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Relevant bibliographies by topics / Meiosis. Oogenesis

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Academic literature on the topic 'Meiosis. Oogenesis'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Meiosis. Oogenesis"

1

Verlhac, Marie-Hélène. "Meiosis and oogenesis." Molecular Biology of the Cell 23, no. 6 (March 15, 2012): 971. http://dx.doi.org/10.1091/mbc.e11-12-0982.

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2

Matsuura, Rieko, Tomoko Ashikawa, Yuka Nozaki, and Daiju Kitagawa. "LIN-41 inactivation leads to delayed centrosome elimination and abnormal chromosome behavior during female meiosis in Caenorhabditis elegans." Molecular Biology of the Cell 27, no. 5 (March 2016): 799–811. http://dx.doi.org/10.1091/mbc.e15-10-0713.

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During oogenesis, two successive meiotic cell divisions occur without functional centrosomes because of the inactivation and subsequent elimination of maternal centrosomes during the diplotene stage of meiosis I. Despite being a conserved phenomenon in most metazoans, the means by which this centrosome behavior is controlled during female meiosis remain elusive. Here, we conducted a targeted RNAi screening in the Caenorhabditis elegans gonad to identify novel regulators of centrosome behavior during oogenesis. We screened 513 genes known to be essential for embryo production and directly visualized GFP–γ-tubulin to monitor centrosome behavior at all stages of oogenesis. In the screening, we found that RNAi-mediated inactivation of 33 genes delayed the elimination of GFP–γ-tubulin at centrosomes during oogenesis, whereas inactivation of nine genes accelerated the process. Depletion of the TRIM-NHL protein LIN-41 led to a significant delay in centrosome elimination and to the separation and reactivation of centrosomes during oogenesis. Upon LIN-41 depletion, meiotic chromosomes were abnormally condensed and pulled toward one of the two spindle poles around late pachytene even though the spindle microtubules emanated from both centrosomes. Overall, our work provides new insights into the regulation of centrosome behavior to ensure critical meiotic events and the generation of intact oocytes.

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Singh, Vijay Pratap, Wei-Ting Yueh, Jennifer L. Gerton, and Francesca E. Duncan. "Oocyte-specific deletion of Hdac8 in mice reveals stage-specific effects on fertility." Reproduction 157, no. 3 (March 2019): 305–16. http://dx.doi.org/10.1530/rep-18-0560.

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Eighteen histone deacetylases exist in mammals. The class 1 histone deacetylases HDAC1 and HDAC2 are important for oogenesis and fertility in mice, likely via their effects on histones. The reproductive function of HDAC8, another class 1 enzyme, has not been explored. One key target of HDAC8 is the SMC3 subunit of cohesin, an essential complex mediating sister chromatid cohesion and chromosome segregation. In current models, HDAC8 activity is required for SMC3 recycling, but this function should be dispensable in oocytes since cohesion is established during pre-meiotic S phase and maintained until meiotic resumption during ovulation. Whether other oocyte-specific HDAC8-mediated deacetylation events are required for oogenesis and female fertility is unknown. We used two Cre drivers to remove Hdac8 at specific stages of oocyte development to address whether HDAC8 is required for female fertility in mice. When HDAC8 was knocked out in oocytes in primary and later stage follicles (Zp3-Cre), oogenesis and folliculogenesis appeared normal and mice were fertile. However, females were subfertile when HDAC8 was knocked out prior to pre-meiotic S phase and cohesion establishment (Vasa-Cre). This subfertility was independent of chromosome segregation errors during meiosis but rather appeared to be the result of defects in oogenesis that resulted in smaller fully grown oocytes with a reduced ability to resume meiosis. In all cases, we did not observe compensatory changes in HDAC1, HDAC2 and HDAC3 levels. Thus, although oocyte-specific expression of HDAC8 is not essential for mouse oogenesis after meiotic S phase, it contributes to optimal fertility. We infer that oocyte-specific expression of the deacetylase HDAC8 is required early in oogenesis for optimal fertility.

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4

Extavour, Cassandra. "Oogenesis: Making the Mos of Meiosis." Current Biology 19, no. 12 (June 2009): R489—R491. http://dx.doi.org/10.1016/j.cub.2009.05.015.

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5

Blokhina, Yana P., Michelle A. Frees, An Nguyen, Masuda Sharifi, Daniel B. Chu, Kristi Bispo, Ivan Olaya, Bruce W. Draper, and Sean M. Burgess. "Rad21l1 cohesin subunit is dispensable for spermatogenesis but not oogenesis in zebrafish." PLOS Genetics 17, no. 6 (June 17, 2021): e1009127. http://dx.doi.org/10.1371/journal.pgen.1009127.

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During meiosis I, ring-shaped cohesin complexes play important roles in aiding the proper segregation of homologous chromosomes. RAD21L is a meiosis-specific vertebrate cohesin that is required for spermatogenesis in mice but is dispensable for oogenesis in young animals. The role of this cohesin in other vertebrate models has not been explored. Here, we tested if the zebrafish homolog Rad21l1 is required for meiotic chromosome dynamics during spermatogenesis and oogenesis. We found that Rad21l1 localizes to unsynapsed chromosome axes. It is also found between the axes of the mature tripartite synaptonemal complex (SC) in both sexes. We knocked out rad21l1 and found that nearly all rad21l1-/- mutants develop as fertile males, suggesting that the mutation causes a defect in juvenile oogenesis, since insufficient oocyte production triggers female to male sex reversal in zebrafish. Sex reversal was partially suppressed by mutation of the checkpoint gene tp53, suggesting that the rad21l1 mutation activates Tp53-mediated apoptosis or arrest in females. This response, however, is not linked to a defect in repairing Spo11-induced double-strand breaks since deletion of spo11 does not suppress the sex reversal phenotype. Compared to tp53 single mutant controls, rad21l1-/- tp53-/- double mutant females produce poor quality eggs that often die or develop into malformed embryos. Overall, these results indicate that the absence of rad21l1-/- females is due to a checkpoint-mediated response and highlight a role for a meiotic-specific cohesin subunit in oogenesis but not spermatogenesis.

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6

Wang, Lina, Zhiliang Xu, Muhammad Babar Khawar, Chao Liu, and Wei Li. "The histone codes for meiosis." Reproduction 154, no. 3 (September 2017): R65—R79. http://dx.doi.org/10.1530/rep-17-0153.

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Meiosis is a specialized process that produces haploid gametes from diploid cells by a single round of DNA replication followed by two successive cell divisions. It contains many special events, such as programmed DNA double-strand break (DSB) formation, homologous recombination, crossover formation and resolution. These events are associated with dynamically regulated chromosomal structures, the dynamic transcriptional regulation and chromatin remodeling are mainly modulated by histone modifications, termed ‘histone codes’. The purpose of this review is to summarize the histone codes that are required for meiosis during spermatogenesis and oogenesis, involving meiosis resumption, meiotic asymmetric division and other cellular processes. We not only systematically review the functional roles of histone codes in meiosis but also discuss future trends and perspectives in this field.

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7

Karashima, T., A. Sugimoto, and M. Yamamoto. "Caenorhabditis elegans homologue of the human azoospermia factor DAZ is required for oogenesis but not for spermatogenesis." Development 127, no. 5 (March 1, 2000): 1069–79. http://dx.doi.org/10.1242/dev.127.5.1069.

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DAZ (Deleted in Azoospermia), the putative azoospermia factor gene in human, encodes a ribonucleoprotein-type RNA-binding protein required for spermatogenesis. A Drosophila homologue of DAZ, called boule, is also essential for spermatogenesis. A mouse homologue, Dazla, is implicated in both spermatogenesis and oogenesis. Here, we report the identification and characterization of daz-1, the single DAZ homologue in the nematode Caenorhabditis elegans. Loss of daz-1 function caused sterility in hermaphrodites, by blocking oogenesis at the pachytene stage of meiosis I. Epistasis analysis suggested that this gene executes its function succeeding gld-1, which governs the early pachytene stage in the oogenic pathway. Spermatogenesis did not appear to be affected in daz-1 hermaphrodites. Males defective in daz-1 produced sperm fully competent in fertilization. Analysis employing sex-determination mutants indicated that the daz-1 function was required for meiosis of female germline regardless of the sex of the soma. Transcription of daz-1 was restricted to the germline, starting prior to the onset of meiosis and was most conspicuous in cells undergoing oogenesis. Thus, daz-1 in C. elegans is an essential factor for female meiosis but, unlike other DAZ family members so far reported, it is dispensable for male meiosis.

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Reunov, Arkadiy, Yana Alexandrova, Yulia Reunova, Alina Komkova, and Liliana Milani. "Germ plasm provides clues on meiosis: the concerted action of germ plasm granules and mitochondria in gametogenesis of the clam Ruditapes philippinarum." Zygote 27, no. 1 (December 7, 2018): 25–35. http://dx.doi.org/10.1017/s0967199418000588.

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SummaryGerm plasm-related structures (GPRS) are known to accompany meiotic cell differentiation but their dynamics are still poorly understood. In this study, we analyzed the ultrastructural mechanisms of GPRS transformation during oogenesis and spermatogenesis of the bivalve mollusc Ruditapes philippinarum (Manila clam), exploring patterns of GPRS activity occurring at meiosis onset, sex-specific difference/similarity of such patterns, and the involvement of mitochondria during GPRS-assigned events. In the two sexes, the zygotene–pachytene stage of meiosis is anticipated by three shared steps. First, the dispersion of germ plasm granules containing the germ line determinant VASA occurs. Second, the VASA protein deriving from germ plasm granules enters neighbouring mitochondria and appears to induce mitochondrial matter release, as supported by cytochrome B localization outside the mitochondria. Third, intranuclear VASA entrance occurs and the protein appears involved in chromatin reorganization, as supported by VASA localization in synaptonemal complexes. In spermatogenesis, these three steps are sufficient for the normal course of meiosis. In oogenesis, these are followed by the action of ‘germ plasm granule formation complex’, a novel type of structure that appears alternative to the Balbiani body. The possibility of germ plasm involvement in reproductive technologies is also suggested.

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Keefe, David L., and Lin Liu. "Telomeres and reproductive aging." Reproduction, Fertility and Development 21, no. 1 (2009): 10. http://dx.doi.org/10.1071/rd08229.

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Infertility, miscarriage and aneuploid offspring increase with age in women, and meiotic dysfunction underlies reproductive aging. How aging disrupts meiotic function in women remains unclear, but as women increasingly delay having children, solving this problem becomes an urgent priority. Telomeres consist of a (TTAGGG)n repeated sequence and associated proteins at chromosome ends, mediate aging in mitotic cells and may also mediate aging during meiosis. Telomeres shorten both during DNA replication and from the response to oxidative DNA damage. Oocytes do not divide in adult mammals, but their precursors do replicate during fetal oogenesis; eggs ovulated from older females have traversed more mitotic cell cycles before entering meiosis during fetal oogenesis than eggs ovulated from younger females. Telomeres also would be expected to shorten from inefficient DNA repair of oxidative damage, because the interval between fetal oogenesis and ovulation is exceptionally prolonged in women. We have tested the hypothesis that telomere shortening disrupts meiosis by shortening telomeres experimentally in mice, which normally do not exhibit age-related meiotic dysfunction. Interestingly, mouse telomeres are much longer than human telomeres, but genetic or pharmacological shortening of mouse telomeres recapitulates in mice the human reproductive aging phenotype as the mouse telomeres reach the length of telomeres from older women. These observations led us to propose a telomere theory of reproductive aging. Moreover, chronological oxidative stress increases with reproductive aging, leading to DNA damage preferentially at (TTAGGG)n repeats. Finally, if telomeres shorten with aging, how do they reset across generations? Telomerase could not play a significant role in telomere elongation during early development, because this enzyme is not active until the blastocyst stage, well after the stage when telomere elongation takes place. Rather, telomeres lengthen during the early cell cycles of development by a novel mechanism involving recombination and sister chromatid exchange. Telomere dysfunction resulting from oxidative stress, a DNA damage response or aberrant telomere recombination may contribute to reproductive aging-associated meiotic defects, miscarriage and infertility.

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Zhao, Zheng-Hui, Heide Schatten, and Qing-Yuan Sun. "High-throughput sequencing reveals landscapes of female germ cell development." Molecular Human Reproduction 26, no. 10 (August 31, 2020): 738–47. http://dx.doi.org/10.1093/molehr/gaaa059.

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Abstract Female germ cell development is a highly complex process that includes meiosis initiation, oocyte growth recruitment, oocyte meiosis retardation and resumption and final meiotic maturation. A series of coordinated molecular signaling factors ensure successful oogenesis. The recent rapid development of high-throughput sequencing technologies allows for the dynamic omics in female germ cells, which is essential for further understanding the regulatory mechanisms of molecular events comprehensively. In this review, we summarize the current literature of multi-omics sequenced by epigenome-, transcriptome- and proteome-associated technologies, which provide valuable information for understanding the regulation of key events during female germ cell development.

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Dissertations / Theses on the topic "Meiosis. Oogenesis"

1

Zhao, Xinbei. "Studies of Drosophila Greatwall kinase in mitosis, meiosis and oogenesis." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611158.

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Fazio, Cynthia Marie. "The influence of meiotic onset on and the role of apoptosis in oocyte death during the meiotic prophase /." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97951.

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Loss of germ cells that entered meiosis at different developmental stages was compared. Mice were injected with BrdU at 13.3, 14.3 or 15.3 days post coitum (dpc) and sacrificed either 3 days after BrdU injection or 4 days post partum (dpp). BrdU-labeled germ cells were detected in ovarian sections through double immunofluorescent staining for BrdU and either GCNA-1 or MVH as a germ cell marker. The results show that the loss of germ cells that entered meiosis at 13.3 or 15.3 dpc was excessive compared to the loss of total germ cells. Such preferential elimination was not found for germ cells that entered meiosis at 14.3 dpc. We conclude that oocyte loss during meiotic prophase is influenced by the timing of meiotic onset.
The mechanism of germ cell loss during ovarian development was tested by the presence of markers for apoptosis. Mouse ovaries were isolated at 12.5 dpc, 18.5 dpc and 2 dpp and cultured with doxorubicin (DXR) to induce cell death. Ovarian histological sections were double immunofluorescent stained for GCNA-1 and cleaved caspase-3 or PARP-1. The results suggest that caspase-3 is not activated in germ cells throughout ovarian development whereas PARP-1 is activated in germ cells at 12.5 dpc and 2 dpp but not at 18.5 dpc. Thus, no evidence has yet been provided to support the hypothesis that oocyte death during the meiotic prophase is mediated by apooptosis.

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3

Lane, Jonathan David. "The organisation and regulation of microtubules in telotrophic ovarioles of hemipteran insects." Thesis, University of Exeter, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296285.

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4

He, Jing. "Investigating the expression and function of DAZL and BOLL during human oogenesis." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/25481.

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Fetal germ cell development is a key stage of female reproductive life. The DAZ family proteins (DAZ, DAZL and BOLL) are RNA-binding proteins with critical roles in murine germ cell development but their expression and potential targets in the human are largely unknown. The studies in this Thesis investigated the expression and function of DAZL and BOLL in human fetal ovary. Both DAZL and BOLL mRNA are increased dramatically at the time of entry into meiosis. Immunohistochemical analysis with specific meiotic markers suggested that DAZL and BOLL have distinct spatial-temporal expression patterns, with minimal co-expression – BOLL expression was transient prior to follicle formation. This pattern was shown not to be present in the mouse fetal ovary, where Dazl and Boll are co-expressed, indicating a limitation of the mouse for exploring the function of Boll. Two human cell lines, embryonic kidney derived HEK293 cells and germ cell tumour derived TCam-2 cells were used as models to identify the mRNA targets of DAZL and BOLL after transfection of DAZL or BOLL vectors. In HEK293 cells, TEX19 and TEX14 were confirmed as potential targets of both DAZL and BOLL, and CDC25A as a potential DAZL target. Further experiments indicated that DAZL and BOLL did not increase target mRNA transcription but increased stabilisation. A DAZL/GFP co-transfection-FACS system for TCam-2 cells was established as this cell line has very low transfection efficiency. TEX14 and SYCP3 significantly increased in GFP+ve-DAZL+ve cells when compare to the GFP-ve-DAZL-ve cells, whilst SOX17 and DNMT3L significantly decreased in the GFP+ve-DAZL+ve cells. A 3'-UTR luciferase assay confirmed regulation of TEX14 and SOX17 by DAZL through their 3'-UTR. RNA immunoprecipitation further demonstrated direct binding between human TEX14, TEX19, SYCP3, SOX17 mRNA and DAZL protein, and that TEX14 binding is through its 3'-UTR. Dual fluorescence immunohistochemistry showed that SOX17 and DMNT3L are expressed in early germ cells with DAZL, and are later down-regulated co-incident with that of DAZL, consistent with the novel repressive effect of human DAZL on these two potential targets. These studies indicate that DAZL and BOLL are associated with different key meiotic stages of germ cell development in human fetal ovary. Several potential mRNA targets of DAZL and BOLL, and a novel repression function of human DAZL on its mRNA targets were identified giving further insight into the role of these factors in human ovarian development.

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5

Kisielnicka, Edyta. "SCF-mediated degradation of the two translational regulators, CPB-3 and GLD-1, during oogenesis in C. elegans." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2018. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-234186.

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The development of an organism and its adult homeostasis rely on regulatory mechanisms that control the underlying gene expression programs. In certain biological contexts, such as germ cell development, gene expression regulation is largely executed at the post-‐transcriptional level. This relies on RNA-‐binding proteins (RBPs), whose activity and expression are also heavily controlled. While the RNA-‐binding potential of RBPs is currently of intense scrutiny, surprisingly little is known to date about the molecular mechanisms that control RNA-‐binding proteins abundance in the context of germ cell development. This work identifies the molecular mechanisms that shape expression patterns of two evolutionarily conserved RNA-‐binding proteins, CPB-‐3 and GLD-‐ 1, which belong to CPEB and STAR protein family, respectively. By focusing on their regulation in the C. elegans germ line, this work reveals an involvement of the proteasome in reducing levels of CPB-‐3/CPEB and GLD-‐1/STAR at the pachytene-‐to-‐diplotene transition during meiotic prophase I. Furthermore, it documents that CPB-‐3 and GLD-‐1 are targeted to proteasomal degradation by a conserved SCF ubiquitin ligase complex that utilises SEL-‐10/Fbxw7 as a substrate recognition subunit. Importantly, destabilisation of both RBPs is likely triggered by their phosphorylation, which is regulated by the mitogen-‐activated protein kinase, MPK-‐1, and restricted to the meiotic timepoint of pachytene exit. Lastly, this work investigates the potential consequences of target mRNA regulation upon delayed RBP degradation. Altogether, the collected data characterise a molecular pathway of CPEB and STAR protein turnover, and suggest that MPK-‐1 signaling may couple RBP-‐mediated regulation of gene expression to progression through meiosis during oogenesis.

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6

Christmann, Leandro. "Acquisition of meiotic competence in growing porcine oocytes." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339451.

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7

Christou-Kent, Marie. "Caractérisation de l'arrêt de la gamétogenèse chez l'homme du gène à la protéine Échec de maturation ovocytaire: Un rôle essentiel pour la protéine PATL2 dans l’ovogenèse PATL2 is a key actor of oocyte maturation whose invalidation causes infertility in women and mice." Thesis, Université Grenoble Alpes (ComUE), 2019. http://www.theses.fr/2019GREAV071.

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L’infertilité est considérée comme une préoccupation majeure de santé, touchant à plus de 50 millions de couples mondialement. Les techniques actuelles d’Assistance Médicale à la Procréation (AMP) ont comme prérequis des gamètes aptes à la fécondation et au développement embryonnaire. Dans les rares cas où des anomalies génétiques mène à un arrêt de la gamétogenèse et donc à la production de gamètes immatures, défectueux ou dégradés, un traitement n’est pas possible. Afin d’envisager de nouvelles stratégies de traitement, il est nécessaire de comprendre les bases moléculaires de ce type d’infertilité. De plus, ces patients représentent une opportunité unique nous permettant de découvrir de nouveaux acteurs de l’ovogenèse et de la spermatogenèse ainsi que de déchiffrer les voies moléculaires impliquées dans la production de gamètes compétentes.L’analyse génétiques de cohortes de patients consanguins peut permettre l’identification de variants génétiques héritées comme causes possibles de la pathologie. Nous avons identifié, par séquençage exomique, un variant pathogène du gène PATL2 dans les patientes atteintes d’un échec de maturation ovocytaire. Cette pathologie, que nous avons appelé la Déficience Méiotique Ovocytaire (DMO), consiste en l’ovulation récurrent d’ovocytes immatures et non-fécondables. Le gène PATL2 code une ribonucléoprotéine ovocytaire qui a été impliqué dans la régulation de la traduction des ARNm maternelles chez l’amphibien. Sa fonction chez les mammifères était jusqu’à présent mal caractérisé. Nous avons aussi identifié un variant pathogène du gène SPINK2, codant un inhibiteur de protéases qui est important pour la neutralisation de l’acrosine pendant le développement de l’acrosome.Par la génération de lignées de souris déficientes (KO) pour les gènes Patl2 et Spink2, et d’une lignée PATL2 « étiquetée » par la méthode CRISPR-Cas9, nous avons montrés que les deux protéines correspondantes jouent des rôles indispensables dans leur gamétogénèses respectives. Nous avons démontré que Patl2 est fortement exprimé dans l’ovocyte murin en cours de croissance, et que son absence entraîne une dérégulation de nombreux transcrits essentiels pendant la phase de croissance, de maturation méiotique ou de développement pré-implantatoire. Les femelles PATL2 KO sont subfertiles par accouplement naturel, et lors de la stimulation hormonale produisent une grande proportion d’ovocytes sans globule polaire (immatures) et/ou avec des défauts au niveau du fuseau méiotique, mis en évidence par immunomarquage. Suite à la fécondation in vitro, un grand nombre d’ovocytes PATL2 KO ont répondu de manière aberrante à la fécondation. Concernant les mâles SPINK2 KO, nous avons montré que l’absence de la protéine SPINK2, qui se localise dans l’acrosome, entraîne un arrêt de la spermiogenèse et une azoospermie à cause d’une autophagie au stade spermatide-ronde. Cet effet est vraisemblablement dû à une activité aberrante de l’acrosine en absence de son inhibiteur, une hypothèse soutenue par la fragmentation de l’appareil de Golgi et l’absence de l’acrosome, événements observés par immunofluorescence.Nous avons, donc, caractérisé deux sous-types génétiques d’infertilité humaine associés à la mutation de ces deux gènes. Ce faisant, nous avons approfondi notre compréhension des fonctions respectives de ces acteurs clés de la gamétogenèse chez les mammifères, ce qui pourrait ouvrir la voie vers une amélioration des techniques d’AMP actuelles ainsi que le développement de thérapies alternatives et personnalisées
Infertility is considered a global public health issue since it affects more than 50 million couples worldwide. Current assisted reproductive technologies (ARTs) have minimal requirements for gametes that are competent for fertilisation and subsequent embryo development. In cases where genetic abnormalities lead to arrested gametogenesis and the production of immature, defective or degraded gametes, treatment is not usually possible. Identifying the molecular causes of these types of infertility is crucial for developing new strategies to treat affected couples. Moreover, these patients represent a unique opportunity to discover new actors of oogenesis and spermatogenesis and to decipher the molecular pathways involved in the production of competent gametes.Genetic analysis of cohorts of infertile patients with shared ancestry can allow the identification of inherited genetic variants as possible causal factors. Using whole exome sequencing, we identified a homozygous pathogenic variant of the gene PATL2 in a cohort of patients with a phenotype of arrested oogenesis due to oocyte meiotic deficiency (OMD). OMD is a rare pathology characterised by the recurrent ovulation of immature oocytes. PATL2 encodes an oocyte ribonucleoprotein whose amphibian orthologue had been shown to be involved in oocyte translational control and whose function in mammals was poorly characterised. We also identified a pathogenic variant of the gene SPINK2 in a familial case of azoospermia. SPINK2 encodes a serine protease inhibitor essential for the neutralisation of acrosin activity during sperm acrosome formation.We showed, through generation of Patl2 and Spink2 knockout (KO) mice and Patl2 tagged mice (the latter using CRISPR-Cas9), that both corresponding proteins play essential respective roles in gametogenesis. We demonstrated that Patl2 is strongly expressed in growing mouse oocytes and that its absence leads to the dysregulation of numerous transcripts necessary for oocyte growth, meiotic maturation and preimplantation embryo development. This was accompanied by a phenotype of subfertility in KO females in natural mating, a large proportion of ovulated oocytes lacking a polar body (immature) and/or displaying spindle assembly defects in immunostaining, and high rate of oocytes with an aberrant response to fertilisation in IVF experiments. In Spink2 KO mice, we demonstrated that absence of Spink2 protein, which is located in the acrosome of maturing and mature spermatozoa, leads to arrested spermiogenesis and azoospermia due to autophagy at the round-spermatid stage. This is plausibly due to aberrant acrosin activity in the absence of its inhibitor, corroborated by fragmentation of the Golgi and absence of the acrosome in immunostaining.We have thus characterised two genetic subtypes of human infertility associated with mutation of these two genes. In doing so, we have furthered our understanding of the respective roles of these crucial actors of mammalian gametogenesis, potentially paving the way for improvement of current ARTs and development of new, personalised therapies

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8

Kisielnicka, Edyta. "SCF-mediated degradation of the two translational regulators, CPB-3 and GLD-1, during oogenesis in C. elegans." Doctoral thesis, 2017. https://tud.qucosa.de/id/qucosa%3A30871.

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The development of an organism and its adult homeostasis rely on regulatory mechanisms that control the underlying gene expression programs. In certain biological contexts, such as germ cell development, gene expression regulation is largely executed at the post-‐transcriptional level. This relies on RNA-‐binding proteins (RBPs), whose activity and expression are also heavily controlled. While the RNA-‐binding potential of RBPs is currently of intense scrutiny, surprisingly little is known to date about the molecular mechanisms that control RNA-‐binding proteins abundance in the context of germ cell development. This work identifies the molecular mechanisms that shape expression patterns of two evolutionarily conserved RNA-‐binding proteins, CPB-‐3 and GLD-‐ 1, which belong to CPEB and STAR protein family, respectively. By focusing on their regulation in the C. elegans germ line, this work reveals an involvement of the proteasome in reducing levels of CPB-‐3/CPEB and GLD-‐1/STAR at the pachytene-‐to-‐diplotene transition during meiotic prophase I. Furthermore, it documents that CPB-‐3 and GLD-‐1 are targeted to proteasomal degradation by a conserved SCF ubiquitin ligase complex that utilises SEL-‐10/Fbxw7 as a substrate recognition subunit. Importantly, destabilisation of both RBPs is likely triggered by their phosphorylation, which is regulated by the mitogen-‐activated protein kinase, MPK-‐1, and restricted to the meiotic timepoint of pachytene exit. Lastly, this work investigates the potential consequences of target mRNA regulation upon delayed RBP degradation. Altogether, the collected data characterise a molecular pathway of CPEB and STAR protein turnover, and suggest that MPK-‐1 signaling may couple RBP-‐mediated regulation of gene expression to progression through meiosis during oogenesis.

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Books on the topic "Meiosis. Oogenesis"

1

Chen, Bin. Grauzone and Completion of Meiosis During Drosophila Oogenesis. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1409-1.

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2

Grauzone and completion of meiosis during drosophila oogenesis. Boston: Kluwer Academic Publishers, 2001.

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3

H, Kinne Rolf K., ed. Oogenesis, spermatogenesis, and reproduction. Basel: Karger, 1991.

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Chen, Bin. Grauzone and Completion of Meiosis During Drosophila Oogenesis. Springer, 2011.

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Book chapters on the topic "Meiosis. Oogenesis"

1

Verlhac, Marie-Hélène, and Karen Wingman Lee. "Mechanisms of Asymmetric Division in Metazoan Meiosis." In Oogenesis, 291–310. Chichester, UK: John Wiley & Sons, Ltd, 2010. http://dx.doi.org/10.1002/9780470687970.ch11.

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Terret, M. Emilie. "The Control of the Metaphase-to-Anaphase Transition in Meiosis I." In Oogenesis, 311–41. Chichester, UK: John Wiley & Sons, Ltd, 2010. http://dx.doi.org/10.1002/9780470687970.ch12.

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Bin, Chen. "Conclusions and Considerations." In Grauzone and Completion of Meiosis During Drosophila Oogenesis, 61–67. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1409-1_4.

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Bin, Chen. "General Introduction." In Grauzone and Completion of Meiosis During Drosophila Oogenesis, 1–9. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1409-1_1.

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Bin, Chen. "Mapping of Drosophila Mutations Using Site-specific Male Recombination." In Grauzone and Completion of Meiosis During Drosophila Oogenesis, 11–29. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1409-1_2.

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Bin, Chen. "Completion of Meiosis in Drosophila Oocytes Requires Transcriptional Control by Grauzone, a New Zinc Finger Protein." In Grauzone and Completion of Meiosis During Drosophila Oogenesis, 31–59. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1409-1_3.

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Santucci-Darmanin, Sabine, and Frédéric Baudat. "Meiotic Recombination in Mammals." In Oogenesis, 141–77. Chichester, UK: John Wiley & Sons, Ltd, 2010. http://dx.doi.org/10.1002/9780470687970.ch6.

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Verlhac, Marie-Hélène, and Manuel Breuer. "Cytoskeletal Correlates of Oocyte Meiotic Divisions." In Oogenesis, 195–207. London: Springer London, 2012. http://dx.doi.org/10.1007/978-0-85729-826-3_14.

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Dumont, Julien, and Stéphane Brunet. "Meiotic Spindle Assembly and Chromosome Segregation in Oocytes." In Oogenesis, 267–90. Chichester, UK: John Wiley & Sons, Ltd, 2010. http://dx.doi.org/10.1002/9780470687970.ch10.

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Jones, Keith T., Simon I. R. Lane, and Janet E. Holt. "Start and Stop Signals of Oocyte Meiotic Maturation." In Oogenesis, 183–93. London: Springer London, 2012. http://dx.doi.org/10.1007/978-0-85729-826-3_13.

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