Academic literature on the topic 'Mitosis/meiosis transition'

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Journal articles on the topic "Mitosis/meiosis transition"

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Bogdanov, Yuri. "Why is meiosis different from mitosis." Priroda, no. 11 (2024): 18. https://doi.org/10.7868/s0032874x24110021.

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Meiosis was existing already in the last eukaryotic common ancestor (LECA). During evolution and transition from the first eukaryotic ancestor to LECA, a whole complex of genes was formed in the genome of the latter (about 300 genes), which provided the process of meiotic division. This is only a few percent of the genome, but these genes significantly changed the course of cell division, and meiosis arose. The paper describes the features of meiosis and possible ways of its formation.
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Clandinin, T. R., and P. E. Mains. "Genetic studies of mei-1 gene activity during the transition from meiosis to mitosis in Caenorhabditis elegans." Genetics 134, no. 1 (1993): 199–210. http://dx.doi.org/10.1093/genetics/134.1.199.

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Abstract Genetic evidence suggests that the mei-1 locus of Caenorhabditis elegans encodes a maternal product required for female meiosis. However, a dominant gain-of-function allele, mei-1(ct46), can support normal meiosis but causes defects in subsequent mitotic spindles. Previously identified intragenic suppressors of ct46 lack functional mei-1 activity; null alleles suppress only in cis but other alleles arise frequently and suppress both in cis and in trans. Using a different screen for suppressors of the dominant ct46 defect, the present study describes another type of intragenic mutation
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Hiraoka, Daisaku, Enako Hosoda, Kazuyoshi Chiba, and Takeo Kishimoto. "SGK phosphorylates Cdc25 and Myt1 to trigger cyclin B–Cdk1 activation at the meiotic G2/M transition." Journal of Cell Biology 218, no. 11 (2019): 3597–611. http://dx.doi.org/10.1083/jcb.201812122.

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The kinase cyclin B–Cdk1 complex is a master regulator of M-phase in both mitosis and meiosis. At the G2/M transition, cyclin B–Cdk1 activation is initiated by a trigger that reverses the balance of activities between Cdc25 and Wee1/Myt1 and is further accelerated by autoregulatory loops. In somatic cell mitosis, this trigger was recently proposed to be the cyclin A–Cdk1/Plk1 axis. However, in the oocyte meiotic G2/M transition, in which hormonal stimuli induce cyclin B–Cdk1 activation, cyclin A–Cdk1 is nonessential and hence the trigger remains elusive. Here, we show that SGK directly phospho
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Courtois, Aurélien, Melina Schuh, Jan Ellenberg, and Takashi Hiiragi. "The transition from meiotic to mitotic spindle assembly is gradual during early mammalian development." Journal of Cell Biology 198, no. 3 (2012): 357–70. http://dx.doi.org/10.1083/jcb.201202135.

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The transition from meiosis to mitosis, classically defined by fertilization, is a fundamental process in development. However, its mechanism remains largely unexplored. In this paper, we report a surprising gradual transition from meiosis to mitosis over the first eight divisions of the mouse embryo. The first cleavages still largely share the mechanism of spindle formation with meiosis, during which the spindle is self-assembled from randomly distributed microtubule-organizing centers (MTOCs) without centrioles, because of the concerted activity of dynein and kinesin-5. During preimplantatio
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Cairo, Albert, Anna Vargova, Neha Shukla, et al. "Meiotic exit in Arabidopsis is driven by P-body–mediated inhibition of translation." Science 377, no. 6606 (2022): 629–34. http://dx.doi.org/10.1126/science.abo0904.

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Meiosis, at the transition between diploid and haploid life cycle phases, is accompanied by reprograming of cell division machinery and followed by a transition back to mitosis. We show that, in Arabidopsis , this transition is driven by inhibition of translation, achieved by a mechanism that involves processing bodies (P-bodies). During the second meiotic division, the meiosis-specific protein THREE-DIVISION MUTANT 1 (TDM1) is incorporated into P-bodies through interaction with SUPPRESSOR WITH MORPHOGENETIC EFFECTS ON GENITALIA 7 (SMG7). TDM1 attracts eIF4F, the main translation initiation co
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Gomes, José-Eduardo, Nicolas Tavernier, Bénédicte Richaudeau, et al. "Microtubule severing by the katanin complex is activated by PPFR-1–dependent MEI-1 dephosphorylation." Journal of Cell Biology 202, no. 3 (2013): 431–39. http://dx.doi.org/10.1083/jcb.201304174.

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Katanin is an evolutionarily conserved microtubule (MT)-severing complex implicated in multiple aspects of MT dynamics. In Caenorhabditis elegans, the katanin homologue MEI-1 is required for meiosis, but must be inactivated before mitosis. Here we show that PPFR-1, a regulatory subunit of a trimeric protein phosphatase 4 complex, enhanced katanin MT-severing activity during C. elegans meiosis. Loss of ppfr-1, similarly to the inactivation of MT severing, caused a specific defect in meiosis II spindle disassembly. We show that a fraction of PPFR-1 was degraded after meiosis, contributing to kat
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Keating, Leonor, Sandra A. Touati, and Katja Wassmann. "A PP2A-B56—Centered View on Metaphase-to-Anaphase Transition in Mouse Oocyte Meiosis I." Cells 9, no. 2 (2020): 390. http://dx.doi.org/10.3390/cells9020390.

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Meiosis is required to reduce to haploid the diploid genome content of a cell, generating gametes—oocytes and sperm—with the correct number of chromosomes. To achieve this goal, two specialized cell divisions without intermediate S-phase are executed in a time-controlled manner. In mammalian female meiosis, these divisions are error-prone. Human oocytes have an exceptionally high error rate that further increases with age, with significant consequences for human fertility. To understand why errors in chromosome segregation occur at such high rates in oocytes, it is essential to understand the
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Fox, Colette, Juan Zou, Juri Rappsilber, and Adele L. Marston. "Cdc14 phosphatase directs centrosome re-duplication at the meiosis I to meiosis II transition in budding yeast." Wellcome Open Research 2 (January 5, 2017): 2. http://dx.doi.org/10.12688/wellcomeopenres.10507.1.

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Background Gametes are generated through a specialized cell division called meiosis, in which ploidy is reduced by half because two consecutive rounds of chromosome segregation, meiosis I and meiosis II, occur without intervening DNA replication. This contrasts with the mitotic cell cycle where DNA replication and chromosome segregation alternate to maintain the same ploidy. At the end of mitosis, CDKs are inactivated. This low CDK state in late mitosis/G1 allows for critical preparatory events for DNA replication and centrosome/spindle pole body (SPB) duplication. However, their execution is
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Fox, Colette, Juan Zou, Juri Rappsilber, and Adele L. Marston. "Cdc14 phosphatase directs centrosome re-duplication at the meiosis I to meiosis II transition in budding yeast." Wellcome Open Research 2 (February 21, 2017): 2. http://dx.doi.org/10.12688/wellcomeopenres.10507.2.

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Background: Gametes are generated through a specialized cell division called meiosis, in which ploidy is reduced by half because two consecutive rounds of chromosome segregation, meiosis I and meiosis II, occur without intervening DNA replication. This contrasts with the mitotic cell cycle where DNA replication and chromosome segregation alternate to maintain the same ploidy. At the end of mitosis, cyclin-dependent kinases (CDKs) are inactivated. This low CDK state in late mitosis/G1 allows for critical preparatory events for DNA replication and centrosome/spindle pole body (SPB) duplication.
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Borgers, Mareike, Martin Wolter, Anna Hentrich, Martin Bergmann, Angelika Stammler, and Lutz Konrad. "Role of compensatory meiosis mechanisms in human spermatogenesis." REPRODUCTION 148, no. 3 (2014): 315–20. http://dx.doi.org/10.1530/rep-14-0279.

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Disturbances of checkpoints in distinct stages of spermatogenesis (mitosis, meiosis, and spermiogenesis) contribute to impaired spermatogenesis; however, the efficiency of meiotic entry has not been investigated in more detail. In this study, we analyzed azoospermic patients with defined spermatogenic defects by the use of octamer-binding protein 2 for type A spermatogonia, sarcoma antigen 1 for mitosis–meiosis transition and SMAD3 for pachytene spermatocytes. Especially patients with maturation arrest (MA) at the level of primary spermatocytes showed significantly reduced numbers of spermatog
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Dissertations / Theses on the topic "Mitosis/meiosis transition"

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Hazra, Ditipriya. "Insights into the control of mRNA decay by YTH proteins during the transition from meiosis to mitosis in yeasts." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLX041.

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Aperçu du contrôle de la dégradation des ARNm par les protéines YTHpendant la transition de la méiose à la mitose chez les levures.Le cycle cellulaire est contrôlé par des processus complexes et interconnectés. Un gène est transcrit en ARNm qui est traduit en protéines mais de nombreux processus de régulation travaillent pour contrôler chaque étape de ce processus apparemment simple. Parmi ces points de contrôle, la régulation post-transcriptionnelle est importante, et la formation d'un complexe protéine-ARN peut diriger le destin cellulaire. Parmi ces protéines de liaison à l'ARN, les protéin
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Detti, Mélanie. "Méthylation des adénosines (m6A) des ARN dans les cellules germinales et infertilité." Electronic Thesis or Diss., Université Côte d'Azur, 2024. http://www.theses.fr/2024COAZ6044.

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La différenciation sexuelle est un mécanisme complexe, où une gonade indifférenciée, va se développer en testicule chez les mâles ou en ovaire chez les femelles. Le sexe chromosomique est à l'origine de la détermination sexuelle, en activant des voies de signalisation sexe-spécifique. Découvert en 1990, le gène SRY, présent sur le chromosome Y des mâles, est un gène qui a longtemps été décrit comme le régisseur de toute la différenciation sexuelle. En sa présence, les embryons XY se différencient en mâles, mais son absence est suffisante pour induire la différenciation femelle, « par défaut ».
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Book chapters on the topic "Mitosis/meiosis transition"

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Courtois, Aurélien, and Takashi Hiiragi. "Gradual Meiosis-To-Mitosis Transition in the Early Mouse Embryo." In Results and Problems in Cell Differentiation. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-30406-4_6.

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Bernstein, Harris, and Carol Bernstein. "Origin of DNA Repair in the RNA World." In DNA Repair [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.93822.

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The early history of life on Earth likely included a stage in which life existed as self-replicating protocells with single-stranded RNA (ssRNA) genomes. In this RNA world, genome damage from a variety of sources (spontaneous hydrolysis, UV, etc.) would have been a problem for survival. Selection pressure for dealing with genome damage would have led to adaptive strategies for mitigating the damage. In today’s world, RNA viruses with ssRNA genomes are common, and these viruses similarly need to cope with genome damage. Thus ssRNA viruses can serve as models for understanding the early evolution of genome repair. As the ssRNA protocells in the early RNA world evolved, the RNA genome likely gave rise, through a series of evolutionary stages, to the double-stranded DNA (dsDNA) genome. In ssRNA to dsDNA evolution, genome repair processes also likely evolved to accommodate this transition. Some of the basic features of ssRNA genome repair appear to have been retained in descendants with dsDNA genomes. In particular, a type of strand-switching recombination occurs when ssRNA replication is blocked by a damage in the template strand. Elements of this process appear to have a central role in recombinational repair processes during meiosis and mitosis of descendant dsDNA organisms.
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Larochelle, D. A., and C. W. Walker. "Changing properties of somatic accessory and germinal cells during the amitotic/mitotic and premeiotic/meiotic transitions of spermatogenesis in Asterias vulgaris." In Echinodermata. CRC Press, 2020. http://dx.doi.org/10.1201/9781003079224-125.

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