Journal articles: '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 (May 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 that also arises at high frequency. These latter alleles appear to have reduced meiotic activity and retain a weakened dominant effect. Characterization of these alleles in trans-heterozygous combinations with previously identified mei-1 alleles has enabled us to define more clearly the role of the mei-1 gene product during normal embryogenesis. We propose that a certain level of mei-1 activity is required for meiosis but must be eliminated prior to mitosis. The dominant mutation causes mei-1 activity to function at mitosis; intragenic trans-suppressors act in an antimorphic manner to inactivate multimeric mei-1 complexes. We propose that inactivation of meiosis-specific functions may be an essential precondition of mitosis; failure to eliminate such functions may allow ectopic meiotic activity during mitosis and cause embryonic lethality.

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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 (September 19, 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 phosphorylates Cdc25 and Myt1 to trigger cyclin B–Cdk1 activation in starfish oocytes. Upon hormonal stimulation of the meiotic G2/M transition, SGK is activated by cooperation between the Gβγ-PI3K pathway and an unidentified pathway downstream of Gβγ, called the atypical Gβγ pathway. These findings identify the trigger in oocyte meiosis and provide insights into the role and activation of SGK.

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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 (July 30, 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 preimplantation development, the number of cellular MTOCs progressively decreased, the spindle pole gradually became more focused, and spindle length progressively scaled down with cell size. The typical mitotic spindle with centrin-, odf2-, kinesin-12–, and CP110-positive centrosomes was established only in the blastocyst. Overall, the transition from meiosis to mitosis progresses gradually throughout the preimplantation stage in the mouse embryo, thus providing a unique system to study the mechanism of centrosome biogenesis in vivo.

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Cairo, Albert, Anna Vargova, Neha Shukla, Claudio Capitao, Pavlina Mikulkova, Sona Valuchova, Jana Pecinkova, Petra Bulankova, and Karel Riha. "Meiotic exit in Arabidopsis is driven by P-body–mediated inhibition of translation." Science 377, no. 6606 (August 5, 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 complex, temporarily sequestering it in P-bodies and inhibiting translation. The failure of tdm1 mutants to terminate meiosis can be overcome by chemical inhibition of translation. We propose that TDM1-containing P-bodies down-regulate expression of meiotic transcripts to facilitate transition of cell fates to postmeiotic gametophyte differentiation.

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Gomes, José-Eduardo, Nicolas Tavernier, Bénédicte Richaudeau, Etienne Formstecher, Thomas Boulin, Paul E. Mains, Julien Dumont, and Lionel Pintard. "Microtubule severing by the katanin complex is activated by PPFR-1–dependent MEI-1 dephosphorylation." Journal of Cell Biology 202, no. 3 (August 5, 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 katanin inactivation. PPFR-1 interacted with MEL-26, the substrate recognition subunit of the CUL-3 RING E3 ligase (CRL3MEL-26), which also targeted MEI-1 for post-meiotic degradation. Reversible protein phosphorylation of MEI-1 may ensure temporal activation of the katanin complex during meiosis, whereas CRL3MEL-26-mediated degradation of both MEI-1 and its activator PPFR-1 ensure efficient katanin inactivation in the transition to mitosis.

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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 (February 7, 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 molecular players at work controlling these divisions. In this review, we look at the interplay of kinase and phosphatase activities at the transition from metaphase-to-anaphase for correct segregation of chromosomes. We focus on the activity of PP2A-B56, a key phosphatase for anaphase onset in both mitosis and meiosis. We start by introducing multiple roles PP2A-B56 occupies for progression through mitosis, before laying out whether or not the same principles may apply to the first meiotic division in oocytes, and describing the known meiosis-specific roles of PP2A-B56 and discrepancies with mitotic cell cycle regulation.

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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 inhibited until S phase, where further preparatory events are also prevented. This “licensing” ensures that both the chromosomes and the centrosomes/SPBs replicate exactly once per cell cycle, thereby maintaining constant ploidy. Crucially, between meiosis I and meiosis II, centrosomes/SPBs must be re-licensed, but DNA re-replication must be avoided. In budding yeast, the Cdc14 protein phosphatase triggers CDK down regulation to promote exit from mitosis. Cdc14 also regulates the meiosis I to meiosis II transition, though its mode of action has remained unclear. Methods Fluorescence and electron microscopy was combined with proteomics to probe SPB duplication in cells with inactive or hyperactive Cdc14. Results We demonstrate that Cdc14 ensures two successive nuclear divisions by re-licensing SPBs at the meiosis I to meiosis II transition. We show that Cdc14 is asymmetrically enriched on a single SPB during anaphase I and provide evidence that this enrichment promotes SPB re-duplication. Cells with impaired Cdc14 activity fail to promote extension of the SPB half-bridge, the initial step in morphogenesis of a new SPB. Conversely, cells with hyper-active Cdc14 duplicate SPBs, but fail to induce their separation. Conclusion Our findings implicate reversal of key CDK-dependent phosphorylations in the differential licensing of cyclical events at the meiosis I to meiosis I transition.

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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. However, their execution is inhibited until S phase, where further preparatory events are also prevented. This “licensing” ensures that both the chromosomes and the centrosomes/SPBs replicate exactly once per cell cycle, thereby maintaining constant ploidy. Crucially, between meiosis I and meiosis II, centrosomes/SPBs must be re-licensed, but DNA re-replication must be avoided. In budding yeast, the Cdc14 protein phosphatase triggers CDK down regulation to promote exit from mitosis. Cdc14 also regulates the meiosis I to meiosis II transition, though its mode of action has remained unclear. Methods: Fluorescence and electron microscopy was combined with proteomics to probe SPB duplication in cells with inactive or hyperactive Cdc14. Results: We demonstrate that Cdc14 ensures two successive nuclear divisions by re-licensing SPBs at the meiosis I to meiosis II transition. We show that Cdc14 is asymmetrically enriched on a single SPB during anaphase I and provide evidence that this enrichment promotes SPB re-duplication. Cells with impaired Cdc14 activity fail to promote extension of the SPB half-bridge, the initial step in morphogenesis of a new SPB. Conversely, cells with hyper-active Cdc14 duplicate SPBs, but fail to induce their separation. Conclusion: Our findings implicate reversal of key CDK-dependent phosphorylations in the differential licensing of cyclical events at the meiosis I to meiosis II transition.

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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 (September 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 spermatogonia compared with patients with histologically intact spermatogenesis or patients with hypospermatogenesis (Hyp). For a detailed individual classification of the patients, we distinguished between ‘high efficiency of meiotic entry’ (high numbers of pachytene spermatocytes) and ‘low efficiency of meiotic entry’ (low numbers of pachytene spermatocytes). Only patients with histologically normal spermatogenesis (Nsp) and patients with Hyp showed normal numbers of spermatogonia and a high efficiency of meiotic entry. Of note, only patients with histologically Nsp or patients with Hyp could compensate low numbers of spermatogonia with a high efficiency of meiotic entry. In contrast, patients with MA always showed a low efficiency of meiotic entry. This is the first report on patients with impaired spermatogenesis, showing that half of the patients with Hyp but all patients with MA cannot compensate reduced numbers in spermatogonia with a highly efficient meiosis. Thus, we suggest that compensatory meiosis mechanisms in human spermatogenesis exist.

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Hunt, T., F. C. Luca, and J. V. Ruderman. "The requirements for protein synthesis and degradation, and the control of destruction of cyclins A and B in the meiotic and mitotic cell cycles of the clam embryo." Journal of Cell Biology 116, no. 3 (February 1, 1992): 707–24. http://dx.doi.org/10.1083/jcb.116.3.707.

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Fertilization of clam oocytes initiates a series of cell divisions, of which the first three--meiosis I, meiosis II, and the first mitotic division--are highly synchronous. After fertilization, protein synthesis is required for the successful completion of every division except meiosis I. When protein synthesis is inhibited, entry into meiosis I and the maintenance of M phase for the normal duration of meiosis occur normally, but the chromosomes fail to interact correctly with the spindle in meiosis II metaphase. By contrast, inhibition of protein synthesis immediately after completion of meiosis or mitosis stops cells entering the next mitosis. We describe the behavior of cyclins A and B in relation to these "points of no return." The cyclins are synthesized continuously and are rapidly destroyed shortly before the metaphase-anaphase transition of the mitotic cell cycles, with cyclin A being degraded in advance of cyclin B. Cyclin destruction normally occurs during a 5-min window in mitosis, but in the monopolar mitosis that occurs after parthenogenetic activation of clam oocytes, or when colchicine is added to fertilized eggs about to enter first mitosis, the destruction of cyclin B is strongly delayed, whereas proteolysis of cyclin A is maintained in an activated state for the duration of metaphase arrest. Under either of these abnormal conditions, inhibition of protein synthesis causes a premature return to interphase that correlates with the time when cyclin B disappears.

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Mehsen, Haytham, Vincent Boudreau, Damien Garrido, Mohammed Bourouh, Myreille Larouche, Paul S. Maddox, Andrew Swan, and Vincent Archambault. "PP2A-B55 promotes nuclear envelope reformation after mitosis in Drosophila." Journal of Cell Biology 217, no. 12 (October 11, 2018): 4106–23. http://dx.doi.org/10.1083/jcb.201804018.

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As a dividing cell exits mitosis and daughter cells enter interphase, many proteins must be dephosphorylated. The protein phosphatase 2A (PP2A) with its B55 regulatory subunit plays a crucial role in this transition, but the identity of its substrates and how their dephosphorylation promotes mitotic exit are largely unknown. We conducted a maternal-effect screen in Drosophila melanogaster to identify genes that function with PP2A-B55/Tws in the cell cycle. We found that eggs that receive reduced levels of Tws and of components of the nuclear envelope (NE) often fail development, concomitant with NE defects following meiosis and in syncytial mitoses. Our mechanistic studies using Drosophila cells indicate that PP2A-Tws promotes nuclear envelope reformation (NER) during mitotic exit by dephosphorylating BAF and suggests that PP2A-Tws targets additional NE components, including Lamin and Nup107. This work establishes Drosophila as a powerful model to further dissect the molecular mechanisms of NER and suggests additional roles of PP2A-Tws in the completion of meiosis and mitosis.

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Lee, Janice Y., Aki Hayashi-Hagihara, and Terry L. Orr-Weaver. "Roles and regulation of the Drosophila centromere cohesion protein MEI-S332 family." Philosophical Transactions of the Royal Society B: Biological Sciences 360, no. 1455 (March 29, 2005): 543–52. http://dx.doi.org/10.1098/rstb.2005.1619.

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In meiosis, a physical attachment, or cohesion, between the centromeres of the sister chromatids is retained until their separation at anaphase II. This cohesion is essential for ensuring accurate segregation of the sister chromatids in meiosis II and avoiding aneuploidy, a condition that can lead to prenatal lethality or birth defects. The Drosophila MEI-S332 protein localizes to centromeres when sister chromatids are attached in mitosis and meiosis, and it is required to maintain cohesion at the centromeres after cohesion along the sister chromatid arms is lost at the metaphase I/anaphase I transition. MEI-S332 is the founding member of a family of proteins that protect centromeric cohesion but whose members also affect kinetochore behaviour and spindle microtubule dynamics. We compare the Drosophila MEI-S332 family members, evaluate the role of MEI-S332 in mitosis and meiosis I, and discuss the regulation of localization of MEI-S332 to the centromere and its dissociation at anaphase. We analyse the relationship between MEI-S332 and cohesin, a protein complex that is also necessary for sister-chromatid cohesion in mitosis and meiosis. In mitosis, centromere localization of MEI-S332 is not dependent upon the cohesin complex, and cohesin retains its association with mitotic chromosomes even in the absence of MEI-S332.

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Hayashi, Aki, Haruhiko Asakawa, Tokuko Haraguchi, and Yasushi Hiraoka. "Reconstruction of the Kinetochore during Meiosis in Fission Yeast Schizosaccharomyces pombe." Molecular Biology of the Cell 17, no. 12 (December 2006): 5173–84. http://dx.doi.org/10.1091/mbc.e06-05-0388.

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During the transition from mitosis to meiosis, the kinetochore undergoes significant reorganization, switching from a bipolar to a monopolar orientation. To examine the centromere proteins that are involved in fundamental reorganization in meiosis, we observed the localization of 22 mitotic and 2 meiotic protein components of the kinetochore during meiosis in living cells of the fission yeast. We found that the 22 mitotic proteins can be classified into three groups: the Mis6-like group, the NMS (Ndc80-Mis12-Spc7) group, and the DASH group, based on their meiotic behavior. Mis6-like group proteins remain at the centromere throughout meiosis. NMS group proteins disappear from the centromere at the onset of meiosis and reappear at the centromere in two steps in late prophase. DASH group proteins appear shortly before metaphase of meiosis I. These observations suggest that Mis6-like group proteins constitute the structural basis of the centromere and that the NMS and DASH group proteins reassemble to establish the functional metaphase kinetochore. On the other hand, the meiosis-specific protein Moa1, which plays an important role in forming the meiotic monopolar kinetochore, is loaded onto the centromere significantly earlier than the NMS group, whereas another meiosis-specific protein, Sgo1, is loaded at times similar to the NMS group.

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Furuta, Tokiko, Simon Tuck, Jay Kirchner, Bryan Koch, Roy Auty, Risa Kitagawa, Ann M. Rose, and David Greenstein. "EMB-30: An APC4 Homologue Required for Metaphase-to-Anaphase Transitions during Meiosis and Mitosis in Caenorhabditis elegans." Molecular Biology of the Cell 11, no. 4 (April 2000): 1401–19. http://dx.doi.org/10.1091/mbc.11.4.1401.

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Here we show that emb-30 is required for metaphase-to-anaphase transitions during meiosis and mitosis inCaenorhabditis elegans. Germline-specificemb-30 mutant alleles block the meiotic divisions. Mutant oocytes, fertilized by wild-type sperm, set up a meiotic spindle but do not progress to anaphase I. As a result, polar bodies are not produced, pronuclei fail to form, and cytokinesis does not occur. Severe-reduction-of-function emb-30 alleles (class I alleles) result in zygotic sterility and lead to germline and somatic defects that are consistent with an essential role in promoting the metaphase-to-anaphase transition during mitosis. Analysis of the vulval cell lineages in these emb-30(class I) mutant animals suggests that mitosis is lengthened and eventually arrested when maternally contributed emb-30 becomes limiting. By further reducing maternal emb-30 function contributed to class I mutant animals, we show that emb-30 is required for the metaphase-to-anaphase transition in many, if not all, cells. Metaphase arrest in emb-30 mutants is not due to activation of the spindle assembly checkpoint but rather reflects an essential emb-30 requirement for M-phase progression. A reduction in emb-30 activity can suppress the lethality and sterility caused by a null mutation in mdf-1, a component of the spindle assembly checkpoint machinery. This result suggests that delaying anaphase onset can bypass the spindle checkpoint requirement for normal development. Positional cloning established thatemb-30 encodes the likely C. elegansorthologue of APC4/Lid1, a component of the anaphase-promoting complex/cyclosome, required for the metaphase-to-anaphase transition. Thus, the anaphase-promoting complex/cyclosome is likely to be required for all metaphase-to-anaphase transitions in a multicellular organism.

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Clift, Dean, and Melina Schuh. "Restarting life: fertilization and the transition from meiosis to mitosis." Nature Reviews Molecular Cell Biology 14, no. 9 (August 14, 2013): 549–62. http://dx.doi.org/10.1038/nrm3643.

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Alonso-Ramos, Paula, and Jesús A. Carballo. "Decoding the Nucleolar Role in Meiotic Recombination and Cell Cycle Control: Insights into Cdc14 Function." International Journal of Molecular Sciences 25, no. 23 (November 29, 2024): 12861. http://dx.doi.org/10.3390/ijms252312861.

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The cell cycle, essential for growth, reproduction, and genetic stability, is regulated by a complex network of cyclins, Cyclin-Dependent Kinases (CDKs), phosphatases, and checkpoints that ensure accurate cell division. CDKs and phosphatases are crucial for controlling cell cycle progression, with CDKs promoting it and phosphatases counteracting their activity to maintain balance. The nucleolus, as a biomolecular condensate, plays a key regulatory role by serving as a hub for ribosome biogenesis and the sequestration and release of various cell cycle regulators. This phase separation characteristic of the nucleolus is vital for the specific and timely release of Cdc14, required for most essential functions of phosphatase in the cell cycle. While mitosis distributes chromosomes to daughter cells, meiosis is a specialized division process that produces gametes and introduces genetic diversity. Central to meiosis is meiotic recombination, which enhances genetic diversity by generating crossover and non-crossover products. This process begins with the introduction of double-strand breaks, which are then processed by numerous repair enzymes. Meiotic recombination and progression are regulated by proteins and feedback mechanisms. CDKs and polo-like kinase Cdc5 drive recombination through positive feedback, while phosphatases like Cdc14 are crucial for activating Yen1, a Holliday junction resolvase involved in repairing unresolved recombination intermediates in both mitosis and meiosis. Cdc14 is released from the nucleolus in a regulated manner, especially during the transition between meiosis I and II, where it helps inactivate CDK activity and promote proper chromosome segregation. This review integrates current knowledge, providing a synthesis of these interconnected processes and an overview of the mechanisms governing cell cycle regulation and meiotic recombination.

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Zhang, Qing-Hua, Wai Shan Yuen, Deepak Adhikari, Jennifer A. Flegg, Greg FitzHarris, Marco Conti, Piotr Sicinski, Ibtissem Nabti, Petros Marangos, and John Carroll. "Cyclin A2 modulates kinetochore–microtubule attachment in meiosis II." Journal of Cell Biology 216, no. 10 (August 17, 2017): 3133–43. http://dx.doi.org/10.1083/jcb.201607111.

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Cyclin A2 is a crucial mitotic Cdk regulatory partner that coordinates entry into mitosis and is then destroyed in prometaphase within minutes of nuclear envelope breakdown. The role of cyclin A2 in female meiosis and its dynamics during the transition from meiosis I (MI) to meiosis II (MII) remain unclear. We found that cyclin A2 decreases in prometaphase I but recovers after the first meiotic division and persists, uniquely for metaphase, in MII-arrested oocytes. Conditional deletion of cyclin A2 from mouse oocytes has no discernible effect on MI but leads to disrupted MII spindles and increased merotelic attachments. On stimulation of exit from MII, there is a dramatic increase in lagging chromosomes and an inhibition of cytokinesis. These defects are associated with an increase in microtubule stability in MII spindles, suggesting that cyclin A2 mediates the fidelity of MII by maintaining microtubule dynamics during the rapid formation of the MII spindle.

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Kadyk, L. C., and J. Kimble. "Genetic regulation of entry into meiosis in Caenorhabditis elegans." Development 125, no. 10 (May 15, 1998): 1803–13. http://dx.doi.org/10.1242/dev.125.10.1803.

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The Caenorhabditis elegans germline is composed of mitotically dividing cells at the distal end that give rise to meiotic cells more proximally. Specification of the distal region as mitotic relies on induction by the somatic distal tip cell and the glp-1 signal transduction pathway. However, the genetic control over the transition from mitosis to meiosis is not understood. In this paper, we report the identification of a gene, gld-2, that has at least two functions in germline development. First, gld-2 is required for normal progression through meiotic prophase. Second, gld-2 promotes entry into meiosis from the mitotic cell cycle. With respect to this second function, gld-2 appears to be functionally redundant with a previously described gene, gld-1 (Francis, R., Barton, M. K., Kimble, J. and Schedl, T. (1995) Genetics 139, 579–606). Germ cells in gld-1(o) and gld-2 single mutants enter meiosis at the normal time, but germ cells in gld-2 gld-1(o) double mutants do not enter meiosis. Instead, the double mutant germline is mitotic throughout and forms a large tumor. We suggest that gld-1 and gld-2 define two independent regulatory pathways, each of which can be sufficient for entry into meiosis. Epistasis analyses show that gld-1 and gld-2 work downstream of the glp-1 signal transduction pathway. Therefore, we hypothesize that glp-1 promotes proliferation by inhibiting the meiosis-promoting functions of gld-1 and gld-2.

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Shao, Hua, Ruizhen Li, Chunqi Ma, Eric Chen, and X. Johné Liu. "Xenopus oocyte meiosis lacks spindle assembly checkpoint control." Journal of Cell Biology 201, no. 2 (April 8, 2013): 191–200. http://dx.doi.org/10.1083/jcb.201211041.

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The spindle assembly checkpoint (SAC) functions as a surveillance mechanism to detect chromosome misalignment and to delay anaphase until the errors are corrected. The SAC is thought to control mitosis and meiosis, including meiosis in mammalian eggs. However, it remains unknown if meiosis in the eggs of nonmammalian vertebrate species is also regulated by SAC. Using a novel karyotyping technique, we demonstrate that complete disruption of spindle microtubules in Xenopus laevis oocytes did not affect the bivalent-to-dyad transition at the time oocytes are undergoing anaphase I. These oocytes also acquired the ability to respond to parthenogenetic activation, which indicates proper metaphase II arrest. Similarly, oocytes exhibiting monopolar spindles, via inhibition of aurora B or Eg5 kinesin, underwent monopolar anaphase on time and without additional intervention. Therefore, the metaphase-to-anaphase transition in frog oocytes is not regulated by SAC.

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Yu, Jing, and Mariana F. Wolfner. "The Drosophila Nuclear Lamina Protein YA Binds to DNA and Histone H2B with Four Domains." Molecular Biology of the Cell 13, no. 2 (February 2002): 558–69. http://dx.doi.org/10.1091/mbc.01-07-0336.

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Dramatic changes occur in nuclear organization and function during the critical developmental transition from meiosis to mitosis. TheDrosophila nuclear lamina protein YA binds to chromatin and is uniquely required for this transition. In this study, we dissected YA's binding to chromatin. We found that YA can bind to chromatin directly and specifically. It binds to DNA but not RNA, with a preference for double-stranded DNA (linear or supercoiled) over single-stranded DNA. It also binds to histone H2B. YA's binding to DNA and histone H2B is mediated by four domains distributed along the length of the YA molecule. A model for YA function at the end ofDrosophila female meiosis is proposed.

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Bickel, Sharon E., Dudley W. Wyman, and Terry L. Orr-Weaver. "Mutational Analysis of the Drosophila Sister-Chromatid Cohesion Protein ORD and Its Role in the Maintenance of Centromeric Cohesion." Genetics 146, no. 4 (August 1, 1997): 1319–31. http://dx.doi.org/10.1093/genetics/146.4.1319.

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The ord gene is required for proper segregation of all chromosomes in both male and female Drosophila meiosis. Here we describe the isolation of a null ord allele and examine the consequences of ablating ord function. Cytologically, meiotic sister-chromatid cohesion is severely disrupted in flies lacking ORD protein. Moreover, the frequency of missegregation in genetic tests is consistent with random segregation of chromosomes through both meiotic divisions, suggesting that sister cohesion may be completely abolished. However, only a slight decrease in viability is observed for ord null flies, indicating that ORD function is not essential for cohesion during somatic mitosis. In addition, we do not observe perturbation of germ-line mitotic divisions in flies lacking ORD activity. Our analysis of weaker ord alleles suggests that ORD is required for proper centromeric cohesion after arm cohesion is released at the metaphase I/anaphase I transition. Finally, although meiotic cohesion is abolished in the ord null fly, chromosome loss is not appreciable. Therefore, ORD activity appears to promote centromeric cohesion during meiosis II but is not essential for kinetochore function during anaphase.

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Renault, A. D. "giant nucleiis essential in the cell cycle transition from meiosis to mitosis." Development 130, no. 13 (July 1, 2003): 2997–3005. http://dx.doi.org/10.1242/dev.00501.

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Shan, Lingjuan, Chan Wu, Di Chen, Lei Hou, Xin Li, Lixia Wang, Xiao Chu, Yifeng Hou, and Zhaohui Wang. "Regulators of alternative polyadenylation operate at the transition from mitosis to meiosis." Journal of Genetics and Genomics 44, no. 2 (February 2017): 95–106. http://dx.doi.org/10.1016/j.jgg.2016.12.007.

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25

Ma, Yuxiao, Wenhui Wu, Yun Zhang, Xuzhao Wang, Jiahui Wei, Xiaotong Guo, Man Xue, and Guiyu Zhu. "The Synchronized Progression from Mitosis to Meiosis in Female Primordial Germ Cells between Layers and Broilers." Genes 14, no. 4 (March 23, 2023): 781. http://dx.doi.org/10.3390/genes14040781.

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Layer and broiler hens show a dramatic difference in the volume and frequency of egg production. However, it is unclear whether the intrinsic competency of oocyte generation is also different between the two types of chicken. All oocytes were derived from the primordial germ cells (PGC) in the developing embryo, and female PGC proliferation (mitosis) and the subsequent differentiation (meiosis) determine the ultimate ovarian pool of germ cells available for future ovulation. In this study, we systematically compared the cellular phenotype and gene expression patterns during PGC mitosis (embryonic day 10, E10) and meiosis (E14) between female layers and broilers to determine whether the early germ cell development is also subjected to the selective breeding of egg production traits. We found that PGCs from E10 showed much higher activity in cell propagation and were enriched in cell proliferation signaling pathways than PGCs from E14 in both types of chicken. A common set of genes, namely insulin-like growth factor 2 (IGF2) and E2F transcription factor 4 (E2F4), were identified as the major regulators of cell proliferation in E10 PGCs of both strains. In addition, we found that E14 PGCs from both strains showed an equal ability to initiate meiosis, which was associated with the upregulation of key genes for meiotic initiation. The intrinsic cellular dynamics during the transition from proliferation to differentiation of female germ cells were conserved between layers and broilers. Hence, we surmise that other non-cell autonomous mechanisms involved in germ-somatic cell interactions would contribute to the divergence of egg production performance between layers and broilers.

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Kadyk, Lisa C., Eric J. Lambie, and Judith Kimble. "glp-3 Is Required for Mitosis and Meiosis in the Caenorhabditis elegans Germ Line." Genetics 145, no. 1 (January 1, 1997): 111–21. http://dx.doi.org/10.1093/genetics/145.1.111.

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The germ line is the only tissue in Caenorhabditis elegans in which a stem cell population continues to divide mitotically throughout life; hence the cell cycles of the germ line and the soma are regulated differently. Here we report the genetic and phenotypic characterization of the glp-3 gene. In animals homozygous for each of five recessive loss-of-function alleles, germ cells in both hermaphrodites and males fail to progress through mitosis and meiosis, but somatic cells appear to divide normally. Germ cells in animals grown at 15° appear by DAPI staining to be uniformly arrested at the G2/M transition with <20 germ cells per gonad on average, suggesting a checkpoint-mediated arrest. In contrast, germ cells in mutant animals grown at 25° frequently proliferate slowly during adulthood, eventually forming small germ lines with several hundred germ cells. Nevertheless, cells in these small germ lines never undergo meiosis. Double mutant analysis with mutations in other genes affecting germ cell proliferation supports the idea that glp-3 may encode a gene product that is required for the mitotic and meiotic cell cycles in the C. elegans germ line.

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Boxem, M., D. G. Srinivasan, and S. van den Heuvel. "The Caenorhabditis elegans gene ncc-1 encodes a cdc2-related kinase required for M phase in meiotic and mitotic cell divisions, but not for S phase." Development 126, no. 10 (May 15, 1999): 2227–39. http://dx.doi.org/10.1242/dev.126.10.2227.

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We have identified six protein kinases that belong to the family of cdc2-related kinases in Caenorhabditis elegans. Results from RNA interference experiments indicate that at least one of these kinases is required for cell-cycle progression during meiosis and mitosis. This kinase, encoded by the ncc-1 gene, is closely related to human Cdk1/Cdc2, Cdk2 and Cdk3 and yeast CDC28/cdc2(+). We addressed whether ncc-1 acts to promote passage through a single transition or multiple transitions in the cell cycle, analogous to Cdks in vertebrates or yeasts, respectively. We isolated five recessive ncc-1 mutations in a genetic screen for mutants that resemble larval arrested ncc-1(RNAi) animals. Our results indicate that maternal ncc-1 product is sufficient for embryogenesis, and that zygotic expression is required for cell divisions during larval development. Cells that form the postembryonic lineages in wild-type animals do not enter mitosis in ncc-1 mutants, as indicated by lack of chromosome condensation and nuclear envelope breakdown. However, progression through G1 and S phase appears unaffected, as revealed by expression of ribonucleotide reductase, incorporation of BrdU and DNA quantitation. Our results indicate that C. elegans uses multiple Cdks to regulate cell-cycle transitions and that ncc-1 is the C. elegans ortholog of Cdk1/Cdc2 in other metazoans, required for M phase in meiotic as well as mitotic cell cycles.

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Crittenden, S. L., E. R. Troemel, T. C. Evans, and J. Kimble. "GLP-1 is localized to the mitotic region of the C. elegans germ line." Development 120, no. 10 (October 1, 1994): 2901–11. http://dx.doi.org/10.1242/dev.120.10.2901.

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In C. elegans, germline mitosis depends on induction by the somatic distal tip cell (DTC) and on activity of the glp-1 gene. Using antibodies to GLP-1 protein, we have examined GLP-1 on western blots and by immunocytochemistry. GLP-1 is tightly associated with membranes of mitotic germline cells, supporting its identification as an integral membrane protein. Furthermore, GLP-1 is localized within the germ line to the mitotic region, consistent with the model that GLP-1 acts as a membrane receptor for the distal tip cell signal. Unexpectedly, GLP-1 and the zone of mitosis extend further than the DTC processes. We present three models by which the DTC may influence GLP-1 activity and thereby determine the zone of mitosis. The spatial restriction of GLP-1 appears to be controlled at the translational level in hermaphrodites. We suggest that down-regulation of GLP-1 may be required to effect the transition from mitosis into meiosis.

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Yuan, Ting-Lu, Wei-Jie Huang, Juan He, Dong Zhang, and Wei-Hua Tang. "Stage-Specific Gene Profiling of Germinal Cells Helps Delineate the Mitosis/Meiosis Transition." Plant Physiology 176, no. 2 (November 29, 2017): 1610–26. http://dx.doi.org/10.1104/pp.17.01483.

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30

Andric, Vedrana, and Mathieu Rougemaille. "Long Non-Coding RNAs in the Control of Gametogenesis: Lessons from Fission Yeast." Non-Coding RNA 7, no. 2 (June 11, 2021): 34. http://dx.doi.org/10.3390/ncrna7020034.

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Long non-coding RNAs (lncRNAs) contribute to cell fate decisions by modulating genome expression and stability. In the fission yeast Schizosaccharomyces pombe, the transition from mitosis to meiosis results in a marked remodeling of gene expression profiles, which ultimately ensures gamete production and inheritance of genetic information to the offspring. This key developmental process involves a set of dedicated lncRNAs that shape cell cycle-dependent transcriptomes through a variety of mechanisms, including epigenetic modifications and the modulation of transcription, post-transcriptional and post-translational regulations, and that contribute to meiosis-specific chromosomal events. In this review, we summarize the biology of these lncRNAs, from their identification to mechanism of action, and discuss their regulatory role in the control of gametogenesis.

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Maezawa, So, Akihiko Sakashita, Masashi Yukawa, Xiaoting Chen, Kazuki Takahashi, Kris G. Alavattam, Ippo Nakata, Matthew T. Weirauch, Artem Barski, and Satoshi H. Namekawa. "Super-enhancer switching drives a burst in gene expression at the mitosis-to-meiosis transition." Nature Structural & Molecular Biology 27, no. 10 (September 7, 2020): 978–88. http://dx.doi.org/10.1038/s41594-020-0488-3.

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Nakagawa, Tadashi, Teng Zhang, Ryo Kushi, Seiji Nakano, Takahiro Endo, Makiko Nakagawa, Noriko Yanagihara, David Zarkower, and Keiko Nakayama. "Regulation of mitosis-meiosis transition by the ubiquitin ligase β-TrCP in male germ cells." Development 144, no. 22 (October 5, 2017): 4137–47. http://dx.doi.org/10.1242/dev.158485.

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Sackton, Katharine L., Jacqueline M. Lopez, Cindy L. Berman, and Mariana F. Wolfner. "YA is needed for proper nuclear organization to transition between meiosis and mitosis in Drosophila." BMC Developmental Biology 9, no. 1 (2009): 43. http://dx.doi.org/10.1186/1471-213x-9-43.

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Wu, Jianbo, Xin Li, Zhiyang Gao, Lin Pang, Xian Liu, Xiahe Huang, Yingchun Wang, and Zhaohui Wang. "RNA kinase CLP1/Cbc regulates meiosis initiation in spermatogenesis." Human Molecular Genetics 30, no. 17 (April 16, 2021): 1569–78. http://dx.doi.org/10.1093/hmg/ddab107.

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Abstract CLP1, TSEN complex, and VCP are evolutionarily conserved proteins whose mutations are associated with neurodegenerative diseases. In this study, we have found that they are also involved in germline differentiation. To optimize both quantity and quality in gametes production, germ cells expand themselves through limited mitotic cycles prior to meiosis. Stemming from our previous findings on the correlation between mRNA 3′-processing and meiosis entry, here we identify that the RNA kinase Cbc, the Drosophila member of the highly conserved CLP1 family, is a component of the program regulating the transition from mitosis to meiosis. Using genetic manipulations in Drosophila testis, we demonstrate that nuclear Cbc is required to promote meiosis entry. Combining biochemical and genetic methods, we reveal that Cbc physically and/or genetically intersects with Tsen54 and TER94 (VCP ortholog) in this process. The C-terminal half of Tsen54 is both necessary and sufficient for its binding with Cbc. Further, we illustrate the functional conservation between Cbc and mammalian CLP1 in the assays of subcellular localization and Drosophila fertility. As CLP1, TSEN complex, and VCP have also been identified in neurodegenerations of animal models, a mechanism involving these factors seems to be shared in gametogenesis and neurogenesis.

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Pajpach, Filip, Tianyu Wu, Linda Shearwin-Whyatt, Keith Jones, and Frank Grützner. "Flavors of Non-Random Meiotic Segregation of Autosomes and Sex Chromosomes." Genes 12, no. 9 (August 28, 2021): 1338. http://dx.doi.org/10.3390/genes12091338.

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Segregation of chromosomes is a multistep process occurring both at mitosis and meiosis to ensure that daughter cells receive a complete set of genetic information. Critical components in the chromosome segregation include centromeres, kinetochores, components of sister chromatid and homologous chromosomes cohesion, microtubule organizing centres, and spindles. Based on the cytological work in the grasshopper Brachystola, it has been accepted for decades that segregation of homologs at meiosis is fundamentally random. This ensures that alleles on chromosomes have equal chance to be transmitted to progeny. At the same time mechanisms of meiotic drive and an increasing number of other examples of non-random segregation of autosomes and sex chromosomes provide insights into the underlying mechanisms of chromosome segregation but also question the textbook dogma of random chromosome segregation. Recent advances provide a better understanding of meiotic drive as a prominent force where cellular and chromosomal changes allow autosomes to bias their segregation. Less understood are mechanisms explaining observations that autosomal heteromorphism may cause biased segregation and regulate alternating segregation of multiple sex chromosome systems or translocation heterozygotes as an extreme case of non-random segregation. We speculate that molecular and cytological mechanisms of non-random segregation might be common in these cases and that there might be a continuous transition between random and non-random segregation which may play a role in the evolution of sexually antagonistic genes and sex chromosome evolution.

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Sipiczki, M., and A. Grallert. "Polarity, spatial organisation of cytoskeleton, and nuclear division in morphologically altered cells of Schizosaccharomyces pombe." Canadian Journal of Microbiology 43, no. 11 (November 1, 1997): 991–98. http://dx.doi.org/10.1139/m97-143.

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To gain more information about the determination of cell polarity and its relationship to the organisation of cytoskeleton, we have examined the mycelial mutant sep1-1 and the multinucleate multipolar syncytia of the triple mutant sep1-1 spl1-1 cdc4-8 by indirect immunofluorescence techniques. We have found that polarity is predetermined by the shape of the cell. During transition from mitosis to interphase the microtubules of the arising cytoplasmic cytoskeleton gradually form a basket-like pattern that reflects the curvatures of the cell envelope. The presumable growing poles, where actin accumulates, usually correlates with the sites where the cell tapers and the microtubules converge. However, no growth can be launched at these sites if the cell surface has not been properly processed. Mitosis and meiosis are not affected significantly by changes in cell morphology and polarity, but larger cells are less effective during sporulation. The azygotic asci produced by multinucleate syncytia frequently contain over 20 ascospores.Key words: cell division cycle, cytokinesis, cytoskeleton, fission yeast.

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Carroll, John, Greg FitzHarris, Petros Marangos, and Guillaume Halet. "Ca2+ signalling and cortical re-organisation during the transition from meiosis to mitosis in mammalian oocytes." European Journal of Obstetrics & Gynecology and Reproductive Biology 115 (July 2004): S61—S67. http://dx.doi.org/10.1016/j.ejogrb.2004.01.024.

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38

Lamitina, S. Todd, and Steven W. L'Hernault. "Dominant mutations in the Caenorhabditis elegans Myt1 orthologwee-1.3 reveal a novel domain that controls M-phase entry during spermatogenesis." Development 129, no. 21 (November 1, 2002): 5009–18. http://dx.doi.org/10.1242/dev.129.21.5009.

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Regulatory phosphorylation of the Cdc2p kinase by Wee1p-type kinases prevents eukaryotic cells from entering mitosis or meiosis at an inappropriate time. The canonical Wee1p kinase is a soluble protein that functions in the eukaryotic nucleus. All metazoa also have a membrane-associated Wee1p-like kinase named Myt1, and we describe the first genetic characterization of this less well-studied kinase. The Caenorhabditis elegans Myt1 ortholog is encoded by the wee-1.3 gene, and six dominant missense mutants prevent primary spermatocytes from entering M phase but do not affect either oocyte meiosis or any mitotic division. These six dominantwee-1.3(gf) mutations are located in a four amino acid region near the C terminus and they cause self-sterility of hermaphrodites. Second-site intragenic suppressor mutations in wee-1.3(gf) restore self-fertility to these dominant sterile hermaphrodites, permitting genetic dissection of this kinase. Ten intragenic wee-1.3 suppressor mutations were recovered and they form an allelic series that includes semi-dominant,hypomorphic and null mutations. These mutants reveal that WEE-1.3 protein is required for embryonic development, germline proliferation and initiation of meiosis during spermatogenesis. This suggests that a novel, sperm-specific pathway negatively regulates WEE-1.3 to allow the G2/M transition of male meiosis I, and that dominant wee-1.3 mutants prevent this negative regulation.

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Deak, J. C., and F. P. Doerder. "High Frequency Intragenic Recombination During Macronuclear Development in Tetrahymena thermophila Restores the Wild-type SerH1 Gene." Genetics 148, no. 3 (March 1, 1998): 1109–15. http://dx.doi.org/10.1093/genetics/148.3.1109.

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Abstract Macronuclear development in ciliates is characterized by extensive rearrangement of genetic material, including sequence elimination, chromosome fragmentation and telomere addition. Intragenic recombination is a relatively rare, but evolutionarily important phenomenon occurring in mitosis and meiosis in a wide variety of organisms. Here, we show that high frequency intragenic recombination, on the order of 30%, occurs in the developing amitotic macronucleus of the ciliate Tetrahymena thermophila. Such recombination, occurring between two nonsense transition mutations separated by 726 nucleotides, reproducibly restores wild-type expression of the SerH1 surface protein gene, thus mimicking complementation in trans heterozygotes. Recombination must be considered a potentially important aspect of macronuclear development, producing gene combinations not present in the germinal micronucleus.

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40

Li, Wei, Leah R. DeBella, Tugba Guven-Ozkan, Rueyling Lin, and Lesilee S. Rose. "An eIF4E-binding protein regulates katanin protein levels in C. elegans embryos." Journal of Cell Biology 187, no. 1 (September 28, 2009): 33–42. http://dx.doi.org/10.1083/jcb.200903003.

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In Caenorhabditis elegans, the MEI-1–katanin microtubule-severing complex is required for meiosis, but must be down-regulated during the transition to embryogenesis to prevent defects in mitosis. A cullin-dependent degradation pathway for MEI-1 protein has been well documented. In this paper, we report that translational repression may also play a role in MEI-1 down-regulation. Reduction of spn-2 function results in spindle orientation defects due to ectopic MEI-1 expression during embryonic mitosis. MEL-26, which is both required for MEI-1 degradation and is itself a target of the cullin degradation pathway, is present at normal levels in spn-2 mutant embryos, suggesting that the degradation pathway is functional. Cloning of spn-2 reveals that it encodes an eIF4E-binding protein that localizes to the cytoplasm and to ribonucleoprotein particles called P granules. SPN-2 binds to the RNA-binding protein OMA-1, which in turn binds to the mei-1 3′ untranslated region. Thus, our results suggest that SPN-2 functions as an eIF4E-binding protein to negatively regulate translation of mei-1.

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McClusky, L. M. "Stage and season effects on cell cycle and apoptotic activities of germ cells and Sertoli cells during spermatogenesis in the spiny dogfish (Squalus acanthias)." Reproduction 129, no. 1 (January 2005): 89–102. http://dx.doi.org/10.1530/rep.1.00177.

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To understand the processes involved in the spatial and temporal maturation of testicular cells in Squalus acanthias, we used standard morphometry, proliferating-cell nuclear antigen (PCNA) and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelling (TUNEL) immunohistochemistry. Except for immature spermatocysts (germinal zone, GZ; early-stage pre-meiotic, E-PrM), the number of cysts in all subsequent stages and the total number of cysts in the spermatogenic progression varied seasonally. The spermatogenic cycle spans about 2 years and is interrupted by germcell clone deletion via apoptosis at the mitosis–meiosis transition in April/May, manifesting as a zone of degeneration (ZD). Rate of displacement of the ZD across the testis diameter indicates that late-stage premeiotic (L-PrM) generations 12–13 require 9–10 months to reach the mature-spermatid stage. Also, the number of cysts completing spermatogenesis is approximately 4–5-fold less than the number that entered spermatogenesis proper 2 years earlier. Pronounced gonocytogenesis in the germinal ridge was coincident with ZD formation in April/May, but it was absent in the fall when mature spermatogonial and meiotic activities had resumed. Whereas strong Sertoli cell PCNA immunoreactivity dominated the GZ cyst cell-cycle activities throughout the year, except during the spring/summer months, the spermatogonial- and Sertoli-cell PCNA indices in E-PrM cysts were inversely related. PCNA immunoreactivity in spermatocytes was seasonal and dependent on the stage of meiosis. TUNEL labelling was limited to spermatogonia and increased stage-dependently in the PrM region (L-PrM = mid-stage PrM ≫E-PrM ≫GZ), correlating with ZD formation, in a season-dependent manner. Results imply that effects of normal regulatory factors in Squalus are stage- and process-specific.

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Prosée, Reinier F., Joanna M. Wenda, Isa Özdemir, Caroline Gabus, Kamila Delaney, Francoise Schwager, Monica Gotta, and Florian A. Steiner. "Transgenerational inheritance of centromere identity requires the CENP-A N-terminal tail in the C. elegans maternal germ line." PLOS Biology 19, no. 7 (July 6, 2021): e3000968. http://dx.doi.org/10.1371/journal.pbio.3000968.

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Centromere protein A (CENP-A) is a histone H3 variant that defines centromeric chromatin and is essential for centromere function. In most eukaryotes, CENP-A-containing chromatin is epigenetically maintained, and centromere identity is inherited from one cell cycle to the next. In the germ line of the holocentric nematode Caenorhabditis elegans, this inheritance cycle is disrupted. CENP-A is removed at the mitosis-to-meiosis transition and is reestablished on chromatin during diplotene of meiosis I. Here, we show that the N-terminal tail of CENP-A is required for the de novo establishment of centromeres, but then its presence becomes dispensable for centromere maintenance during development. Worms homozygous for a CENP-A tail deletion maintain functional centromeres during development but give rise to inviable offspring because they fail to reestablish centromeres in the maternal germ line. We identify the N-terminal tail of CENP-A as a critical domain for the interaction with the conserved kinetochore protein KNL-2 and argue that this interaction plays an important role in setting centromere identity in the germ line. We conclude that centromere establishment and maintenance are functionally distinct in C. elegans.

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McLeod, Maureen, Boris Shor, Anthony Caporaso, Wei Wang, Hua Chen, and Lin Hu. "Cpc2, a Fission Yeast Homologue of Mammalian RACK1 Protein, Interacts with Ran1 (Pat1) Kinase To Regulate Cell Cycle Progression and Meiotic Development." Molecular and Cellular Biology 20, no. 11 (June 1, 2000): 4016–27. http://dx.doi.org/10.1128/mcb.20.11.4016-4027.2000.

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ABSTRACT The Schizosaccharomyces pombe ran1/pat1 gene regulates the transition between mitosis and meiosis. Inactivation of Ran1 (Pat1) kinase is necessary and sufficient for cells to exit the cell cycle and undergo meiosis. The yeast two-hybrid interaction trap was used to identify protein partners for Ran1/Pat1. Here we report the identification of one of these, Cpc2. Cpc2 encodes a homologue of RACK1, a WD protein with homology to the β subunit of heterotrimeric G proteins. RACK1 is a highly conserved protein, although its function remains undefined. In mammalian cells, RACK1 physically associates with some signal transduction proteins, including Src and protein kinase C. Fission yeast cells containing a cpc2 null allele are viable but cell cycle delayed. cpc2Δ cells fail to accumulate in G1 when starved of nitrogen. This leads to defects in conjugation and meiosis. Copurification studies show that although Cpc2 and Ran1 (Pat1) physically associate, Cpc2 does not alter Ran1 (Pat1) kinase activity in vitro. Using a Ran1 (Pat1) fusion to green fluorescent protein, we show that localization of the kinase is impaired in cpc2Δ cells. Thus, in parallel with the proposed role of RACK1 in mammalian cells, fission yeast cpc2 may function as an anchoring protein for Ran1 (Pat1) kinase. All defects associated with loss of cpc2 are reversed in cells expressing mammalian RACK1, demonstrating that the fission yeast and mammalian gene products are indeed functional homologues.

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Rhee, K., and D. J. Wolgemuth. "The NIMA-related kinase 2, Nek2, is expressed in specific stages of the meiotic cell cycle and associates with meiotic chromosomes." Development 124, no. 11 (June 1, 1997): 2167–77. http://dx.doi.org/10.1242/dev.124.11.2167.

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The Aspergillus nimA gene encodes a Ser/Thr protein kinase which is required for mitosis, in addition to Cdc2, and which has been suggested to have a role in chromosomal condensation. In this study, we isolated a potential murine homologue of nimA, Nek2, which was shown to be expressed most abundantly in the testis of the adult tissues examined. Its expression in the testis was restricted to the germ cells, with highest levels detected in spermatocytes at pachytene and diplotene stages. Immunohistochemical analysis revealed that Nek2 localized to nuclei, exhibiting a non-uniform distribution within the nucleus. Nek2 appeared to be associated with meiotic chromosomes, an association that was better defined by immunolocalization to hypotonically dispersed meiotic chromosomes. This localization was more apparent in regions of dense chromatin, including the sex vesicle, and was also obvious at some of the chromosome ends. The presence of Nek2 protein was not unique to male germ cells, as it was found in meiotic pachytene stage oocytes as well. Furthermore, in an in vitro experimental setting in which meiotic chromosome condensation was induced with okadaic acid, a concomitant induction of Nek2 kinase activity was observed. The expression of Nek2 in meiotic prophase is consistent with the hypothesis that in vivo, Nek2 is involved in the G2/M phase transition of the cell cycle. Our results further provide evidence that in vivo, mouse Nek2 is involved in events of meiosis, including but not limited to chromosomal condensation.

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Crosio, Claudia, Gian Maria Fimia, Romain Loury, Masashi Kimura, Yukio Okano, Hongyi Zhou, Subrata Sen, C. David Allis, and Paolo Sassone-Corsi. "Mitotic Phosphorylation of Histone H3: Spatio-Temporal Regulation by Mammalian Aurora Kinases." Molecular and Cellular Biology 22, no. 3 (February 1, 2002): 874–85. http://dx.doi.org/10.1128/mcb.22.3.874-885.2002.

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ABSTRACT Phosphorylation at a highly conserved serine residue (Ser-10) in the histone H3 tail is considered to be a crucial event for the onset of mitosis. This modification appears early in the G2 phase within pericentromeric heterochromatin and spreads in an ordered fashion coincident with mitotic chromosome condensation. Mutation of Ser-10 is essential in Tetrahymena, since it results in abnormal chromosome segregation and extensive chromosome loss during mitosis and meiosis, establishing a strong link between signaling and chromosome dynamics. Although mitotic H3 phosphorylation has been long recognized, the transduction routes and the identity of the protein kinases involved have been elusive. Here we show that the expression of Aurora-A and Aurora-B, two kinases of the Aurora/AIK family, is tightly coordinated with H3 phosphorylation during the G2/M transition. During the G2 phase, the Aurora-A kinase is coexpressed while the Aurora-B kinase colocalizes with phosphorylated histone H3. At prophase and metaphase, Aurora-A is highly localized in the centrosomic region and in the spindle poles while Aurora-B is present in the centromeric region concurrent with H3 phosphorylation, to then translocate by cytokinesis to the midbody region. Both Aurora-A and Aurora-B proteins physically interact with the H3 tail and efficiently phosphorylate Ser10 both in vitro and in vivo, even if Aurora-A appears to be a better H3 kinase than Aurora-B. Since Aurora-A and Aurora-B are known to be overexpressed in a variety of human cancers, our findings provide an attractive link between cell transformation, chromatin modifications and a specific kinase system.

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Pierce, Michael, Kirsten R. Benjamin, Sherwin P. Montano, Millie M. Georgiadis, Edward Winter, and Andrew K. Vershon. "Sum1 and Ndt80 Proteins Compete for Binding to Middle Sporulation Element Sequences That Control Meiotic Gene Expression." Molecular and Cellular Biology 23, no. 14 (July 15, 2003): 4814–25. http://dx.doi.org/10.1128/mcb.23.14.4814-4825.2003.

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ABSTRACT A key transition in meiosis is the exit from prophase and entry into the nuclear divisions, which in the yeast Saccharomyces cerevisiae depends upon induction of the middle sporulation genes. Ndt80 is the primary transcriptional activator of the middle sporulation genes and binds to a DNA sequence element termed the middle sporulation element (MSE). Sum1 is a transcriptional repressor that binds to MSEs and represses middle sporulation genes during mitosis and early sporulation. We demonstrate that Sum1 and Ndt80 have overlapping yet distinct sequence requirements for binding to and acting at variant MSEs. Whole-genome expression analysis identified a subset of middle sporulation genes that was derepressed in a sum1 mutant. A comparison of the MSEs in the Sum1-repressible promoters and MSEs from other middle sporulation genes revealed that there are distinct classes of MSEs. We show that Sum1 and Ndt80 compete for binding to MSEs and that small changes in the sequence of an MSE can yield large differences in which protein is bound. Our results provide a mechanism for differentially regulating the expression of middle sporulation genes through the competition between the Sum1 repressor and the Ndt80 activator.

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LIN, Fei, Shi-Bing CAO, Xue-Shan MA, and Hai-Xiang SUN. "Inhibition of casein kinase 2 blocks G₂/M transition in early embryo mitosis but not in oocyte meiosis in mouse." Journal of Reproduction and Development 63, no. 3 (2017): 319–24. http://dx.doi.org/10.1262/jrd.2016-064.

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Tatemoto, Hideki, and Norio Muto. "Mitogen-activated protein kinase regulates normal transition from metaphase to interphase following parthenogenetic activation in porcine oocytes." Zygote 9, no. 1 (February 2001): 15–23. http://dx.doi.org/10.1017/s0967199401001034.

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The decrease in maturation-promoting factor (MPF) activity precedes that in mitogen-activated protein kinase (MAPK) activity after egg activation, but the cellular functions of this delayed inactivation of MAPK are still unclear. The present study was conducted to examine the essential role of MAPK activity for supporting the transition from metaphase to interphase in porcine oocytes matured in vitro. The increases in the phosphorylated forms of MAPK and the activities of MAPK and histone H1 kinase (H1K) were shown in oocytes arrested at the metaphase II (MII) stage. After additional incubation of MII-arrested oocytes in medium with added U0126, a specific inhibitor of MAPK kinase, 24% of oocytes completed the second meiotic division and underwent entry into interphase with pronucleus (PN) formation, but not second polar body (PB-2) emission. The intensities of the phosphorylated forms of MAPK and the activities of MAPK and H1K in matured oocytes treated with U0126 were significantly decreased by the treatment with U0126. Electrostimulation to induce artificial activation caused both H1K and MAPK inactivation; the inactivation of H1K preceded the inactivation of MAPK and sustained high levels of MAPK activity were detected during the period of PB-2 emission. However, the time sequence required for MAPK inactivation was significantly reduced by the addition of U0126 to the culture medium following electrostimulation, resulting in the dramatic inactivation of MAPK distinct from that of H1K. In these oocytes, PB-2 emission was markedly inhibited but little difference was found in the time course of PN formation compared with oocytes not treated with U0126. These findings suggest that the decrease in MAPK activity is partly involved in driving matured oocytes out of metaphase to induce PN development, and that the delayed MAPK inactivation after the onset of MPF inactivation in activated oocytes has a crucial role for PB-2 emission to accomplish the transition from meiosis to mitosis.

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Pintard, Lionel, Thimo Kurz, Sarah Glaser, John H. Willis, Matthias Peter, and Bruce Bowerman. "Neddylation and Deneddylation of CUL-3 Is Required to Target MEI-1/Katanin for Degradation at the Meiosis-to-Mitosis Transition in C. elegans." Current Biology 13, no. 11 (May 2003): 911–21. http://dx.doi.org/10.1016/s0960-9822(03)00336-1.

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Yang, Wenjing, Hailong Yan, Ke Wang, Yang Cui, Tong Zhou, Han Xu, Haijing Zhu, et al. "Goat PDGFRB : unique mRNA expression profile in gonad and significant association between genetic variation and litter size." Royal Society Open Science 6, no. 1 (January 2019): 180805. http://dx.doi.org/10.1098/rsos.180805.

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β-Type platelet-derived growth factor receptor ( PDGFRB ) is a typical tyrosine kinase, as a candidate gene associated with reproduction. Its main roles include regulation of gonocytes (migration and proliferation) and of the cell cycle. The objectives of this study were to identify mRNA expression of the goat PDGFRB gene, as well as insertion/deletion (indel) variants and their association with litter size in 1122 healthy Shaanbei white cashmere goats. The results revealed that PDGFRB was widely expressed in all tested tissues, and the expression levels in testes at different developmental stages indicated a potential association with the mitosis-to-meiosis transition. Furthermore, the expression of PDGFRB was relatively higher in the ovary tissue of mothers of two lambs compared with mothers of single lamb. These results implied that PDGFRB was related to goat fertility. Meanwhile, two intronic indels, 5 bp ( n = 501) and 10 bp ( n = 1122), were identified. Statistical analysis revealed that only the 10 bp indel was associated with first-born litter size ( n = 1122, p = 6.030 × 10 −5 ), and that individuals of the genotype insertion/deletion had larger litter sizes than those of genotype insertion/insertion. Overall, these results indicated that the 10 bp indel of PDGFRB could be used in marker-assisted selection during goat genetic breeding.

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Journal articles on the topic 'Mitosis/meiosis transition'

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