and female oocyte maturation during adulthood. Therefore, it remains unclear how the different stages of meiotic prophase I between human oogenesis and spermatogenesis compare. Analysis of single-cell transcriptomics data from human fetal germ cells (FGC) allowed us to identify the molecular signatures of female meiotic prophase I stages leptotene, zygotene, pachytene and diplotene. We have compared those between male and female germ cells in similar stages of meiotic prophase I and revealed conserved and specific features between sexes. We identified not only key players involved in the process of meiosis, but also highlighted the molecular components that could be responsible for changes in cellular morphology that occur during this developmental period, when the female FGC acquire their typical (sex-specific) oocyte shape as well as sex-differences in the regulation of DNA methylation. Analysis of X-linked expression between sexes during meiotic prophase I suggested a transient X-linked enrichment during female pachytene, that contrasts with the meiotic sex chromosome inactivation in males. Our study of the events that take place during meiotic prophase I provide a better understanding not only of female meiosis during development, but also highlights biomarkers that can be used to study infertility and offers insights in germline sex dimorphism in humans.
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Baarends, Willy M., Evelyne Wassenaar, Roald van der Laan, Jos Hoogerbrugge, Esther Sleddens-Linkels, Jan H. J. Hoeijmakers, Peter de Boer, and J. Anton Grootegoed. "Silencing of Unpaired Chromatin and Histone H2A Ubiquitination in Mammalian Meiosis." Molecular and Cellular Biology 25, no. 3 (February 1, 2005): 1041–53. http://dx.doi.org/10.1128/mcb.25.3.1041-1053.2005.
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ABSTRACT During meiotic prophase in male mammals, the X and Y chromosomes are incorporated in the XY body. This heterochromatic body is transcriptionally silenced and marked by increased ubiquitination of histone H2A. This led us to investigate the relationship between histone H2A ubiquitination and chromatin silencing in more detail. First, we found that ubiquitinated H2A also marks the silenced X chromosome of the Barr body in female somatic cells. Next, we studied a possible relationship between H2A ubiquitination, chromatin silencing, and unpaired chromatin in meiotic prophase. The mouse models used carry an unpaired autosomal region in male meiosis or unpaired X and Y chromosomes in female meiosis. We show that ubiquitinated histone H2A is associated with transcriptional silencing of large chromatin regions. This silencing in mammalian meiotic prophase cells concerns unpaired chromatin regions and resembles a phenomenon described for the fungus Neurospora crassa and named meiotic silencing by unpaired DNA.
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Havekes, Francis W. J., J. Hans de Jong, and Christa Heyting. "Comparative analysis of female and male meiosis in three meiotic mutants of tomato." Genome 40, no. 6 (December 1, 1997): 879–86. http://dx.doi.org/10.1139/g97-814.
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Female meiosis was analysed in squash preparations of ovules from three meiotic mutants and wild-type plants of tomato. In the completely asynaptic mutant as6, chromosome pairing and chiasma formation were virtually absent in both sexes. In the partially asynaptic mutant asb, with intermediate levels of chromosome pairing at pachytene, there were a higher number of chiasmate chromosome arms in female meiosis than in male meiosis, whereas in the desynaptic mutant as5 there were normal levels of chromosome pairing at pachytene and a similar reduction in chiasma frequency in the two sexes. In wild-type tomato, we found slightly higher numbers of chiasmate chromosome arms in female meiosis than in male meiosis. We propose that the higher female chiasma frequencies in mutant asb and wild-type tomato result from a longer duration of female meiotic prophase. This would allow chromosomes more time to pair and recombine. It is possible that a longer duration of prophase I does not affect mutants as5 and as6, either because the meiotic defect acts before the pairing process begins (in as6) or because it acts at a later stage and involves chiasma maintenance (in as5).Key words: female meiosis, tomato, chiasma, mutant.
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Jones, K. T. "032. Cdh1: A CELL CYCLE PROTEIN INVOLVED IN FEMALE MEIOSIS AND PREVENTION OF ANEUPLOIDY." Reproduction, Fertility and Development 22, no. 9 (2010): 10. http://dx.doi.org/10.1071/srb10abs032.
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Mammalian oocytes are arrested at the dictyate stage of prophase I in the ovary. In growing follicles, oocytes can become responsive to Luteinising Hormone and will undergo meiotic resumption just before ovulation. During the first meiotic division, homologous chromosomes are segregated, a process that is very error prone in human oocytes. By ovulation the oocyte has extruded its first polar body and has re-arrested at metaphase of the first meiotic division. Recent work from our lab has established that the protein Cdh1 is involved uniquely in both in the process of prophase I arrest and the correct segregation of homologs in meiosis I. Thus in cultured oocytes, in vitro antisense knockdown of Cdh1 induces both meiotic resumption and high rates of aneuploidy as a result of non-disjunction during first meiosis. Cdh1 causes prophase I arrest by inducing cyclin B1 degradation and maintaining low levels of the kinase CDK1, whose activity induces meiotic resumption. Cdh1 is an activator of the Anaphase-Promoting Complex (APC), a ubiquitin ligase that earmarks proteins such as cyclin B1 for proteolysis. Cdh1 prevents aneuploidy by causing the degradation of Cdc20, a protein that is responsible for activating the APC once all homologs are correctly aligned at metaphase. Thus loss of Cdh1 seems to prematurely activate APC(Cdc20) activity. It is interesting that a single protein can affect two important meiotic transitions in oocytes. However to explore its functions more fully, and confirm that an in vitro knockdown is faithfully replicated by in vivo loss, a targeted knockout of Cdh1 is needed. Therefore we have generated an oocyte specific Cdh1 knockout by ZP3 promoter driven Cre- recombinase activity in oocytes carrying loxP insertions in the single copy Cdh1 gene. This talk will therefore focus on the effects of an in vivo Cdh1 knockout.
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Su, Yongchun, Yunfei Li, and Ping Ye. "Mammalian meiosis is more conserved by sex than by species: conserved co-expression networks of meiotic prophase." REPRODUCTION 142, no. 5 (November 2011): 675–87. http://dx.doi.org/10.1530/rep-11-0260.
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Despite the importance of meiosis to human reproduction, we know remarkably little about the genes and pathways that regulate meiotic progression through prophase in any mammalian species. Microarray expression profiles of mammalian gonads provide a valuable resource for probing gene networks. However, expression studies are confounded by mixed germ cell and somatic cell populations in the gonad and asynchronous germ cell populations. Further, widely used clustering methods for analyzing microarray profiles are unable to prioritize candidate genes for testing. To derive a comprehensive understanding of gene expression in mammalian meiotic prophase, we constructed conserved co-expression networks by linking expression profiles of male and female gonads across mouse and human. We demonstrate that conserved gene co-expression dramatically improved the accuracy of detecting known meiotic genes compared with using co-expression in individual studies. Interestingly, our results indicate that meiotic prophase is more conserved by sex than by species. The co-expression networks allowed us to identify genes involved in meiotic recombination, chromatin cohesion, and piRNA metabolism. Further, we were able to prioritize candidate genes based on quantitative co-expression links with known meiotic genes. Literature studies of these candidate genes suggest that some are human disease genes while others are associated with mammalian gonads. In conclusion, our co-expression networks provide a systematic understanding of cross-sex and cross-species conservations observed during meiotic prophase. This approach further allows us to prioritize candidate meiotic genes for in-depth mechanistic studies in the future.
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Agashe, Bhavna, Chellapilla Krishna Prasad, and Imran Siddiqi. "Identification and analysis ofDYAD: a gene required for meiotic chromosome organisation and female meiotic progression inArabidopsis." Development 129, no. 16 (August 15, 2002): 3935–43. http://dx.doi.org/10.1242/dev.129.16.3935.
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The dyad mutant of Arabidopsis was previously identified as being defective in female meiosis. We report here the analysis of the DYAD gene. In ovules and anthers DYAD RNA is detected specifically in female and male meiocytes respectively, in premeiotic interphase/meiotic prophase. Analysis of chromosome spreads in female meiocytes showed that in the mutant, chromosomes did not undergo synapsis and formed ten univalents instead of five bivalents. Unlike mutations in AtDMC1 and AtSPO11 which also affect bivalent formation as the univalent chromosomes segregate randomly, the dyad univalents formed an ordered metaphase plate and underwent an equational division. This suggests a requirement for DYAD for chromosome synapsis and centromere configuration in female meiosis. The dyad mutant showed increased and persistent expression of a meiosis-specific marker, pAtDMC1::GUS during female meiosis, indicative of defective meiotic progression. The sequence of the putative protein encoded by DYAD did not reveal strong similarity to other proteins. DYAD is therefore likely to encode a novel protein required for meiotic chromosome organisation and female meiotic progression.
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Barlow, C., M. Liyanage, P. B. Moens, M. Tarsounas, K. Nagashima, K. Brown, S. Rottinghaus, et al. "Atm deficiency results in severe meiotic disruption as early as leptonema of prophase I." Development 125, no. 20 (October 15, 1998): 4007–17. http://dx.doi.org/10.1242/dev.125.20.4007.
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Infertility is a common feature of the human disorder ataxia-telangiectasia and Atm-deficient mice are completely infertile. To gain further insight into the role of ATM in meiosis, we examined meiotic cells in Atm-deficient mice during development. Spermatocyte degeneration begins between postnatal days 8 and 16.5, soon after entry into prophase I of meiosis, while oocytes degenerate late in embryogenesis prior to dictyate arrest. Using electron microscopy and immunolocalization of meiotic proteins in mutant adult spermatocytes, we found that male and female gametogenesis is severely disrupted in Atm-deficient mice as early as leptonema of prophase I, resulting in apoptotic degeneration. A small number of mutant cells progress into later stages of meiosis, but no cells proceed beyond prophase I. ATR, a protein related to ATM, DMC1, a RAD51 family member, and RAD51 are mislocalized to chromatin and have reduced localization to developing synaptonemal complexes in spermatocytes from Atm-deficient mice, suggesting dysregulation of the orderly progression of meiotic events. ATM protein is normally present at high levels primarily in ova cytoplasm of developing ovarian follicles, and in the nucleus of spermatogonia and to a lesser extent in spermatoctyes, but without localization to the synaptonemal complex. We propose a model in which ATM acts to monitor meiosis by participation in the regulation or surveillance of meiotic progression, similar to its role as a monitor of mitotic cell cycle progression.
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Delves, C. J., R. E. Howells, and R. J. Post. "Gametogenesis and fertilization in Dirofilaria immitis (Nematoda: Filarioidea)." Parasitology 92, no. 1 (February 1986): 181–97. http://dx.doi.org/10.1017/s003118200006354x.
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SUMMARYGametogenesis in Dirofilaria immitis has been studied principally by means of the aceto-orcein chromosomal squash technique, but with additional ultrastructural observations. A terminal germinative zone, in which a continuous and rapid division of germ cells occurs, has been identified in the gonoduct of both male and female worms. Approximately 20% of cells within these germinative zones were in arrested mitotic division following the incubation in vitro of excised gonads in 0·01% colchicine for 4 h. All primary spermatocytes within a 1–2 cm length of the testis proximal to the germinative zone were at the prophase of the 1st meiotic division. In the corresponding region of the ovary, the primary oocytes were similarly at the prophase of the 1st meiotic division in 75% of female worms examined but in the remaining 25% all primary oocytes possessed markedly less condensed, probably interphase nuclei. A possible hormonal control of the cyclical development of primary oocytes, but not primary spermatocytes in D. immitis is suggested. In most of the remaining length of the gonoducts beyond this region of cells at meiotic prophase, the chromatin material of both primary spermatocytes and oocytes is decondensed. Recondensation of chromosomes in the spermatocytes is observed just prior to entry into the seminal vesicle, where meiosis I is completed and meiosis II takes place. In the primary oocyte, completion of meiosis only occurs after fertilization within the seminal receptacle by an entire male gamete. Following the 2 meiotic divisions in the oocyte and subsequent extrusion of the 2 polar bodies, the haploid chromosome complement of the female unites with that of the male, re-establishing the diploid number of the zygote (2n = 10). Male chromosomes within the oocyte remain visible throughout late oogenesis and fusion occurs without the formation of pronuclei.
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Li, Miao, Tao Huang, Meng-Jing Li, Chuan-Xin Zhang, Xiao-Chen Yu, Ying-Ying Yin, Chao Liu, et al. "The histone modification reader ZCWPW1 is required for meiosis prophase I in male but not in female mice." Science Advances 5, no. 8 (August 2019): eaax1101. http://dx.doi.org/10.1126/sciadv.aax1101.
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Meiosis is a specialized type of cell division that creates haploid germ cells and ensures their genetic diversity through homologous recombination. We show that the H3K4me3 reader ZCWPW1 is specifically required for meiosis prophase I progression in male but not in female germ cells in mice. Loss of Zcwpw1 in male mice caused a complete failure of synapsis, resulting in meiotic arrest at the zygotene to pachytene stage, accompanied by incomplete DNA double-strand break repair and lack of crossover formation, leading to male infertility. In oocytes, deletion of Zcwpw1 only somewhat slowed down meiosis prophase I progression; Zcwpw1−/− oocytes were able to complete meiosis, and Zcwpw1−/− female mice had normal fertility until mid-adulthood. We conclude that the H3K4me3 reader ZCWPW1 is indispensable for meiosis synapsis in males but is dispensable for females. Our results suggest that ZCWPW1 may represent a previously unknown, sex-dependent epigenetic regulator of germ cell meiosis in mammals.
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Francis, R., E. Maine, and T. Schedl. "Analysis of the multiple roles of gld-1 in germline development: interactions with the sex determination cascade and the glp-1 signaling pathway." Genetics 139, no. 2 (February 1, 1995): 607–30. http://dx.doi.org/10.1093/genetics/139.2.607.
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Abstract The Caenorhabditis elegans gene gld-1 is essential for oocyte development; in gld-1 (null) hermaphrodites, a tumor forms where oogenesis would normally occur. We use genetic epistasis analysis to demonstrate that tumor formation is dependent on the sexual fate of the germline. When the germline sex determination pathway is set in the female mode (terminal fem/fog genes inactive), gld-1 (null) germ cells exit meiotic prophase and proliferate to form a tumor, but when the pathway is set in the male mode, they develop into sperm. We conclude that the gld-1 (null) phenotype is cell-type specific and that gld-1(+) acts at the end of the cascade to direct oogenesis. We also use cell ablation and epistasis analysis to examine the dependence of tumor formation on the glp-1 signaling pathway. Although glp-1 activity promotes tumor growth, it is not essential for tumor formation by gld-1 (null) germ cells. These data also reveal that gld-1(+) plays a nonessential (and sex nonspecific) role in regulating germ cell proliferation before their entry into meiosis. Thus gld-1(+) may negatively regulate proliferation at two distinct points in germ cell development: before entry into meiotic prophase in both sexes (nonessential premeiotic gld-1 function) and during meiotic prophase when the sex determination pathway is set in the female mode (essential meiotic gld-1 function).
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Li, Jian, Ji-Xin Tang, Jin-Mei Cheng, Bian Hu, Yu-Qian Wang, Batool Aalia, Xiao-Yu Li, et al. "Cyclin B2 can compensate for Cyclin B1 in oocyte meiosis I." Journal of Cell Biology 217, no. 11 (August 10, 2018): 3901–11. http://dx.doi.org/10.1083/jcb.201802077.
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Mammalian oocytes are arrested at the prophase of the first meiotic division for months and even years, depending on species. Meiotic resumption of fully grown oocytes requires activation of M-phase–promoting factor (MPF), which is composed of Cyclin B1 and cyclin-dependent kinase 1 (CDK1). It has long been believed that Cyclin B1 synthesis/accumulation and its interaction with CDK1 is a prerequisite for MPF activation in oocytes. In this study, we revealed that oocyte meiotic resumption occurred in the absence of Cyclin B1. Ccnb1-null oocytes resumed meiosis and extruded the first polar body. Without Cyclin B1, CDK1 could be activated by up-regulated Cyclin B2. Ccnb1 and Ccnb2 double knockout permanently arrested the oocytes at the prophase of the first meiotic division. Oocyte-specific Ccnb1-null female mice were infertile due to failed MPF activity elevation and thus premature interphase-like stage entry in the second meiotic division. These results have revealed a hidden compensatory mechanism between Cyclin B1 and Cyclin B2 in regulating MPF and oocyte meiotic resumption.
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Stringer, Jessica M., Amy Winship, Nadeen Zerafa, Matthew Wakefield, and Karla Hutt. "Oocytes can efficiently repair DNA double-strand breaks to restore genetic integrity and protect offspring health." Proceedings of the National Academy of Sciences 117, no. 21 (May 7, 2020): 11513–22. http://dx.doi.org/10.1073/pnas.2001124117.
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Female fertility and offspring health are critically dependent on an adequate supply of high-quality oocytes, the majority of which are maintained in the ovaries in a unique state of meiotic prophase arrest. While mechanisms of DNA repair during meiotic recombination are well characterized, the same is not true for prophase-arrested oocytes. Here we show that prophase-arrested oocytes rapidly respond to γ-irradiation–induced DNA double-strand breaks by activating Ataxia Telangiectasia Mutated, phosphorylating histone H2AX, and localizing RAD51 to the sites of DNA damage. Despite mobilizing the DNA repair response, even very low levels of DNA damage result in the apoptosis of prophase-arrested oocytes. However, we show that, when apoptosis is inhibited, severe DNA damage is corrected via homologous recombination repair. The repair is sufficient to support fertility and maintain health and genetic fidelity in offspring. Thus, despite the preferential induction of apoptosis following exogenously induced genotoxic stress, prophase-arrested oocytes are highly capable of functionally efficient DNA repair. These data implicate DNA repair as a key quality control mechanism in the female germ line and a critical determinant of fertility and genetic integrity.
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Delves, C. J., H. H. Rees, and R. E. Howells. "Egg production in Brugia pahangi(Nematoda: Filarioidea)." Parasitology 98, no. 1 (February 1989): 105–13. http://dx.doi.org/10.1017/s0031182000059746.
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SummaryOogenesis in Brugia pahangi has been studied by means of the aceto-orcein chromosomal squash technique and light-microscope autoradiography. The use of colchicine has demonstrated a 2–3 mm terminal germinative zone within the ovary, in which continuous and rapid mitotic division of germ cells occurs. In 80% of the gonads, oocytes within a 1–2 mm length of the ovary proximal to the germinative zone were at the prophase of meiosis I. Primary oocytes with markedly less condensed chromatin, apparently interphase cells, were observed in the corresponding region of the ovary in the remaining 20% of material examined. A cyclical or phased development of primary oocytes is suggested. Autoradiographic studies, concerned with the incorporation of [5-3H]uridine into germ cells of B. pahangi in vitro, further suggest that the onset of meiotic prophase is associated with the initiation of high RNA synthetic activity. Following meiotic prophase, oocytes complete meiosis I before entering a period of growth during which the chromatin material is decondensed. Recondensation of chromosomes prior to meiosis II is only observed after fertilization within the seminal receptacle. On completion of meiosis II, with the extrusion of a polar body, the haploid chromosome complement of the female unites with that of the male, re-establishing the diploid number of the zygote (2n = 10).
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Zhou, Changyin, Yilong Miao, Zhaokang Cui, Xiayan ShiYang, Yu Zhang, and Bo Xiong. "The cohesin release factor Wapl interacts with Bub3 to govern SAC activity in female meiosis I." Science Advances 6, no. 15 (April 2020): eaax3969. http://dx.doi.org/10.1126/sciadv.aax3969.
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During mitotic prophase, cohesins are removed from chromosome arms by Wapl to ensure faithful sister chromatid separation. However, during female meiosis I, the resolution of chiasmata requires the proteolytic cleavage of cohesin subunit Rec8 along chromosome arms by Separase to separate homologs, and thus the role of Wapl remained unknown. Here, we report that Wapl functions as a regulator of spindle assembly checkpoint (SAC) to prevent aneuploidy in meiosis I. Depletion of Wapl accelerates meiotic progression, inactivates SAC, and causes meiotic defects such as aberrant spindle/chromosome structure and incorrect kinetochore-microtubule (K-MT) attachment, consequently leading to aneuploid eggs. Notably, we identify Bub3 as a binding partner of Wapl by immunoprecipitation and mass spectrometry analysis. We further determine that Wapl controls the SAC activity by maintaining Bub3 protein level and document that exogenous Bub3 restores the normal meiosis in Wapl-depleted oocytes. Together, our findings uncover unique, noncanonical roles for Wapl in mediating control of the SAC in female meiosis I.
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Roig, I., P. Robles, R. Garcia, I. Martínez-Flores, Ll Cabero, J. Egozcue, B. Liebe, H. Scherthan, and M. Garcia. "Chromosome 18 pairing behavior in human trisomic oocytes. Presence of an extra chromosome extends bouquet stage." Reproduction 129, no. 5 (May 2005): 565–75. http://dx.doi.org/10.1530/rep.1.00568.
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Little is known about the first meiotic prophase stages in the human female because these occur during fetal life, and only a few studies have addressed aneuploid human oocytes. In this paper, the synaptic process in the meiotic prophase in three 47, XX + 18 cases is analyzed. A complete study of the dynamics of centromeres and telomeres, cohesin core and synapsis development in aneuploid female meiosis was performed. Investigation of chromosome dynamics in prophase of trisomy 18 oocytes show that these events follow the major patterns seen earlier in euploid oocytes. However, there is a significant delay in the resolution of bouquet topology which could relate to the presence of a surplus chromosome 18 axial element in zygotene oocytes. Pachytene oocytes displayed normal synapsis among the three chromosome 18s. However, in some oocytes the surplus chromosome 18 core was aligned to the bivalent 18. As ataxia telangiectasia and Rad3 related kinase (ATR) has been described as a marker for late-pairing chromosomes in mice, ATR distribution was analyzed in human meiocytes –spermatocytes, euploid oocytes and trisomic oocytes. In contrast to the observations made in mice, no preferential staining for late-pairing chromosomes was observed in humans. In the cases studied, bivalent synapses progressed as in a normal ovary, contrasting with the hypothesis that a surplus chromosome can modify pairing of other chromosomes.
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Rosario, Roseanne, Hazel L. Stewart, Emily Walshe, and Richard A. Anderson. "Reduced retinoic acid synthesis accelerates prophase I and follicle activation." Reproduction 160, no. 3 (September 2020): 331–41. http://dx.doi.org/10.1530/rep-20-0221.
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In female mammals, reproductive potential is determined during fetal life by the formation of a non-renewable pool of primordial follicles. Initiation of meiosis is one of the defining features of germ cell differentiation and is well established to commence in response to retinoic acid. WIN 18,446 inhibits the conversion of retinol to retinoic acid, and therefore it was used to explore the impact of reduced retinoic acid synthesis on meiotic progression and thus germ cell development and subsequent primordial follicle formation. e13.5 mouse fetal ovaries were cultured in vitro and treated with WIN 18,446 for the first 3 days of a total of up to 12 days. Doses as low as 0.01 µM reduced transcript levels of the retinoic acid response genes Stra8 and Rarβ without affecting germ cell number. Higher doses resulted in germ cell loss, rescued with the addition of retinoic acid. WIN 18,446 significantly accelerated the progression of prophase I; this was seen as early as 48 h post treatment using meiotic chromosome spreads and was still evident after 12 days of culture using Tra98/Msy2 immunostaining. Furthermore, ovaries treated with WIN 18,446 at e13.5 but not at P0 had a higher proportion of growing follicles compared to vehicle controls, thus showing evidence of increased follicle activation. These data therefore indicate that retinoic acid is not necessary for meiotic progression but may have a role in the regulation of its progression and germ cell survival at that time and provide evidence for a link between meiotic arrest and follicle growth initiation.
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Freixa, L., M. García, and J. Egozcue. "The timing of first meiotic prophase in oocytes from female domestic dogs (Canis familiaris)." Genome 29, no. 1 (February 1, 1987): 208–10. http://dx.doi.org/10.1139/g87-036.
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Meiotic studies in 15 female puppies (Canis familiaris) revealed that in this species first meiotic prophase begins postnatally. Leptotene is observed until day 5, zygotene from day 5 to day 15, pachytene from day 10 to day 30, diplotene from day 15 to day 30, and dictyotene appears by day 30. These results are not in agreement with previous reports on the timing of oogenesis in this species. Key words: Canis familiaris, oogenesis.
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Larsen, J. K., A. G. Byskov, and I. J. Christensen. "Flow cytometry and sorting of meiotic prophase cells of female rabbits." Reproduction 76, no. 2 (March 1, 1986): 587–96. http://dx.doi.org/10.1530/jrf.0.0760587.
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Ryu, Kwon-Yul, Shamim A. Sinnar, Laura G. Reinholdt, Sergio Vaccari, Susan Hall, Manuel A. Garcia, Tatiana S. Zaitseva, et al. "The Mouse Polyubiquitin Gene Ubb Is Essential for Meiotic Progression." Molecular and Cellular Biology 28, no. 3 (December 10, 2007): 1136–46. http://dx.doi.org/10.1128/mcb.01566-07.
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ABSTRACT Ubiquitin is encoded in mice by two polyubiquitin genes, Ubb and Ubc, that are considered to be stress inducible and two constitutively expressed monoubiquitin (Uba) genes. Here we report that targeted disruption of Ubb results in male and female infertility due to failure of germ cells to progress through meiosis I and hypogonadism. In the absence of Ubb, spermatocytes and oocytes arrest during meiotic prophase, before metaphase of the first meiotic division. Although cellular ubiquitin levels are believed to be maintained by a combination of functional redundancy among the four ubiquitin genes, stress inducibility of the two polyubiquitin genes, and ubiquitin recycling by proteasome-associated isopeptidases, our results indicate that ubiquitin is required for and consumed during meiotic progression. The striking similarity of the meiotic phenotype in Ubb −/− germ cells to the sporulation defect in fission yeast (Schizosaccharomyces pombe) lacking a polyubiquitin gene suggests that a meiotic role of the polyubiquitin gene has been conserved throughout eukaryotic evolution.
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Tu, Zhaowei, Mustafa Bilal Bayazit, Hongbin Liu, Jingjing Zhang, Kiran Busayavalasa, Sanjiv Risal, Jingchen Shao, et al. "Speedy A–Cdk2 binding mediates initial telomere–nuclear envelope attachment during meiotic prophase I independent of Cdk2 activation." Proceedings of the National Academy of Sciences 114, no. 3 (December 28, 2016): 592–97. http://dx.doi.org/10.1073/pnas.1618465114.
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Telomere attachment to the nuclear envelope (NE) is a prerequisite for chromosome movement during meiotic prophase I that is required for pairing of homologous chromosomes, synapsis, and homologous recombination. Here we show that Speedy A, a noncanonical activator of cyclin-dependent kinases (Cdks), is specifically localized to telomeres in prophase I male and female germ cells in mice, and plays an essential role in the telomere–NE attachment. Deletion of Spdya in mice disrupts telomere–NE attachment, and this impairs homologous pairing and synapsis and leads to zygotene arrest in male and female germ cells. In addition, we have identified a telomere localization domain on Speedy A covering the distal N terminus and the Cdk2-binding Ringo domain, and this domain is essential for the localization of Speedy A to telomeres. Furthermore, we found that the binding of Cdk2 to Speedy A is indispensable for Cdk2’s localization on telomeres, suggesting that Speedy A and Cdk2 might be the initial components that are recruited to the NE for forming the meiotic telomere complex. However, Speedy A-Cdk2–mediated telomere–NE attachment is independent of Cdk2 activation. Our results thus indicate that Speedy A and Cdk2 might mediate the initial telomere–NE attachment for the efficient assembly of the telomere complex that is essential for meiotic prophase I progression.
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Tang, Lois, Thomas Machacek, Yasmine M. Mamnun, Alexandra Penkner, Jiradet Gloggnitzer, Christina Wegrostek, Robert Konrat, Michael F. Jantsch, Josef Loidl, and Verena Jantsch. "Mutations in Caenorhabditis elegans him-19 Show Meiotic Defects That Worsen with Age." Molecular Biology of the Cell 21, no. 6 (March 15, 2010): 885–96. http://dx.doi.org/10.1091/mbc.e09-09-0811.
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From a screen for meiotic Caenorhabditis elegans mutants based on high incidence of males, we identified a novel gene, him-19, with multiple functions in prophase of meiosis I. Mutant him-19(jf6) animals show a reduction in pairing of homologous chromosomes and subsequent bivalent formation. Consistently, synaptonemal complex formation is spatially restricted and possibly involves nonhomologous chromosomes. Also, foci of the recombination protein RAD-51 occur delayed or cease altogether. Ultimately, mutation of him-19 leads to chromosome missegregation and reduced offspring viability. The observed defects suggest that HIM-19 is important for both homology recognition and formation of meiotic DNA double-strand breaks. It therefore seems to be engaged in an early meiotic event, resembling in this respect the regulator kinase CHK-2. Most astonishingly, him-19(jf6) hermaphrodites display worsening of phenotypes with increasing age, whereas defects are more severe in female than in male meiosis. This finding is consistent with depletion of a him-19-dependent factor during the production of oocytes. Further characterization of him-19 could contribute to our understanding of age-dependent meiotic defects in humans.
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Bella, J. L., J. Gosálvez, and J. De la Torre. "Males vs. female meiotic prophase in a grasshopper, Arcyptera microptera (Orthoptera: Acridiae)." Genetica 82, no. 3 (November 1990): 151–56. http://dx.doi.org/10.1007/bf00056357.
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Marec, František, and Walther Traut. "Synaptonemal complexes in female and male meiotic prophase of Ephestia kuehniella (Lepidoptera)." Heredity 71, no. 4 (October 1993): 394–404. http://dx.doi.org/10.1038/hdy.1993.154.
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Cusidó, L., R. Pujol, J. Egozcue, and M. García. "Cyclophosphamide-induced synaptonemal complex damage during meiotic prophase of female Rattus norvegicus." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 329, no. 2 (July 1995): 131–41. http://dx.doi.org/10.1016/0027-5107(95)00029-i.
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Kupriyanova, L. A., L. D. Safronova, and A. I. Chekunova. "Meiotic Chromosomes, Synaptonemal Complexes in a Female Viviparous Lizard (Zootoca vivipara) in Prophase I of Meiosis." Russian Journal of Genetics 55, no. 6 (June 2019): 774–78. http://dx.doi.org/10.1134/s1022795419060085.
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Hodges, Craig A., Renée LeMaire-Adkins, and Patricia A. Hunt. "Coordinating the segregation of sister chromatids during the first meiotic division: evidence for sexual dimorphism." Journal of Cell Science 114, no. 13 (July 1, 2001): 2417–26. http://dx.doi.org/10.1242/jcs.114.13.2417.
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Errors during the first meiotic division are common in our species, but virtually all occur during female meiosis. The reason why oogenesis is more error prone than spermatogenesis remains unknown. Normal segregation of homologous chromosomes at the first meiotic division (MI) requires coordinated behavior of the sister chromatids of each homolog. Failure of sister kinetochores to act cooperatively at MI, or precocious sister chromatid segregation (PSCS), has been postulated to be a major contributor to human nondisjunction. To investigate the factors that influence PSCS we utilized the XO mouse, since the chromatids of the single X chromosome frequently segregate at MI, and the propensity for PSCS is influenced by genetic background. Our studies demonstrate that the strain-specific differences in PSCS are due to the actions of an autosomal trans-acting factor or factors. Since components of the synaptonemal complex are thought to play a role in centromere cohesion and kinetochore orientation, we evaluated the behavior of the X chromosome at prophase to determine if this factor influenced the propensity of the chromosome for self-synapsis. We were unable to directly correlate synaptic differences with subsequent segregation behavior. However, unexpectedly, we uncovered a sexual dimorphism that may partially explain sex-specific differences in the fidelity of meiotic chromosome segregation. Specifically, in the male remnants of the synaptonemal complex remain associated with the centromeres until anaphase of the second meiotic division (MII), whereas in the female, all traces of synaptonemal complex (SC) protein components are lost from the chromosomes before the onset of the first meiotic division. This finding suggests a sex-specific difference in the components used to correctly segregate chromosomes during meiosis, and may provide a reason for the high error frequency during female meiosis.
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Larson, Stephanie M., Hyo J. Lee, Pei-hsuan Hung, Lauren M. Matthews, Douglas N. Robinson, and Janice P. Evans. "Cortical Mechanics and Meiosis II Completion in Mammalian Oocytes Are Mediated by Myosin-II and Ezrin-Radixin-Moesin (ERM) Proteins." Molecular Biology of the Cell 21, no. 18 (September 15, 2010): 3182–92. http://dx.doi.org/10.1091/mbc.e10-01-0066.
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Cell division is inherently mechanical, with cell mechanics being a critical determinant governing the cell shape changes that accompany progression through the cell cycle. The mechanical properties of symmetrically dividing mitotic cells have been well characterized, whereas the contribution of cellular mechanics to the strikingly asymmetric divisions of female meiosis is very poorly understood. Progression of the mammalian oocyte through meiosis involves remodeling of the cortex and proper orientation of the meiotic spindle, and thus we hypothesized that cortical tension and stiffness would change through meiotic maturation and fertilization to facilitate and/or direct cellular remodeling. This work shows that tension in mouse oocytes drops about sixfold during meiotic maturation from prophase I to metaphase II and then increases ∼1.6-fold upon fertilization. The metaphase II egg is polarized, with tension differing ∼2.5-fold between the cortex over the meiotic spindle and the opposite cortex, suggesting that meiotic maturation is accompanied by assembly of a cortical domain with stiffer mechanics as part of the process to achieve asymmetric cytokinesis. We further demonstrate that actin, myosin-II, and the ERM (Ezrin/Radixin/Moesin) family of proteins are enriched in complementary cortical domains and mediate cellular mechanics in mammalian eggs. Manipulation of actin, myosin-II, and ERM function alters tension levels and also is associated with dramatic spindle abnormalities with completion of meiosis II after fertilization. Thus, myosin-II and ERM proteins modulate mechanical properties in oocytes, contributing to cell polarity and to completion of meiosis.
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Golubovskaya, Inna, Nadezhda Avalkina, and William F. Sheridan. "New Insights Into the Role of the Maize ameiotic1 Locus." Genetics 147, no. 3 (November 1, 1997): 1339–50. http://dx.doi.org/10.1093/genetics/147.3.1339.
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In maize the am1-1 mutant allele results in both the male and female meiocytes undergoing mitosis in place of the meiotic divisions. A second mutant allele am1-praI enables both the male and female meiocytes to proceed to the early zygotene stage of meiotic prophase I before being blocked. Here we report on three new alleles that allow all male meiocytes to undergo mitosis but in female meiocytes approximately one quarter (am1-2), one half (am1-485, or all (am1-489) of them are blocked at an abnormal interphase stage. Previous analysis has shown that am1-praI is dominant to am1-1 in male meiocytes. Cytological analysis of heteroallelic combinations in female meiocytes now indicates a dominance relationship of am1-praI > am1-1 > am1-2/am1-485 > am1-489. The evidence provided by the female phenotypes of the new mutant alleles suggest that, whereas the normal am1 allele is required for the meiocytes to proceed through meiosis, a partially functional allele may be required for their diversion into a mitotic division. The partial or complete blockage of mitosis in female meiocytes carrying the new am1 alleles rules out the possibility that the mitotic division of mutant meiocytes reflects a simple default pathway for cells that cannot initiate meiosis. This locus may have a dual function.
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Matveevsky, Sergey, Tsenka Chassovnikarova, Tatiana Grishaeva, Maret Atsaeva, Vasilii Malygin, Irina Bakloushinskaya, and Oxana Kolomiets. "Kinase CDK2 in Mammalian Meiotic Prophase I: Screening for Hetero- and Homomorphic Sex Chromosomes." International Journal of Molecular Sciences 22, no. 4 (February 17, 2021): 1969. http://dx.doi.org/10.3390/ijms22041969.
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Cyclin-dependent kinases (CDKs) are crucial regulators of the eukaryotic cell cycle. The critical role of CDK2 in the progression of meiosis was demonstrated in a single mammalian species, the mouse. We used immunocytochemistry to study the localization of CDK2 during meiosis in seven rodent species that possess hetero- and homomorphic male sex chromosomes. To compare the distribution of CDK2 in XY and XX male sex chromosomes, we performed multi-round immunostaining of a number of marker proteins in meiotic chromosomes of the rat and subterranean mole voles. Antibodies to the following proteins were used: RAD51, a member of the double-stranded DNA break repair machinery; MLH1, a component of the DNA mismatch repair system; and SUN1, which is involved in the connection between the meiotic telomeres and nuclear envelope, alongside the synaptic protein SYCP3 and kinetochore marker CREST. Using an enhanced protocol, we were able to assess the distribution of as many as four separate proteins in the same meiotic cell. We showed that during prophase I, CDK2 localizes to telomeric and interstitial regions of autosomes in all species investigated (rat, vole, hamster, subterranean mole voles, and mole rats). In sex bivalents following synaptic specificity, the CDK2 signals were distributed in three different modes. In the XY bivalent in the rat and mole rat, we detected numerous CDK2 signals in asynaptic regions and a single CDK2 focus on synaptic segments, similar to the mouse sex chromosomes. In the mole voles, which have unique XX sex chromosomes in males, CDK2 signals were nevertheless distributed similarly to the rat XY sex chromosomes. In the vole, sex chromosomes did not synapse, but demonstrated CDK2 signals of varying intensity, similar to the rat X and Y chromosomes. In female mole voles, the XX bivalent had CDK2 pattern similar to autosomes of all species. In the hamster, CDK2 signals were revealed in telomeric regions in the short synaptic segment of the sex bivalent. We found that CDK2 signals colocalize with SUN1 and MLH1 signals in meiotic chromosomes in rats and mole voles, similar to the mouse. The difference in CDK2 manifestation at the prophase I sex chromosomes can be considered an example of the rapid chromosome evolution in mammals.
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Alton, Michelle, Mau Pan Lau, Michele Villemure, and Teruko Taketo. "The behavior of the X- and Y-chromosomes in the oocyte during meiotic prophase in the B6.YTIR sex-reversed mouse ovary." REPRODUCTION 135, no. 2 (February 2008): 241–52. http://dx.doi.org/10.1530/rep-07-0383.
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Sexual differentiation of the germ cells follows gonadal differentiation, which is determined by the presence or the absence of the Y-chromosome. Consequently, oogenesis and spermatogenesis take place in the germ cells with XX and XY sex chromosomal compositions respectively. It is unclear how sexual dimorphic regulation of meiosis is associated with the sex-chromosomal composition. In the present study, we examined the behavior of the sex chromosomes in the oocytes of the B6.YTIRsex-reversed female mouse, in comparison with XO and XX females. As the sex chromosomes fail to pair in both XY and XO oocytes during meiotic prophase, we anticipated that the pairing failure may lead to excessive oocyte loss. However, the total number of germ cells, identified by immunolabeling of germ cell nuclear antigen 1 (GCNA1), did not differ between XY and XX ovaries or XO and XX ovaries up to the day of delivery. The progression of meiotic prophase, assessed by immunolabeling of synaptonemal complex components, was also similar between the two genotypes of ovaries. These observations suggest that the failure in sex-chromosome pairing is not sufficient to cause oocyte loss. On the other hand, labeling of phosphorylated histone γH2AX, known to be associated with asynapsis and transcriptional repression, was seen over the X-chromosome but not over the Y-chromosome in the majority of XY oocytes at the pachytene stage. For comparison, γH2AX labeling was seen only in the minority of XX oocytes at the same stage. We speculate that the transcriptional activity of sex chromosomes in the XY oocyte may be incompatible with ooplasmic maturation.
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Turner, James M. A., Paul S. Burgoyne, and Prim B. Singh. "M31 and macroH2A1.2 colocalise at the pseudoautosomal region during mouse meiosis." Journal of Cell Science 114, no. 18 (September 15, 2001): 3367–75. http://dx.doi.org/10.1242/jcs.114.18.3367.
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Progression through meiotic prophase is associated with dramatic changes in chromosome condensation. Two proteins that have been implicated in effecting these changes are the mammalian HP1-like protein M31 (HP1β or MOD1) and the unusual core histone macroH2A1.2. Previous analyses of M31 and macroH2A1.2 localisation in mouse testis sections have indicated that both proteins are components of meiotic centromeric heterochromatin and of the sex body, the transcriptionally inactive domain of the X and Y chromosomes. This second observation has raised the possibility that these proteins co-operate in meiotic sex chromosome inactivation. In order to investigate the roles of M31 and macroH2A1.2 in meiosis in greater detail, we have examined their localisation patterns in surface-spread meiocytes from male and female mice. Using this approach, we report that, in addition to their previous described staining patterns, both proteins localise to a focus within the portion of the pseudoautosomal region (PAR) that contains the steroid sulphatase (Sts) gene. In light of the timing of its appearance and of its behaviour in sex-chromosomally variant mice, we suggest a role for this heterochromatin focus in preventing complete desynapsis of the terminally associated X and Y chromosomes prior to anaphase I.
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Robles, P., I. Roig, R. Garcia, A. Ortega, J. Egozcue, L. L. Cabero, and M. Garcia. "Pairing and synapsis in oocytes from female fetuses with euploid and aneuploid chromosome complements." Reproduction 133, no. 5 (May 2007): 899–907. http://dx.doi.org/10.1530/rep-06-0243.
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Only little is known about the meiotic prophase events in human oocytes, although some of them are involved in the origin of aneuploidies. Here, a broad study of the pairing and synaptic processes in 3263 human euploid and 2613 aneuploid oocytes (47,XX, +21 and 47,XX, +13), using different techniques and methods, is presented in order to elucidate the characteristics of this essential meiotic process. Our results reaffirm the existence of a common high efficiency in the pairing process leading to the obtainment of a bivalent for all chromosomes studied in euploid and aneuploid cases. Nevertheless, this high efficiency was insufficient to consistently produce trivalents in aneuploid oocytes. Trivalent 21 was only observed in 48.8% of the 47,XX, +21 pachytene-stage oocytes studied, and trivalent 13 was found in 68.7% of the 47,XX, +13 pachytene-stage oocytes analyzed. Our data confirm the hypothesis which suggests that in human oocytes the presence of an extra chromosome could interfere in bouquet dynamics. In addition, the pairing process of the X chromosome is altered in trisomic 21 oocytes, providing evidence of the influence that an extra chromosome 21 may cause meiotic progression.
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Pujol, R., L. Cusidó, A. Rubio, J. Egozcue, and M. Garcia. "X-ray-induced synaptonemal complex damage during meiotic prophase in female fetuses of Rattus norvegicus." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 379, no. 2 (October 1997): 127–34. http://dx.doi.org/10.1016/s0027-5107(97)00115-2.
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Gupta, Anumegha, Meenakshi Tiwari, Alka Sharma, Ashutosh N. Pandey, Pramod K. Yadav, Anil K. Yadav, Shilpa Prasad, Ajai K. Pandey, Tulsidas G. Shrivastav, and Shail K. Chaube. "Cyclic nucleotides regulate oocyte meiotic maturation and quality in mammals." Journal of Reproductive Health and Medicine 3 (November 6, 2020): 1. http://dx.doi.org/10.25259/jrhm_7_2020.
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Oocyte meiosis is a prolong series of events that are comprised several intermittent channels in mammals. Oocyte meiosis starts during fetal life and then gets arrested at diplotene stage of first meiotic prophase in follicular oocyte. The continuous transfer of cyclic adenosine 3’, 5’-monophosphate (cAMP) and cyclic guanosine 3’, 5’-monophosphate (cGMP) from encircling granulosa cells to the oocyte through gap junctions helps in the maintenance of their high level required to achieve the long-lasting diplotene arrest so-called germinal vesicle stage. Phosphodiesterase inhibitors have been used to elevate intracellular level of both cyclic nucleotides and prevent spontaneous resumption of meiosis in oocytes under in vitro culture conditions. On the other hand, disruption of gap junction either by pituitary gonadotropin or by physical removal of encircling granulosa cells interrupts transfer of these nucleotides to the oocyte. As a result, intraoocyte cAMP as well as cGMP levels are decreased drastically that initiate downstream pathways to destabilize maturation-promoting factor (MPF). The destabilized MPF initiates meiotic resumption from diplotene arrest in mammalian oocytes. Oocyte meiosis further progresses from metaphase I to metaphase II stage and extrudes first polar body to get converted into haploid female gamete at the time of ovulation. Indeed, high level of cAMP as well as cGMP levels maintains diplotene arrest for a long time in follicular oocytes. On the other hand, transient decrease of their levels drives resumption from diplotene arrest, thereby meiotic maturation process, which enables oocyte to achieve developmental competency. Any defect in this process directly affects oocyte quality and thereby reproductive outcome in mammals including human.
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Ma, Jun-Yu, Li-Ying Yan, Zhen-Bo Wang, Shi-Ming Luo, William S. B. Yeung, Xiang-Hong Ou, Qing-Yuan Sun, and Jie Qiao. "Meiotic chromatid recombination and segregation assessed with human single cell genome sequencing data." Journal of Medical Genetics 56, no. 3 (December 4, 2018): 156–63. http://dx.doi.org/10.1136/jmedgenet-2018-105612.
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BackgroundThe human oocyte transmits one set of haploid genome into female pronucleus (FPN) while discards the remaining genome into the first polar body (PB1) and the second polar body (PB2). The FPN genome carries an assembly of maternal and paternal genome that resulted from homologous recombination during the prophase of the first meiosis. However, how parental genome has been shuffled and transmitted is difficult to assess by analysing only the progeny’s genome.ObjectiveTo assess meiotic chromatid recombination and segregation in human oocytes.MethodsSingle cell genome sequencing data of PB1, PB2 and FPN that originated from the same oocyte were used to analyse the human oocyte homologous chromosome interaction and segregation. To analyse whether chromosomes were non-randomly segregated into polar bodies or pronucleus, we analysed the ratio of crossover in PB2 and FPN, and constructed a model to detect the randomness of oocyte chromosome segregation.ResultsWe found that during oocyte meiosis, in addition to homologous chromosome recombination, there was also a genome conversion phenomenon which generated a non-reciprocal genetic information transmission between homologous chromosomes. We also inferred that during meiosis, DNA breaks and repairs frequently occurred at centromere-adjacent regions. From our data we did not find obvious evidence supporting the crossover number-based or SNP-based meiotic drive in oocytes.ConclusionIn addition to the crossover-based recombination, during human oocyte meiosis, a direct genome conversion between homologous chromosomes is used in some oocytes. Our findings are helpful in understanding the specific features of meiotic chromatid recombination and segregation in human oocytes.
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Dichinnson, H. "Cytoplasniic differentiation during microsporogenesis in higher plants." Acta Societatis Botanicorum Poloniae 50, no. 1-2 (2014): 3–12. http://dx.doi.org/10.5586/asbp.1981.001.
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Conspicuous cytoplasmic dedifferentiation in the pollen mother cells takes place early in the meiotic prophase of many plants. This event involves the removal of much of the cytoplasmic RNA. and the differentiation of both plastids and mitochondria to approaching the sole expression of their genomes. Much of the RNA removed from the cytoplasm passes to the nucleoplasm where it is utilised in the construction of a new `generation' of ribusomes. These new ribosomes are incorporated into cytoplasmic `nuclewhich disintegrate in the post-meiotic cytoplasm, restoring its ribosomes to pre-prophase levels. These changes are interpreted as evidence of a process by which the cytoplasm is cleansed of sporophytic control elements, both for the expression of the new gametophytic genome, and in the female cells of higher plants, for transmission to the new generation. The absence of control elements (presumably long-term messenger RNA) from the cytoplasm would result in the dedifferentiation observed in the organelles, and the low levels of reserves in these cells presumably results in characteristically lengthy and unusual redifferentiation of both plastids and mitochondria, once information-carrying molecules again enter the cytosol.
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Jing, Juli, Ting Zhang, Yazhong Wang, Zhenhai Cui, and Yan He. "ZmRAD51C Is Essential for Double-Strand Break Repair and Homologous Recombination in Maize Meiosis." International Journal of Molecular Sciences 20, no. 21 (November 5, 2019): 5513. http://dx.doi.org/10.3390/ijms20215513.
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Radiation sensitive 51 (RAD51) recombinases play crucial roles in meiotic double-strand break (DSB) repair mediated by homologous recombination (HR) to ensure the correct segregation of homologous chromosomes. In this study, we identified the meiotic functions of ZmRAD51C, the maize homolog of Arabidopsis and rice RAD51C. The Zmrad51c mutants exhibited regular vegetative growth but complete sterility for both male and female inflorescence. However, the mutants showed hypersensitivity to DNA damage by mitomycin C. Cytological analysis indicated that homologous chromosome pairing and synapsis were rigorously inhibited, and meiotic chromosomes were often entangled from diplotene to metaphase I, leading to chromosome fragmentation at anaphase I. Immunofluorescence analysis showed that although the signals of the axial element absence of first division (AFD1) and asynaptic1 (ASY1) were normal, the assembly of the central element zipper1 (ZYP1) was severely disrupted. The DSB formation was normal in Zmrad51c meiocytes, symbolized by the regular occurrence of γH2AX signals. However, RAD51 and disrupted meiotic cDNA 1 (DMC1) signals were never detected at the early stage of prophase I in the mutant. Taken together, our results indicate that ZmRAD51C functions crucially for both meiotic DSB repair and homologous recombination in maize.
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Bellani, Marina A., Kingsley A. Boateng, Dianne McLeod, and R. Daniel Camerini-Otero. "The Expression Profile of the Major Mouse SPO11 Isoforms Indicates that SPO11β Introduces Double Strand Breaks and Suggests that SPO11α Has an Additional Role in Prophase in both Spermatocytes and Oocytes." Molecular and Cellular Biology 30, no. 18 (July 20, 2010): 4391–403. http://dx.doi.org/10.1128/mcb.00002-10.
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ABSTRACT Both in mice and humans, two major SPO11 isoforms are generated by alternative splicing: SPO11α (exon 2 skipped) and SPO11β. Thus, the alternative splicing event must have emerged before the mouse and human lineages diverged and was maintained during 90 million years of evolution, arguing for an essential role for both isoforms. Here we demonstrate that developmental regulation of alternative splicing at the Spo11 locus governs the sequential expression of SPO11 isoforms in male meiotic prophase. Protein quantification in juvenile mice and in prophase mutants indicates that early spermatocytes synthesize primarily SPO11β. Estimation of the number of SPO11 dimers (ββ/αβ/αα) in mutants in which spermatocytes undergo a normal number of double strand breaks but arrest in midprophase due to inefficient repair argues for a role for SPO11β-containing dimers in introducing the breaks in leptonema. Expression kinetics in males suggested a role for SPO11α in pachytene/diplotene spermatocytes. Nevertheless, we found that both alternative transcripts can be detected in oocytes throughout prophase I, arguing against a male-specific function for this isoform. Altogether, our data support a role for SPO11α in mid- to late prophase, presumably acting as a topoisomerase, that would be conserved in male and female meiocytes.
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Quartuccio, Suzanne M., Shweta S. Dipali, and Karen Schindler. "Haspin inhibition reveals functional differences of interchromatid axis–localized AURKB and AURKC." Molecular Biology of the Cell 28, no. 17 (August 15, 2017): 2233–40. http://dx.doi.org/10.1091/mbc.e16-12-0850.
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Aneuploidy is the leading genetic abnormality contributing to infertility, and chromosome segregation errors are common during female mammalian meiosis I (MI). Previous results indicate that haspin kinase regulates resumption of meiosis from prophase arrest, chromosome condensation, and kinetochore–microtubule attachments during early prometaphase of MI. Here we report that haspin inhibition in late prometaphase I causes acceleration of MI, bypass of the spindle assembly checkpoint (SAC), and loss of interchromatid axis–localized Aurora kinase C. Meiotic cells contain a second chromosomal passenger complex (CPC) population, with Aurora kinase B (AURKB) bound to INCENP. Haspin inhibition in oocytes from Aurkc−/− mice, where AURKB is the sole CPC kinase, does not alter MI completion timing, and no change in localization of the SAC protein, MAD2, is observed. These data suggest that AURKB on the interchromatid axis is not needed for SAC activation and illustrate a key difference between the functional capacities of the two AURK homologues.
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Sumiyoshi, Eisuke, Asako Sugimoto, and Masayuki Yamamoto. "Protein phosphatase 4 is required for centrosome maturation in mitosis and sperm meiosis inC. elegans." Journal of Cell Science 115, no. 7 (April 1, 2002): 1403–10. http://dx.doi.org/10.1242/jcs.115.7.1403.
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The centrosome consists of two centrioles surrounded by the pericentriolar material (PCM). In late G2 phase, centrosomes enlarge by recruiting extra PCM,and concomitantly its microtubule nucleation activity increases dramatically. The regulatory mechanisms of this dynamic change of centrosomes are not well understood. Protein phosphatase 4 (PP4) is known to localize to mitotic centrosomes in mammals and Drosophila. An involvement of PP4 in the mitotic spindle assembly has been implicated in Drosophila, but in vivo functions of PP4 in other organisms are largely unknown. Here we characterize two Caenorhabditis elegans PP4 genes, named pph-4.1 and pph-4.2. Inhibition of the function of each gene by RNA-mediated interference (RNAi) revealed that PPH-4.1 was essential for embryogenesis but PPH-4.2 was not. More specifically, PPH-4.1 was required for the formation of spindles in mitosis and sperm meiosis. However, this phosphatase was apparently dispensable for female meiotic divisions, which do not depend on centrosomes. In the cell depleted of pph-4.1 activity,localization of γ-tubulin and a Polo-like kinase homologue to the centrosome was severely disturbed. Immunofluorescence staining revealed that PPH-4.1 was present at centrosomes from prophase to telophase, but not during interphase. These results indicate that PPH-4.1 is a centrosomal protein involved in the recruitment of PCM components to the centrosome, and is essential for the activation of microtubule nucleation potential of the centrosome. Furthermore, chiasmata between homologous chromosomes were often absent in oocytes that lacked pph-4.1 activity. Thus, besides promoting spindle formation, PPH-4.1 appears to play a role in either the establishment or the maintenance of chiasmata during meiotic prophase I.
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Cullen, C. Fiona, Amy L. Brittle, Takashi Ito, and Hiroyuki Ohkura. "The conserved kinase NHK-1 is essential for mitotic progression and unifying acentrosomal meiotic spindles in Drosophila melanogaster." Journal of Cell Biology 171, no. 4 (November 21, 2005): 593–602. http://dx.doi.org/10.1083/jcb.200508127.
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Conventional centrosomes are absent from the spindle in female meiosis in many species, but it is not clear how multiple chromosomes form one shared bipolar spindle without centrosomes. We identified a female sterile mutant in which each bivalent chromosome often forms a separate bipolar metaphase I spindle. Unlike wild type, prophase I chromosomes fail to form a single compact structure within the oocyte nucleus, although the integrity of metaphase I chromosomes appears to be normal. Molecular analysis indicates that the mutant is defective in the conserved kinase nucleosomal histone kinase-1 (NHK-1). Isolation of further alleles and RNA interference in S2 cells demonstrated that NHK-1 is also required for mitotic progression. NHK-1 itself is phosphorylated in mitosis and female meiosis, suggesting that this kinase is part of the regulatory system coordinating progression of mitosis and meiosis.
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Hagihara, Yota, Satoshi Asada, Takahiro Maeda, Toru Nakano, and Shinpei Yamaguchi. "Tet1 regulates epigenetic remodeling of the pericentromeric heterochromatin and chromocenter organization in DNA hypomethylated cells." PLOS Genetics 17, no. 6 (June 24, 2021): e1009646. http://dx.doi.org/10.1371/journal.pgen.1009646.
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Pericentromeric heterochromatin (PCH), the constitutive heterochromatin of pericentromeric regions, plays crucial roles in various cellular events, such as cell division and DNA replication. PCH forms chromocenters in the interphase nucleus, and chromocenters cluster at the prophase of meiosis. Chromocenter clustering has been reported to be critical for the appropriate progression of meiosis. However, the molecular mechanisms underlying chromocenter clustering remain elusive. In this study, we found that global DNA hypomethylation, 5hmC enrichment in PCH, and chromocenter clustering of Dnmt1-KO ESCs were similar to those of the female meiotic germ cells. Tet1 is essential for the deposition of 5hmC and facultative histone marks of H3K27me3 and H2AK119ub at PCH, as well as chromocenter clustering. RING1B, one of the core components of PRC1, is recruited to PCH by TET1, and PRC1 plays a critical role in chromocenter clustering. In addition, the rearrangement of the chromocenter under DNA hypomethylated condition was mediated by liquid-liquid phase separation. Thus, we demonstrated a novel role of Tet1 in chromocenter rearrangement in DNA hypomethylated cells.
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Dietrich, A. J. J. "The influence of hypotonic treatment on the morphology of meiotic stages II. Prophase of the first meiotic division of female mice up to dictyotene." Genetica 70, no. 3 (October 1986): 161–65. http://dx.doi.org/10.1007/bf00122182.
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Cao, Yun-Kao, Zhi-Sheng Zhong, Da-Yuan Chen, Gui-Xue Zhang, Heide Schatten, and Qing-Yuan Sun. "Cell cycle-dependent localization and possible roles of the small GTPase Ran in mouse oocyte maturation, fertilization and early cleavage." Reproduction 130, no. 4 (October 2005): 431–40. http://dx.doi.org/10.1530/rep.1.00391.
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The small GTPase Ran controls numerous cellular processes of the mitotic cell cycle. In this experiment, we investigated the localization and possible roles of Ran during mouse oocyte meiotic maturation, fertilization and early cleavage by using confocal laser scanning microscopy, antibody microinjection and microtubule disturbance. The results showed that Ran was localized mainly in the nucleus (except for the nucleolus) in the oocyte, zygote and early embryo. At pro-metaphase of meiosis I, Ran distributed throughout the cell, but predominantly concentrated around the condensed chromosomes. During the completion of meiosis I and meiosis II, it concentrated to the meiotic spindle microtubules except for the midbody region. After sperm penetration, Ran dispersed with the extrusion of the second polar body and gradually concentrated in the male and female pronuclei thereafter. Ran was also observed to exist diffusely in the cytoplasm in prophase; it concentrated at the mitotic spindle, and migrated to the nucleus during early cleavage. Ran’s concentration around the spindle disappeared when microtubule assembly was inhibited by colchicine, while it was concentrated around the chromosomes after microtubule stabilization with taxol treatment. Ran did not display any role in cytokinesis during division when pseudo-cleavage of germinal vesicle-intact oocytes was induced. Anti-Ran antibody microinjection decreased the germinal vesicle breakdown and the first polar body extrusion, and distorted spindle organization and chromosome alignment. Our results indicate that Ran has a cell cycle-dependent localization and may have regulatory roles in cell cycle progression and microtubule organization in mouse oocytes, fertilized eggs and early embryos.
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Chastant-Maillard, Sylvie, Christine Viaris de Lesegno, Martine Chebrout, Sandra Thoumire, Thierry Meylheuc, Alain Fontbonne, Marc Chodkiewicz, Marie Saint-Dizier, and Karine Reynaud. "The canine oocyte: uncommon features of in vivo and in vitro maturation." Reproduction, Fertility and Development 23, no. 3 (2011): 391. http://dx.doi.org/10.1071/rd10064.
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The biology of the canine oocyte is unusual compared with that of other mammalian females. The present paper reviews both in vivo and in vitro specificities of canine oocytes. Final follicular growth in the bitch is characterised by an early appearance of LH binding sites in the granulosa, a high proportion of polyovular follicles and a preovulatory luteinisation, starting at the time of the LH surge. Through follicular fluid, preovulatory oocytes are thus exposed to high levels of progesterone, as high as 1000-fold plasma concentrations. The composition of the follicular fluid is affected by the size of the female. The more specific aspect of oocyte biology in the bitch is ovulation: oocytes are expelled immature, at the Prophase I stage. Ovulatory follicles are 6–8 mm in diameter, releasing oocytes from 110 µm, with dark cytoplasm. Resumption of meiosis occurs from 48 h postovulation, MII stages appearing 48–54 h after ovulation. The mechanisms controlling such a late meiotic resumption are still unknown. Granulosa cells seem to play a central role as in other mammalian species, but not with cAMP as the principal mediator. The importance of a transient reactivation of oocyte transcription a few hours before meiotic resumption is to be explored. These specific features may contribute to the low efficiency of IVM. Only 10–20% oocytes reach the metaphase stage and suffer from a poor cytoplasmic maturation. Moreover, in vitro culture of canine oocytes is associated with a high proportion of degeneration. To date, IVM of the oocytes is the main limiting factor for the development of assisted reproductive techniques in the canine. A better knowledge of the basic physiology of folliculogenesis and the molecular mechanisms controlling oocyte meiosis resumption in this species may allow us to overcome this obstacle.
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Garner, Tyler Bruce, James Malcolm Hester, Allison Carothers, and Francisco J. Diaz. "Role of zinc in female reproduction." Biology of Reproduction 104, no. 5 (February 17, 2021): 976–94. http://dx.doi.org/10.1093/biolre/ioab023.
Full textAbstract:
Abstract Zinc is a critical component in a number of conserved processes that regulate female germ cell growth, fertility, and pregnancy. During follicle development, a sufficient intracellular concentration of zinc in the oocyte maintains meiotic arrest at prophase I until the germ cell is ready to undergo maturation. An adequate supply of zinc is necessary for the oocyte to form a fertilization-competent egg as dietary zinc deficiency or chelation of zinc disrupts maturation and reduces the oocyte quality. Following sperm fusion to the egg to initiate the acrosomal reaction, a quick release of zinc, known as the zinc spark, induces egg activation in addition to facilitating zona pellucida hardening and reducing sperm motility to prevent polyspermy. Symmetric division, proliferation, and differentiation of the preimplantation embryo rely on zinc availability, both during the oocyte development and post-fertilization. Further, the fetal contribution to the placenta, fetal limb growth, and neural tube development are hindered in females challenged with zinc deficiency during pregnancy. In this review, we discuss the role of zinc in germ cell development, fertilization, and pregnancy with a focus on recent studies in mammalian females. We further detail the fundamental zinc-mediated reproductive processes that have only been explored in non-mammalian species and speculate on the role of zinc in similar mechanisms of female mammals. The evidence collected over the last decade highlights the necessity of zinc for normal fertility and healthy pregnancy outcomes, which suggests zinc supplementation should be considered for reproductive age women at risk of zinc deficiency.
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Dai, Xiangyan, Xinkai Cheng, Jianfei Huang, Yanping Gao, Deshou Wang, Zhi Feng, Gang Zhai, et al. "Rbm46, a novel germ cell-specific factor, modulates meiotic progression and spermatogenesis." Biology of Reproduction 104, no. 5 (February 2, 2021): 1139–53. http://dx.doi.org/10.1093/biolre/ioab016.
Full textAbstract:
Abstract It has been suggested that many novel RNA-binding proteins (RBPs) are required for gametogenesis, but the necessity of few of these proteins has been functionally verified. Here, we identified one RBP, Rbm46, and investigated its expression pattern and role in zebrafish reproduction. We found that rbm46 is maternally provided and specifically expressed in the germ cells of gonadal tissues using in situ hybridization, reverse transcription-PCR, and quantitative real-time polymerase chain reaction (qRT-PCR). Two independent rbm46 mutant zebrafish lines were generated via the transcription activator-like effector nuclease technique. Specific disruption of rbm46 resulted in masculinization and infertility in the mutants. Although the spermatogonia appeared grossly normal in the mutants, spermatogenesis was impaired, and meiosis events were not observed. The introduction of a tp53M214K mutation could not rescue the female-to-male sex-reversal phenotype, indicating that rbm46 acts independently of the p53-dependent apoptotic pathway. RNA sequencing and qRT-PCR subsequently indicated that Rbm46 might be involved in the posttranscriptional regulation of functional genes essential for germ cell development, such as nanos3, dazl, and sycp3, during gametogenesis. Together, our results reveal for the first time the crucial role of rbm46 in regulating germ cell development in vivo through promotion of germ cell progression through meiosis prophase I.
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Ueda, T., K. Yamazaki, R. Suzuki, H. Fujimoto, H. Sasaki, Y. Sakaki, and T. Higashinakagawa. "Parental methylation patterns of a transgenic locus in adult somatic tissues are imprinted during gametogenesis." Development 116, no. 4 (December 1, 1992): 831–39. http://dx.doi.org/10.1242/dev.116.4.831.
Full textAbstract:
The methylation status of a mouse metallothionein-I/human transthyretin fusion gene was studied during gametogenesis in transgenic mice. In the adult tissues of this mouse line, the promoter region of the transgene on chromosome 11 is methylated when it is maternally inherited and undermethylated when it is paternally inherited. Germ cells from various developmental stages of gametogenesis were isolated, and their DNAs were assayed using methylation-sensitive restriction endonucleases and the polymerase chain reaction. Only low to nonexistent levels of transgene methylation were detected in germ cells from 14.5-day-old male and female fetuses irrespective of the parental origin of the transgene. This undermethylated state persisted in oocytes from newborn females as well as in testicular spermatogenic cells and sperm. By contrast, the transgene promoter was completely methylated in fully grown oocytes arrested at the first meiotic prophase. The endogenous metallothionein-I gene promoter, located on a different chromosome, remained undermethylated at all stages examined, consistent with previous findings reported for a typical CpG island. Taken together, the results suggest that parental-specific adult patterns of transgene methylation are established during gametogenesis.
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Palomeque, T., E. Chica, and R. Díaz de la Guardia. "Karyotype, C-banding, chromosomal location of active nucleolar organizing regions, and B-chromosomes in Lasius niger (Hymenoptera, Formicidae)." Genome 33, no. 2 (April 1, 1990): 267–72. http://dx.doi.org/10.1139/g90-041.
Full textAbstract:
The karyotype of Lasius niger (n = 15) was analysed using C-banding and observation of nucleolar organizing region (NOR) sites. C-banding showed the existence of heterochromatin in the paracentromeric regions of all chromosomes. Two sites with primary NORs were found in chromosomes 6 and 8. Chromosome 13 showed a secondary NOR. In both cases, the NORs were located in the paracentromeric region. B-chromosomes were found in male and female germ cells. They exhibited intra- and inter-individual numerical variation. No B-chromosomes were observed in somatic cells (cerebral ganglion cells) of all castes. The Bs are telocentric, small, and clearly distinguishable from the regular members of the complement. They show positive heteropycnosis in meiotic prophase and they are highly C-band positive. The activity of NORs does not change when Bs are present. Several aspects of the behaviour of these Bs are examined.Key words: C-bands, nucleolar organizing region (primary), nucleolar oganizing region (secondary), B-chromosomes, Formicidae.
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He, Wen-Bin, Chao-Feng Tu, Qiang Liu, Lan-Lan Meng, Shi-Min Yuan, Ai-Xiang Luo, Fu-Sheng He, et al. "DMC1 mutation that causes human non-obstructive azoospermia and premature ovarian insufficiency identified by whole-exome sequencing." Journal of Medical Genetics 55, no. 3 (January 13, 2018): 198–204. http://dx.doi.org/10.1136/jmedgenet-2017-104992.
Full textAbstract:
BackgroundThe genetic causes of the majority of male and female infertility caused by human non-obstructive azoospermia (NOA) and premature ovarian insufficiency (POI) with meiotic arrest are unknown.ObjectiveTo identify the genetic cause of NOA and POI in two affected members from a consanguineous Chinese family.MethodsWe performed whole-exome sequencing of DNA from both affected patients. The identified candidate causative gene was further verified by Sanger sequencing for pedigree analysis in this family. In silico analysis was performed to functionally characterise the mutation, and histological analysis was performed using the biopsied testicle sample from the male patient with NOA.ResultsWe identified a novel homozygous missense mutation (NM_007068.3: c.106G>A, p.Asp36Asn) in DMC1, which cosegregated with NOA and POI phenotypes in this family. The identified missense mutation resulted in the substitution of a conserved aspartic residue with asparaginate in the modified H3TH motif of DMC1. This substitution results in protein misfolding. Histological analysis demonstrated a lack of spermatozoa in the male patient’s seminiferous tubules. Immunohistochemistry using a testis biopsy sample from the male patient showed that spermatogenesis was blocked at the zygotene stage during meiotic prophase I.ConclusionsTo the best of our knowledge, this is the first report identifying DMC1 as the causative gene for human NOA and POI. Furthermore, our pedigree analysis shows an autosomal recessive mode of inheritance for NOA and POI caused by DMC1 in this family.