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Journal articles on the topic 'Meiosis; Meiotic'
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1
Hasenkampf, C. A., A. A. Taylor, N. U. Siddiqui, and C. D. Riggs. "meiotin-1 gene expression in normal anthers and in anthers exhibiting prematurely condensed chromosomes." Genome 43, no. 4 (August 1, 2000): 604–12. http://dx.doi.org/10.1139/g00-021.
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We have cloned and sequenced the promoter of a meiotin-1 gene, and have determined the precise temporal and spatial pattern of meiotin-1 gene expression. The expression of the meiotin-1 gene is controlled in two increments. The meiotin-1 gene is not expressed in any of the vegetative tissues examined. Early in microsporogenesis, low levels of meiotin-1 RNA can be detected. At the onset of meiosis, there is a dramatic increase in meiotin-1 RNA levels in both tapetal and meiotic cells. However, while meiotin-1 RNA is observed in both the nucleus and cytoplasm of meiotic cells, it is found only in the nucleus of the tapetal cells. We have also examined the expression of the meiotin-1 gene in aberrant meiotic nuclei that prematurely condense their chromosomes; these nuclei have reduced levels of the meiotin-1 protein. The aberrant nuclei have only the basal level of meiotin-1 RNA; they do not exhibit the transcriptional induction seen for normal cells at the onset of meiosis. Implications for the function of meiotin-1 in regulating chromatin condensation, and in coordinating meiotic and tapetal cell activities are discussed.Key words: anther development, chromatin, meiosis, meiotin-1, promoter.
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Goldway, M., A. Sherman, D. Zenvirth, T. Arbel, and G. Simchen. "A short chromosomal region with major roles in yeast chromosome III meiotic disjunction, recombination and double strand breaks." Genetics 133, no. 2 (February 1, 1993): 159–69. http://dx.doi.org/10.1093/genetics/133.2.159.
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Abstract A multicopy plasmid was isolated from a yeast genomic library, whose presence resulted in a twofold increase in meiotic nondisjunction of chromosome III. The plasmid contains a 7.5-kb insert from the middle of the right arm of chromosome III, including the gene THR4. Using chromosomal fragments derived from chromosome III, we determined that the cloned region caused a significant, specific, cis-acting increase in chromosome III nondisjunction in the first meiotic division. The plasmid containing this segment exhibited high spontaneous meiotic integration into chromosome III (in 2.4% of the normal meiotic divisions) and a sixfold increase (15.5%) in integration in nondisjunctant meioses. Genetic analysis of the cloned region revealed that it contains a "hot spot" for meiotic recombination. In DNA of rad50S mutant cells, a strong meiosis-induced double strand break (DSB) signal was detected in this region. We discuss the possible relationships between meiosis-induced DSBs, recombination and chromosome disjunction, and propose that recombinational hot spots may be "pairing sites" for homologous chromosomes in meiosis.
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Tsuchiya, Dai, Claire Gonzalez, and Soni Lacefield. "The spindle checkpoint protein Mad2 regulates APC/C activity during prometaphase and metaphase of meiosis I in Saccharomyces cerevisiae." Molecular Biology of the Cell 22, no. 16 (August 15, 2011): 2848–61. http://dx.doi.org/10.1091/mbc.e11-04-0378.
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In many eukaryotes, disruption of the spindle checkpoint protein Mad2 results in an increase in meiosis I nondisjunction, suggesting that Mad2 has a conserved role in ensuring faithful chromosome segregation in meiosis. To characterize the meiotic function of Mad2, we analyzed individual budding yeast cells undergoing meiosis. We find that Mad2 sets the duration of meiosis I by regulating the activity of APCCdc20. In the absence of Mad2, most cells undergo both meiotic divisions, but securin, a substrate of the APC/C, is degraded prematurely, and prometaphase I/metaphase I is accelerated. Some mad2Δ cells have a misregulation of meiotic cell cycle events and undergo a single aberrant division in which sister chromatids separate. In these cells, both APCCdc20 and APCAma1 are prematurely active, and meiosis I and meiosis II events occur in a single meiotic division. We show that Mad2 indirectly regulates APCAma1 activity by decreasing APCCdc20 activity. We propose that Mad2 is an important meiotic cell cycle regulator that ensures the timely degradation of APC/C substrates and the proper orchestration of the meiotic divisions.
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Cooper, Katrina F., and Randy Strich. "Saccharomyces cerevisiae C-Type Cyclin Ume3p/Srb11p Is Required for Efficient Induction and Execution of Meiotic Development." Eukaryotic Cell 1, no. 1 (February 2002): 66–74. http://dx.doi.org/10.1128/ec.01.1.66-74.2002.
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ABSTRACT The yeast C-type cyclin Ume3p/Srb11p and its cyclin-dependent kinase partner Ume5p/Srb10p repress the transcription of several genes required for meiotic recombination or meiosis I nuclear division. To relieve this repression, Srb11p is destroyed early in meiosis, prior to the first meiotic division. This report identifies two roles for Srb11p in regulating meiotic development. First, SRB11 is required for the normal exit from the mitotic cell cycle prior to meiotic induction. Specifically, mutants lacking SRB11 (srb11Δ) uncouple bud growth from chromosome segregation, producing small buds with nuclei. The bud growth defect is most likely due to the failure of srb11Δ mutants to reestablish polarized actin fibers at the bud tip following exposure to sporulation medium. Second, Srb11p is required for the efficient execution of meiosis I. srb11Δ mutants either exhibited a delay in performing meiosis I and meiosis II or skipped meiosis I entirely. This meiotic defect is not due to the activation of the recombination or spindle assembly checkpoint pathways. However, the expression of several meiotic genes is delayed and reduced in the mutant strains. These results suggest a positive role for Srb10-Srb11p in regulating the transcription program. This model is supported by the finding that overexpression of the meiotic inducer IME2 partially restored the ability of srb11 mutants to perform meiosis I. In conclusion, these findings indicate that Srb11p is required for both entry into and execution of the meiotic program, thus describing multiple roles for a C-type cyclin in the regulation of a developmental pathway.
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Page, A. W., and T. L. Orr-Weaver. "The Drosophila genes grauzone and cortex are necessary for proper female meiosis." Journal of Cell Science 109, no. 7 (July 1, 1996): 1707–15. http://dx.doi.org/10.1242/jcs.109.7.1707.
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In Drosophila, normal female meiosis arrests at metaphase I. After meiotic arrest is released by egg activation, the two meiotic divisions are rapidly completed, even in unfertilized eggs. Since little is known about the regulation of the meiotic cell cycle after the meiotic arrest, we screened for mutants that arrest in meiosis. Here we describe the phenotype of eggs laid by sterile mothers mutant for either grauzone or cortex. These eggs arrest in metaphase of meiosis II, and although they can enter into an aberrant anaphase II, they never exit meiosis. Prolonged sister-chromatid cohesion is not the cause of this arrest, since a premature release of sister cohesion does not rescue the meiotic arrest of cortex eggs. Aberrant chromosome segregation at meiosis I was the earliest observable defect, suggesting that grauzone and cortex are first required immediately after egg activation. The cortical microtubules are also defective, remaining in a pre-activated state in activated mutant eggs. The mutations had no observable effect on either male meiosis or mitosis. We believe these genes will provide insight into the developmental regulation of meiosis in a genetically tractable organism.
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Nelms, Brad, and Virginia Walbot. "Defining the developmental program leading to meiosis in maize." Science 364, no. 6435 (April 4, 2019): 52–56. http://dx.doi.org/10.1126/science.aav6428.
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In multicellular organisms, the entry into meiosis is a complex process characterized by increasing meiotic specialization. Using single-cell RNA sequencing, we reconstructed the developmental program into maize male meiosis. A smooth continuum of expression stages before meiosis was followed by a two-step transcriptome reorganization in leptotene, during which 26.7% of transcripts changed in abundance by twofold or more. Analysis of cell-cycle gene expression indicated that nearly all pregerminal cells proliferate, eliminating a stem-cell model to generate meiotic cells. Mutants defective in somatic differentiation or meiotic commitment expressed transcripts normally present in early meiosis after a delay; thus, the germinal transcriptional program is cell autonomous and can proceed despite meiotic failure.
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Nag, D. K., M. P. Koonce, and J. Axelrod. "SSP1, a gene necessary for proper completion of meiotic divisions and spore formation in Saccharomyces cerevisiae." Molecular and Cellular Biology 17, no. 12 (December 1997): 7029–39. http://dx.doi.org/10.1128/mcb.17.12.7029.
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During meiosis, a diploid cell undergoes two rounds of nuclear division following one round of DNA replication to produce four haploid gametes. In yeast, haploid meiotic products are packaged into spores. To gain new insights into meiotic development and spore formation, we followed differential expression of genes in meiotic versus vegetatively growing cells in the yeast Saccharomyces cerevisiae. Our results indicate that there are at least five different classes of transcripts representing genes expressed at different stages of the sporulation program. Here we describe one of these differentially expressed genes, SSP1, which plays an essential role in meiosis and spore formation. SSP1 is expressed midway through meiosis, and homozygous ssp1 diploid cells fail to sporulate. In the ssp1 mutant, meiotic recombination is normal but viability declines rapidly. Both meiotic divisions occur at the normal time; however, the fraction of cells completing meiosis is significantly reduced, and nuclei become fragmented soon after meiosis II. The ssp1 defect does not appear to be related to a microtubule-cytoskeletal-dependent event and is independent of two rounds of chromosome segregation. The data suggest that Ssp1 is likely to function in a pathway that controls meiotic nuclear divisions and coordinates meiosis and spore formation.
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Li, Qianyan, Sara Hariri, and JoAnne Engebrecht. "Meiotic Double-Strand Break Processing and Crossover Patterning Are Regulated in a Sex-Specific Manner by BRCA1–BARD1 in Caenorhabditis elegans." Genetics 216, no. 2 (August 12, 2020): 359–79. http://dx.doi.org/10.1534/genetics.120.303292.
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Meiosis is regulated in a sex-specific manner to produce two distinct gametes, sperm and oocytes, for sexual reproduction. To determine how meiotic recombination is regulated in spermatogenesis, we analyzed the meiotic phenotypes of mutants in the tumor suppressor E3 ubiquitin ligase BRC-1-BRD-1 complex in Caenorhabditis elegans male meiosis. Unlike in mammals, this complex is not required for meiotic sex chromosome inactivation, the process whereby hemizygous sex chromosomes are transcriptionally silenced. Interestingly, brc-1 and brd-1 mutants show meiotic recombination phenotypes that are largely opposing to those previously reported for female meiosis. Fewer meiotic recombination intermediates marked by the recombinase RAD-51 were observed in brc-1 and brd-1 mutants, and the reduction in RAD-51 foci could be suppressed by mutation of nonhomologous-end-joining proteins. Analysis of GFP::RPA-1 revealed fewer foci in the brc-1brd-1 mutant and concentration of BRC-1-BRD-1 to sites of meiotic recombination was dependent on DNA end resection, suggesting that the complex regulates the processing of meiotic double-strand breaks to promote repair by homologous recombination. Further, BRC-1-BRD-1 is important to promote progeny viability when male meiosis is perturbed by mutations that block the pairing and synapsis of different chromosome pairs, although the complex is not required to stabilize the RAD-51 filament as in female meiosis under the same conditions. Analyses of crossover designation and formation revealed that BRC-1-BRD-1 inhibits supernumerary COs when meiosis is perturbed. Together, our findings suggest that BRC-1-BRD-1 regulates different aspects of meiotic recombination in male and female meiosis.
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Loidl, Josef. "Tetrahymena meiosis: Simple yet ingenious." PLOS Genetics 17, no. 7 (July 15, 2021): e1009627. http://dx.doi.org/10.1371/journal.pgen.1009627.
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The presence of meiosis, which is a conserved component of sexual reproduction, across organisms from all eukaryotic kingdoms, strongly argues that sex is a primordial feature of eukaryotes. However, extant meiotic structures and processes can vary considerably between organisms. The ciliated protist Tetrahymena thermophila, which diverged from animals, plants, and fungi early in evolution, provides one example of a rather unconventional meiosis. Tetrahymena has a simpler meiosis compared with most other organisms: It lacks both a synaptonemal complex (SC) and specialized meiotic machinery for chromosome cohesion and has a reduced capacity to regulate meiotic recombination. Despite this, it also features several unique mechanisms, including elongation of the nucleus to twice the cell length to promote homologous pairing and prevent recombination between sister chromatids. Comparison of the meiotic programs of Tetrahymena and higher multicellular organisms may reveal how extant meiosis evolved from proto-meiosis.
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Mukherjee, Kaustav, Bruce Futcher, and Janet Leatherwood. "mmi1 and rep2 mRNAs are novel RNA targets of the Mei2 RNA-binding protein during early meiosis in Schizosaccharomyces pombe." Open Biology 8, no. 9 (September 2018): 180110. http://dx.doi.org/10.1098/rsob.180110.
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The RNA-binding protein Mei2 is crucial for meiosis in Schizosaccharomyces pombe. In mei2 mutants, pre-meiotic S-phase is blocked, along with meiosis. Mei2 binds a long non-coding RNA (lncRNA) called meiRNA, which is a ‘sponge RNA’ for the meiotic inhibitor protein Mmi1. The interaction between Mei2, meiRNA and Mmi1 protein is essential for meiosis. But mei2 mutants have stronger and different phenotypes than meiRNA mutants, since mei2Δ arrests before pre-meiotic S, while the meiRNA mutant arrests after pre-meiotic S but before meiosis. This suggests Mei2 may bind additional RNAs. To identify novel RNA targets of Mei2, which might explain how Mei2 regulates pre-meiotic S, we used RNA immunoprecipitation and cross-linking immunoprecipitation. In addition to meiRNA, we found the mRNAs for mmi1 (which encodes Mmi1) and for the S-phase transcription factor rep2 . There were also three other RNAs of uncertain relevance. We suggest that at meiotic initiation, Mei2 may sequester rep2 mRNA to help allow pre-meiotic S, and then may bind both meiRNA and mmi1 mRNA to inactivate Mmi1 at two levels, the protein level (as previously known), and also the mRNA level, allowing meiosis. We call Mei2–meiRNA a ‘double sponge’ (i.e. binding both an mRNA and its encoded protein).
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Giroux, Craig N., Michael E. Dresser, and Howard F. Tiano. "Genetic control of chromosome synapsis in yeast meiosis." Genome 31, no. 1 (January 1, 1989): 88–94. http://dx.doi.org/10.1139/g89-017.
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Both meiosis-specific and general recombination functions, recruited from the mitotic cell cycle, are required for elevated levels of recombination and for chromosome synapsis (assembly of the synaptonemal complex) during yeast meiosis. The meiosis-specific SPO11 gene (previously shown to be required for meiotic recombination) has been isolated and shown to be essential for synaptonemal complex formation but not for DNA metabolism during the vegetative cell cycle. In contrast, the RAD52 gene is required for mitotic and meiotic recombination but not for synaptonemal complex assembly. These data suggest that the synaptonemal complex may be necessary but is clearly not sufficient for meiotic recombination. Cytological analysis of spread meiotic nuclei demonstrates that chromosome behavior in yeast is comparable with that observed in larger eukaryotes. These spread preparations support the immunocytological localization of specific proteins in meiotic nuclei. This combination of genetic, molecular cloning, and cytological approaches in a single experimental system provides a means of addressing the role of specific gene products and nuclear structures in meiotic chromosome behavior.Key words: synaptonemal complex, chromosome behavior, meiosis.
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Yang, Hui-Ju, Haruhiko Asakawa, Tokuko Haraguchi, and Yasushi Hiraoka. "Nup132 modulates meiotic spindle attachment in fission yeast by regulating kinetochore assembly." Journal of Cell Biology 211, no. 2 (October 19, 2015): 295–308. http://dx.doi.org/10.1083/jcb.201501035.
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During meiosis, the kinetochore undergoes substantial reorganization to establish monopolar spindle attachment. In the fission yeast Schizosaccharomyces pombe, the KNL1–Spc7-Mis12-Nuf2 (KMN) complex, which constitutes the outer kinetochore, is disassembled during meiotic prophase and is reassembled before meiosis I. Here, we show that the nucleoporin Nup132 is required for timely assembly of the KMN proteins: In the absence of Nup132, Mis12 and Spc7 are precociously assembled at the centromeres during meiotic prophase. In contrast, Nuf2 shows timely dissociation and reappearance at the meiotic centromeres. We further demonstrate that depletion of Nup132 activates the spindle assembly checkpoint in meiosis I, possibly because of the increased incidence of erroneous spindle attachment at sister chromatids. These results suggest that precocious assembly of the kinetochores leads to the meiosis I defects observed in the nup132-disrupted mutant. Thus, we propose that Nup132 plays an important role in establishing monopolar spindle attachment at meiosis I through outer kinetochore reorganization at meiotic prophase.
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Hanna, Carol, Suzanne Menges, Duane Kraemer, and Charles R. Long. "Synchronisation of canine germinal vesicle stage oocytes prior to in vitro maturation alters the kinetics of nuclear progression during subsequent resumption of meiosis." Reproduction, Fertility and Development 20, no. 5 (2008): 606. http://dx.doi.org/10.1071/rd07227.
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Inhibition of meiosis before in vitro maturation (IVM) can improve meiotic competence in immature mammalian oocytes. Therefore, meiosis-inhibiting agents were evaluated singularly for the ability to arrest and synchronise germinal vesicle (GV) stage canine oocytes, and the most effective treatments were combined to improve meiotic resumption rates. Oocytes cultured in 2 ng mL–1 oestradiol (E2), 10 IU mL–1 eCG, or both (EG) for 72 h resulted in significantly fewer oocytes resuming meiosis in EG than the control, E2, or with eCG. Oocytes cultured in 50 or 100 μmol L–1 of butyrolactone 1 or roscovitine (ROS) for up to 48 h did not resume meiosis nor increase subsequent meiotic resumption rates following IVM. A combination of 50 μmol L–1 ROS and EG treatment for 48 h significantly increased the proportion of canine oocytes in meiotic arrest. More importantly, following 48 h of IVM, ROS+EG-treated oocytes demonstrated a dramatic increase in the ability to resume meiosis compared with the non-treated controls (51.3 ± 8.2% and 10.8 ± 4.5%, respectively; P < 0.05). These data indicate that chemical and biological meiotic inhibitors are effective at inducing GV arrest in canine oocytes. Furthermore, these inhibitors are reversible and beneficial to subsequent meiotic resumption in vitro.
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Kohl, Kathryn P., and Jeff Sekelsky. "Meiotic and Mitotic Recombination in Meiosis." Genetics 194, no. 2 (June 2013): 327–34. http://dx.doi.org/10.1534/genetics.113.150581.
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Byers, Breck, and Nancy M. Hollingsworth. "Meiosis: DNA branching during meiotic recombination." Current Biology 4, no. 5 (May 1994): 448–51. http://dx.doi.org/10.1016/s0960-9822(00)00100-7.
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Dudley, Keith. "Meiotic Inhibition - Molecular Control of Meiosis." FEBS Letters 253, no. 1-2 (August 14, 1989): 293–94. http://dx.doi.org/10.1016/0014-5793(89)80984-6.
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Malapeira, Jordi, Alberto Moldón, Elena Hidalgo, Gerald R. Smith, Paul Nurse, and José Ayté. "A Meiosis-Specific Cyclin Regulated by Splicing Is Required for Proper Progression through Meiosis." Molecular and Cellular Biology 25, no. 15 (August 1, 2005): 6330–37. http://dx.doi.org/10.1128/mcb.25.15.6330-6337.2005.
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ABSTRACT The meiotic cell cycle is modified from the mitotic cell cycle by having a premeiotic S phase which leads to high levels of recombination, a reductional pattern of chromosome segregation at the first division, and a second division with no intervening DNA synthesis. Cyclin-dependent kinases are essential for progression through the meiotic cell cycle, as for the mitotic cycle. Here we show that a fission yeast cyclin, Rem1, is present only during meiosis. Cells lacking Rem1 have impaired meiotic recombination, and Rem1 is required for premeiotic DNA synthesis when Cig2 is not present. rem1 expression is regulated at the level of both transcription and splicing, with Mei4 as a positive and Cig2 a negative factor of rem1 splicing. This regulation ensures the timely appearance of the different cyclins during meiosis, which is required for the proper progression through the meiotic cell cycle. We propose that the meiosis-specific B-type cyclin Rem1 has a central role in bringing about progression through meiosis.
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Scherthan, H., J. Bähler, and J. Kohli. "Dynamics of chromosome organization and pairing during meiotic prophase in fission yeast." Journal of Cell Biology 127, no. 2 (October 15, 1994): 273–85. http://dx.doi.org/10.1083/jcb.127.2.273.
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Interactions between homologous chromosomes (pairing, recombination) are of central importance for meiosis. We studied entire chromosomes and defined chromosomal subregions in synchronous meiotic cultures of Schizosaccharomyces pombe by fluorescence in situ hybridization. Probes of different complexity were applied to spread nuclei, to delineate whole chromosomes, to visualize repeated sequences of centromeres, telomeres, and ribosomal DNA, and to study unique sequences of different chromosomal regions. In diploid nuclei, homologous chromosomes share a joint territory even before entry into meiosis. The centromeres of all chromosomes are clustered in vegetative and meiotic prophase cells, whereas the telomeres cluster near the nucleolus early in meiosis and maintain this configuration throughout meiotic prophase. Telomeres and centromeres appear to play crucial roles for chromosome organization and pairing, both in vegetative cells and during meiosis. Homologous pairing of unique sequences shows regional differences and is most frequent near centromeres and telomeres. Multiple homologous interactions are formed independently of each other. Pairing increases during meiosis, but not all chromosomal regions become closely paired in every meiosis. There is no detectable axial compaction of chromosomes in meiotic prophase. S. pombe does not form mature synaptonemal complexes, but axial element-like structures (linear elements), which were analyzed in parallel. Their appearance coincides with pairing of interstitial chromosomal regions. Axial elements may define minimal structures required for efficient pairing and recombination of meiotic chromosomes.
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Cartagena-Lirola, Hugo, Ilaria Guerini, Nicola Manfrini, Giovanna Lucchini, and Maria Pia Longhese. "Role of the Saccharomyces cerevisiae Rad53 Checkpoint Kinase in Signaling Double-Strand Breaks during the Meiotic Cell Cycle." Molecular and Cellular Biology 28, no. 14 (May 27, 2008): 4480–93. http://dx.doi.org/10.1128/mcb.00375-08.
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ABSTRACT DNA double-strand breaks (DSBs) can arise at unpredictable locations after DNA damage or in a programmed manner during meiosis. DNA damage checkpoint response to accidental DSBs during mitosis requires the Rad53 effector kinase, whereas the meiosis-specific Mek1 kinase, together with Red1 and Hop1, mediates the recombination checkpoint in response to programmed meiotic DSBs. Here we provide evidence that exogenous DSBs lead to Rad53 phosphorylation during the meiotic cell cycle, whereas programmed meiotic DSBs do not. However, the latter can trigger phosphorylation of a protein fusion between Rad53 and the Mec1-interacting protein Ddc2, suggesting that the inability of Rad53 to transduce the meiosis-specific DSB signals might be due to its failure to access the meiotic recombination sites. Rad53 phosphorylation/activation is elicited when unrepaired meiosis-specific DSBs escape the recombination checkpoint. This activation requires homologous chromosome segregation and delays the second meiotic division. Altogether, these data indicate that Rad53 prevents sister chromatid segregation in the presence of unrepaired programmed meiotic DSBs, thus providing a salvage mechanism ensuring genetic integrity in the gametes even in the absence of the recombination checkpoint.
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Ohta, Midori, Masamitsu Sato, and Masayuki Yamamoto. "Spindle pole body components are reorganized during fission yeast meiosis." Molecular Biology of the Cell 23, no. 10 (May 15, 2012): 1799–811. http://dx.doi.org/10.1091/mbc.e11-11-0951.
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During meiosis, the centrosome/spindle pole body (SPB) must be regulated in a manner distinct from that of mitosis to achieve a specialized cell division that will produce gametes. In this paper, we demonstrate that several SPB components are localized to SPBs in a meiosis-specific manner in the fission yeast Schizosaccharomyces pombe. SPB components, such as Cut12, Pcp1, and Spo15, which stay on the SPB during the mitotic cell cycle, disassociate from the SPB during meiotic prophase and then return to the SPB immediately before the onset of meiosis I. Interestingly, the polo kinase Plo1, which normally localizes to the SPB during mitosis, is excluded from them in meiotic prophase, when meiosis-specific, horse-tail nuclear movement occurs. We found that exclusion of Plo1 during this period was essential to properly remodel SPBs, because artificial targeting of Plo1 to SPBs resulted in an overduplication of SPBs. We also found that the centrin Cdc31 was required for meiotic SPB remodeling. Thus Plo1 and a centrin play central roles in the meiotic SPB remodeling, which is essential for generating the proper number of meiotic SPBs and, thereby provide unique characteristics to meiotic divisions.
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Thompson, Dawn A., and Franklin W. Stahl. "Genetic Control of Recombination Partner Preference in Yeast Meiosis: Isolation and Characterization of Mutants Elevated for Meiotic Unequal Sister-Chromatid Recombination." Genetics 153, no. 2 (October 1, 1999): 621–41. http://dx.doi.org/10.1093/genetics/153.2.621.
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Abstract Meiotic exchange occurs preferentially between homologous chromatids, in contrast to mitotic recombination, which occurs primarily between sister chromatids. To identify functions that direct meiotic recombination events to homologues, we screened for mutants exhibiting an increase in meiotic unequal sister-chromatid recombination (SCR). The msc (meiotic sister-chromatid recombination) mutants were quantified in spo13 meiosis with respect to meiotic unequal SCR frequency, disome segregation pattern, sporulation frequency, and spore viability. Analysis of the msc mutants according to these criteria defines three classes. Mutants with a class I phenotype identified new alleles of the meiosis-specific genes RED1 and MEK1, the DNA damage checkpoint genes RAD24 and MEC3, and a previously unknown gene, MSC6. The genes RED1, MEK1, RAD24, RAD17, and MEC1 are required for meiotic prophase arrest induced by a dmc1 mutation, which defines a meiotic recombination checkpoint. Meiotic unequal SCR was also elevated in a rad17 mutant. Our observation that meiotic unequal SCR is elevated in meiotic recombination checkpoint mutants suggests that, in addition to their proposed monitoring function, these checkpoint genes function to direct meiotic recombination events to homologues. The mutants in class II, including a dmc1 mutant, confer a dominant meiotic lethal phenotype in diploid SPO13 meiosis in our strain background, and they identify alleles of UBR1, INP52, BUD3, PET122, ELA1, and MSC1-MSC3. These results suggest that DMC1 functions to bias the repair of meiosis-specific double-strand breaks to homologues. We hypothesize that the genes identified by the class II mutants function in or are regulators of the DMC1-promoted interhomologue recombination pathway. Class III mutants may be elevated for rates of both SCR and homologue exchange.
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Lee, R. H., and S. M. Honigberg. "Nutritional regulation of late meiotic events in Saccharomyces cerevisiae through a pathway distinct from initiation." Molecular and Cellular Biology 16, no. 6 (June 1996): 3222–32. http://dx.doi.org/10.1128/mcb.16.6.3222.
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The IME1 gene is essential for initiation of meiosis in the yeast Saccharomyces cerevisiae, although it is not required for growth. Here we report that in stationary-phase cultures containing low concentration of glucose, cells overexpressing IME1 undergo the early meiotic events, including DNA replication, commitment to recombination, and synaptonemal complex formation and dissolution. In contrast, later meiotic events, such as chromosome segregation, commitment to meiosis, and spore formation, do not occur. Thus, nutrients can repress the late stages of meiosis independently of their block of initiation. Cells arrested at this midpoint in meiosis are relatively stable and can resume meiotic differentiation if transferred to sporulation conditions. Resumption of meiosis does not require repression of IME1 expression, since IME1 RNA levels stay high after transfer of the arrested cells to sporulation medium. These results suggest that meiosis in S. cerevisiae is a paradigm of a differentiation pathway regulated by signal transduction at both early and late stages.
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Borgne, Annie, Hiroshi Murakami, José Ayté, and Paul Nurse. "The G1/S Cyclin Cig2p during Meiosis in Fission Yeast." Molecular Biology of the Cell 13, no. 6 (June 2002): 2080–90. http://dx.doi.org/10.1091/mbc.01-10-0507.
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Cyclin-dependent kinases (CDKs) are important for both mitotic and meiotic cell cycles. In fission yeast, the major CDK, Cdc2p is involved in premeiotic DNA replication and in meiosis II. One of its partners, the mitotic cyclin Cdc13p is known to be required for meiosis, whereas there are no studies on the G1/S cyclin Cig2p. In this article, we have studied the regulation of the Cdc2p/Cdc13p and Cdc2p/Cig2p complexes during synchronous meiosis. We observed that Cdc2p/Cig2p kinase is activated in an unexpected biphasic manner, first at onset of premeiotic S phase and again during meiotic nuclear divisions. The role of Cig2p during meiosis was investigated usingcig2-deleted strains that exhibit delays in onset of both S phase and meiotic divisions as well as an inefficient completion of MII. Furthermore, analysis of cig2 transcripts revealed a meiosis-specific regulation of cig2expression during MI/MII dependent upon the Mei4p transcription factor leading to a different transcription start site at this stage of meiosis.
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Catlett, Michael G., and Susan L. Forsburg. "Schizosaccharomyces pombeRdh54 (TID1) Acts with Rhp54 (RAD54) to Repair Meiotic Double-Strand Breaks." Molecular Biology of the Cell 14, no. 11 (November 2003): 4707–20. http://dx.doi.org/10.1091/mbc.e03-05-0288.
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We report the characterization of rdh54+, the second fission yeast Schizosaccharomyces pombe Rad54 homolog. rdh54+shares sequence and functional homology to budding yeast RDH54/TID1. Rdh54p is present during meiosis with appropriate timing for a meiotic recombination factor. It interacts with Rhp51 and the meiotic Rhp51 homolog Dmc1 in yeast two-hybrid assays. Deletion of rdh54+has no effect on DNA damage repair during the haploid vegetative cell cycle. In meiosis, however, rdh54Δ shows decreased spore viability and homologous recombination with a concomitant increase in sister chromatid exchange. The rdh54Δ single mutant repairs meiotic breaks with similar timing to wild type, suggesting redundancy of meiotic recombination factors. Consistent with this, the rdh54Δ rhp54Δ double mutant fails to repair meiotic double strand breaks. Live cell analysis shows that rdh54Δ rhp54Δ asci do not arrest, but undergo both meiotic divisions with near normal timing, suggesting that failure to repair double strand breaks in S. pombe meiosis does not result in checkpoint arrest.
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Tian, Hui, Timothy Billings, and Petko M. Petkov. "EWSR1 affects PRDM9-dependent histone 3 methylation and provides a link between recombination hotspots and the chromosome axis protein REC8." Molecular Biology of the Cell 32, no. 1 (January 1, 2021): 1–14. http://dx.doi.org/10.1091/mbc.e20-09-0604.
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EWSR1, a protein whose role in meiosis was not previously clarified in detail, binds to both the recombination regulator PRDM9 and the phosphorylated meiosis-specific cohesin pREC8 in male meiotic cells and is essential for promoting PRDM9-dependent histone methylation and normal meiotic progress.
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Li, Jian, Wei-Ping Qian, and Qing-Yuan Sun. "Cyclins regulating oocyte meiotic cell cycle progression†." Biology of Reproduction 101, no. 5 (July 26, 2019): 878–81. http://dx.doi.org/10.1093/biolre/ioz143.
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Abstract Oocyte meiotic maturation is a vital and final process in oogenesis. Unlike somatic cells， the oocyte needs to undergo two continuous meiotic divisions (meiosis I and meiosis II) to become a haploid gamete. Notably, oocyte meiotic progression includes two rounds of unique meiotic arrest and resumption. The first arrest occurs at the G2 (germinal vesicle) stage and meiosis resumption is stimulated by a gonadotropin surge; the second arrest takes place at the metaphase II stage, the stage from which it is released when fertilization takes place. The maturation-promoting factor, which consists of cyclin B1 (CCNB1) and cyclin-dependent kinase 1 (CDK1), is responsible for regulating meiotic resumption and progression, while CDK1 is the unique CDK that acts as the catalytic subunit of maturation-promoting factor. Recent studies showed that except for cyclin B1, multiple cyclins interact with CDK1 to form complexes, which are involved in the regulation of meiotic progression at different stages. Here, we review and discuss the control of oocyte meiotic progression by cyclins A1, A2, B1, B2, B3, and O.
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Yan, Rihui, Sharon E. Thomas, Jui-He Tsai, Yukihiro Yamada, and Bruce D. McKee. "SOLO: a meiotic protein required for centromere cohesion, coorientation, and SMC1 localization in Drosophila melanogaster." Journal of Cell Biology 188, no. 3 (February 8, 2010): 335–49. http://dx.doi.org/10.1083/jcb.200904040.
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Sister chromatid cohesion is essential to maintain stable connections between homologues and sister chromatids during meiosis and to establish correct centromere orientation patterns on the meiosis I and II spindles. However, the meiotic cohesion apparatus in Drosophila melanogaster remains largely uncharacterized. We describe a novel protein, sisters on the loose (SOLO), which is essential for meiotic cohesion in Drosophila. In solo mutants, sister centromeres separate before prometaphase I, disrupting meiosis I centromere orientation and causing nondisjunction of both homologous and sister chromatids. Centromeric foci of the cohesin protein SMC1 are absent in solo mutants at all meiotic stages. SOLO and SMC1 colocalize to meiotic centromeres from early prophase I until anaphase II in wild-type males, but both proteins disappear prematurely at anaphase I in mutants for mei-S332, which encodes the Drosophila homologue of the cohesin protector protein shugoshin. The solo mutant phenotypes and the localization patterns of SOLO and SMC1 indicate that they function together to maintain sister chromatid cohesion in Drosophila meiosis.
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Diener, Andrew C., and Gerald R. Fink. "DLH1 is a Functional Candida albicans Homologue of the Meiosis-Specific Gene DMC1." Genetics 143, no. 2 (June 1, 1996): 769–76. http://dx.doi.org/10.1093/genetics/143.2.769.
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Abstract DMC1/LIM15 homologue 1 (DLH1), a gene related to meiosis-specific genes, has been isolated from Candida albicans, a fungus thought not to undergo meiosis. The deduced protein sequence of DLH1 contains 74% amino acid identity with Dmclp from Saccharomyces cermisiae and 63% with Liml5p from the plant Lilium long)lmm, meiosisspecific homologues of Escherichia coli RecA. Candida DLH1 complements a dmcl/dmcl null mutant in S. cermisiae: High copy expression of DLH1 restores both sporulation and meiotic recombination to a Saccharomyces dmclΔ/dmclΔ strain. Unlike the DMCl gene, which is transcribed only in meiotic cells, the heterologous Candida DLH1 gene is transcribed in both vegetative and meiotic cells of S. cermisiae. Transcription of DLH1 is not detected or induced in C. albicans under conditions that induce DMC1 and meiosis in S. cermisiae. The presence of an intact homologue of a meiosis-specific gene in C. albicans raises the possibility that this organism has a cryptic meiotic pathway.
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Molnar, Monika, Jürg Bähler, Jürg Kohli, and Yasushi Hiraoka. "Live observation of fission yeast meiosis in recombination-deficient mutants." Journal of Cell Science 114, no. 15 (August 1, 2001): 2843–53. http://dx.doi.org/10.1242/jcs.114.15.2843.
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Regular segregation of homologous chromosomes during meiotic divisions is essential for the generation of viable progeny. In recombination-proficient organisms, chromosome disjunction at meiosis I generally occurs by chiasma formation between the homologs (chiasmate meiosis). We have studied meiotic stages in living rec8 and rec7 mutant cells of fission yeast, with special attention to prophase and the first meiotic division. Both rec8 and rec7 are early recombination mutants, and in rec7 mutants, chromosome segregation at meiosis I occurs without any recombination (achiasmate meiosis). Both mutants showed distinct irregularities in nuclear prophase movements. Additionally, rec7 showed an extended first division of variable length and with single chromosomes changing back and forth between the cell poles. Two other early recombination deficient mutants (rec14 and rec15) showed very similar phenotypes to rec7 during the first meiotic division, and the fidelity of achiasmate chromosome segregation slightly exceeded the expected random level. We discuss possible regulatory mechanisms of fission yeast to deal with achiasmate chromosome segregation.
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Sun, H., D. Dawson, and J. W. Szostak. "Genetic and physical analyses of sister chromatid exchange in yeast meiosis." Molecular and Cellular Biology 11, no. 12 (December 1991): 6328–36. http://dx.doi.org/10.1128/mcb.11.12.6328.
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We have used nonessential circular minichromosomes to monitor sister chromatid exchange during yeast meiosis. Genetic analysis shows that a 64-kb circular minichromosome undergoes sister chromatid exchange during 40% of meioses. This frequency is not reduced by the presence of a homologous linear minichromosome. Furthermore, sister chromatid exchange can be stimulated by the presence of a 12-kb ARG4 DNA fragment, which contains initiation sites for meiotic gene conversion. Using physical analysis, we have directly identified a product of sister chromatid exchange: a head-to-tail dimer form of a circular minichromosome. This dimer form is absent in a rad50S mutant strain, which is deficient in processing of the ends of meiosis-specific double-stranded breaks into single-stranded DNA tails. Our studies suggest that meiotic sister chromatid exchange is stimulated by the same mechanism as meiotic homolog exchange.
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Sun, H., D. Dawson, and J. W. Szostak. "Genetic and physical analyses of sister chromatid exchange in yeast meiosis." Molecular and Cellular Biology 11, no. 12 (December 1991): 6328–36. http://dx.doi.org/10.1128/mcb.11.12.6328-6336.1991.
Full textAbstract:
We have used nonessential circular minichromosomes to monitor sister chromatid exchange during yeast meiosis. Genetic analysis shows that a 64-kb circular minichromosome undergoes sister chromatid exchange during 40% of meioses. This frequency is not reduced by the presence of a homologous linear minichromosome. Furthermore, sister chromatid exchange can be stimulated by the presence of a 12-kb ARG4 DNA fragment, which contains initiation sites for meiotic gene conversion. Using physical analysis, we have directly identified a product of sister chromatid exchange: a head-to-tail dimer form of a circular minichromosome. This dimer form is absent in a rad50S mutant strain, which is deficient in processing of the ends of meiosis-specific double-stranded breaks into single-stranded DNA tails. Our studies suggest that meiotic sister chromatid exchange is stimulated by the same mechanism as meiotic homolog exchange.
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Honigberg, Saul M., and Rita H. Lee. "Snf1 Kinase Connects Nutritional Pathways Controlling Meiosis in Saccharomyces cerevisiae." Molecular and Cellular Biology 18, no. 8 (August 1, 1998): 4548–55. http://dx.doi.org/10.1128/mcb.18.8.4548.
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ABSTRACT Glucose inhibits meiosis in Saccharomyces cerevisiae at three different steps (IME1 transcription, IME2transcription, and entry into late stages of meiosis). Because many of the regulatory effects of glucose in yeast are mediated through the inhibition of Snf1 kinase, a component of the glucose repression pathway, we determined the role of SNF1 in regulating meiosis. Deleting SNF1 repressed meiosis at the same three steps that were inhibited by glucose, suggesting that glucose blocks meiosis by inhibiting Snf1. For example, the snf1Δ mutant completely failed to induce IME1 transcripts in sporulation medium. Furthermore, even when this block was bypassed by expression ofIME1 from a multicopy plasmid, IME2transcription and meiotic initiation occurred at only 10 to 20% of the levels seen in wild-type cells. The addition of glucose did not further inhibit IME2 transcription, suggesting that Snf1 is the primary mediator of glucose controls on IME2 expression. Finally, in snf1Δ cells in which both blocks on meiotic initiation were bypassed, early stages of meiosis (DNA replication and commitment to recombination) occurred, but later stages (chromosome segregation and spore formation) did not, suggesting that Snf1 controls later stages of meiosis independently from the two controls on meiotic initiation. Because Snf1 is known to activate the expression of genes required for acetate metabolism, it may also serve to connect glucose and acetate controls on meiotic differentiation.
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Hochegger, Helfrid, Andrea Klotzbücher, Jane Kirk, Mike Howell, Katherine le Guellec, Kate Fletcher, Tod Duncan, Muhammad Sohail, and Tim Hunt. "New B-type cyclin synthesis is required between meiosis I and II duringXenopusoocyte maturation." Development 128, no. 19 (October 1, 2001): 3795–807. http://dx.doi.org/10.1242/dev.128.19.3795.
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Progression through meiosis requires two waves of maturation promoting factor (MPF) activity corresponding to meiosis I and meiosis II. Frog oocytes contain a pool of inactive ‘pre-MPF’ consisting of cyclin-dependent kinase 1 bound to B-type cyclins, of which we now find three previously unsuspected members, cyclins B3, B4 and B5. Protein synthesis is required to activate pre-MPF, and we show here that this does not require new B-type cyclin synthesis, probably because of a large maternal stockpile of cyclins B2 and B5. This stockpile is degraded after meiosis I and consequently, the activation of MPF for meiosis II requires new cyclin synthesis, principally of cyclins B1 and B4, whose translation is strongly activated after meiosis I. If this wave of new cyclin synthesis is ablated by antisense oligonucleotides, the oocytes degenerate and fail to form a second meiotic spindle. The effects on meiotic progression are even more severe when all new protein synthesis is blocked by cycloheximide added after meiosis I, but can be rescued by injection of indestructible B-type cyclins. B-type cyclins and MPF activity are required to maintain c-mos and MAP kinase activity during meiosis II, and to establish the metaphase arrest at the end of meiotic maturation. We discuss the interdependence of c-mos and MPF, and reveal an important role for translational control of cyclin synthesis between the two meiotic divisions.
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Walters, Marta Sherman. "Meiosis readiness in Lilium." Canadian Journal of Genetics and Cytology 27, no. 1 (February 1, 1985): 33–38. http://dx.doi.org/10.1139/g85-007.
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It was observed in five cultivars and two hybrids of Lilium that premeiotic prophase is retarded in anthers approaching meiosis. The occurrence of premeiotic despiralization was related to the degree of retardation of premeiotic prophase. It is proposed that meiosis is initiated by stimuli arising outside the premeiotic cells. It is suggested that an accumulation of meiosis-inducing substances in the cytoplasm of the premeiotic cells causes prophase to slow down; when a critical level ("meiosis readiness") is reached, mitotic division is no longer possible and cells in premeiotic prophase despiralize to interphase.Key words: meiotic prophase, Lilium, meiotic readiness, premeiotic despiralization.
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Kurzbauer, Marie-Therese, Michael Peter Janisiw, Luis F. Paulin, Ignacio Prusén Mota, Konstantin Tomanov, Ondrej Krsicka, Arndt von Haeseler, Veit Schubert, and Peter Schlögelhofer. "ATM controls meiotic DNA double-strand break formation and recombination and affects synaptonemal complex organization in plants." Plant Cell 33, no. 5 (February 5, 2021): 1633–56. http://dx.doi.org/10.1093/plcell/koab045.
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Abstract Meiosis is a specialized cell division that gives rise to genetically distinct gametic cells. Meiosis relies on the tightly controlled formation of DNA double-strand breaks (DSBs) and their repair via homologous recombination for correct chromosome segregation. Like all forms of DNA damage, meiotic DSBs are potentially harmful and their formation activates an elaborate response to inhibit excessive DNA break formation and ensure successful repair. Previous studies established the protein kinase ATM as a DSB sensor and meiotic regulator in several organisms. Here we show that Arabidopsis ATM acts at multiple steps during DSB formation and processing, as well as crossover (CO) formation and synaptonemal complex (SC) organization, all vital for the successful completion of meiosis. We developed a single-molecule approach to quantify meiotic breaks and determined that ATM is essential to limit the number of meiotic DSBs. Local and genome-wide recombination screens showed that ATM restricts the number of interference-insensitive COs, while super-resolution STED nanoscopy of meiotic chromosomes revealed that the kinase affects chromatin loop size and SC length and width. Our study extends our understanding of how ATM functions during plant meiosis and establishes it as an integral factor of the meiotic program.
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Soygur, B., R. G. Jaszczak, A. Fries, D. H. Nguyen, S. Malki, G. Hu, N. Demir, R. Arora, and D. J. Laird. "Intercellular bridges coordinate the transition from pluripotency to meiosis in mouse fetal oocytes." Science Advances 7, no. 15 (April 2021): eabc6747. http://dx.doi.org/10.1126/sciadv.abc6747.
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Meiosis is critical to generating oocytes and ensuring female fertility; however, the mechanisms regulating the switch from mitotic primordial germ cells to meiotic germ cells are poorly understood. Here, we implicate intercellular bridges (ICBs) in this state transition. We used three-dimensional in toto imaging to map meiotic initiation in the mouse fetal ovary and revealed a radial geometry of this transition that precedes the established anterior-posterior wave. Our studies reveal that appropriate timing of meiotic entry across the ovary and coordination of mitotic-meiotic transition within a cyst depend on the ICB componentTex14, which we show is required for functional cytoplasmic sharing. We find thatTex14mutants more rapidly attenuate the pluripotency transcriptDppa3upon meiotic initiation, andDppa3mutants undergo premature meiosis similar toTex14. Together, these results lead to a model that ICBs coordinate and buffer the transition from pluripotency to meiosis through dilution of regulatory factors.
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Agashe, Bhavna, Chellapilla Krishna Prasad, and Imran Siddiqi. "Identification and analysis ofDYAD: a gene required for meiotic chromosome organisation and female meiotic progression inArabidopsis." Development 129, no. 16 (August 15, 2002): 3935–43. http://dx.doi.org/10.1242/dev.129.16.3935.
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The dyad mutant of Arabidopsis was previously identified as being defective in female meiosis. We report here the analysis of the DYAD gene. In ovules and anthers DYAD RNA is detected specifically in female and male meiocytes respectively, in premeiotic interphase/meiotic prophase. Analysis of chromosome spreads in female meiocytes showed that in the mutant, chromosomes did not undergo synapsis and formed ten univalents instead of five bivalents. Unlike mutations in AtDMC1 and AtSPO11 which also affect bivalent formation as the univalent chromosomes segregate randomly, the dyad univalents formed an ordered metaphase plate and underwent an equational division. This suggests a requirement for DYAD for chromosome synapsis and centromere configuration in female meiosis. The dyad mutant showed increased and persistent expression of a meiosis-specific marker, pAtDMC1::GUS during female meiosis, indicative of defective meiotic progression. The sequence of the putative protein encoded by DYAD did not reveal strong similarity to other proteins. DYAD is therefore likely to encode a novel protein required for meiotic chromosome organisation and female meiotic progression.
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Shanks, Robert M. Q., Rebecca J. Kamieniecki, and Dean S. Dawson. "The Kar3-Interacting Protein Cik1p Plays a Critical Role in Passage Through Meiosis I in Saccharomyces cerevisiae." Genetics 159, no. 3 (November 1, 2001): 939–51. http://dx.doi.org/10.1093/genetics/159.3.939.
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Abstract Meiosis I in Saccharomyces cerevisiae is dependent upon the motor protein Kar3. Absence of Kar3p in meiosis results in an arrest in prophase I. Cik1p and Vik1p are kinesin-associated proteins known to modulate the function of Kar3p in the microtubule-dependent processes of karyogamy and mitosis. Experiments were performed to determine whether Cik1p and Vik1p are also important for the function of Kar3p during meiosis. The meiotic phenotypes of a cik1 mutant were found to be similar to those of kar3 mutants. Cells without Cik1p exhibit a meiotic defect in homologous recombination and synaptonemal complex formation. Most cik1 mutant cells, like kar3 mutants, arrest in meiotic prophase; however, in cik1 mutants this arrest is less severe. These data are consistent with the model that Cik1p is necessary for some, but not all, of the roles of Kar3p in meiosis I. vik1 mutants sporulate at wild-type levels, but have reduced spore viability. This loss in viability is partially attributable to vegetative chromosome loss in vik1 diploids. Cellular localization experiments reveal that Kar3p, Cik1p, and Vik1p are present throughout meiosis and are consistent with Cik1p and Vik1p having different meiotic roles.
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Klieger, Yair, Ofer Yizhar, Drora Zenvirth, Neta Shtepel-Milman, Margriet Snoek, and Giora Simchen. "Involvement of Sir2/4 in Silencing of DNA Breakage and Recombination on Mouse YACs during Yeast Meiosis." Molecular Biology of the Cell 16, no. 3 (March 2005): 1449–55. http://dx.doi.org/10.1091/mbc.e04-07-0592.
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Yeast artificial chromosomes (YACs) that contain human DNA backbone undergo DNA double-strand breaks (DSBs) and recombination during yeast meiosis at rates similar to the yeast native chromosomes. Surprisingly, YACs containing DNA covering a recombination hot spot in the mouse major histocompatibility complex class III region do not show meiotic DSBs and undergo meiotic recombination at reduced levels. Moreover, segregation of these YACs during meiosis is seriously compromised. In meiotic yeast cells carrying the mutations sir2 or sir4, but not sir3, these YACs show DSBs, suggesting that a unique chromatin structure of the YACs, involving Sir2 and Sir4, protects the YACs from the meiotic recombination machinery. We speculate that the paucity of DSBs and recombination events on these YACs during yeast meiosis may reflect the refractory nature of the corresponding region in the mouse genome.
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Lenormand, Thomas, Jan Engelstädter, Susan E. Johnston, Erik Wijnker, and Christoph R. Haag. "Evolutionary mysteries in meiosis." Philosophical Transactions of the Royal Society B: Biological Sciences 371, no. 1706 (October 19, 2016): 20160001. http://dx.doi.org/10.1098/rstb.2016.0001.
Full textAbstract:
Meiosis is a key event of sexual life cycles in eukaryotes. Its mechanistic details have been uncovered in several model organisms, and most of its essential features have received various and often contradictory evolutionary interpretations. In this perspective, we present an overview of these often ‘weird’ features. We discuss the origin of meiosis (origin of ploidy reduction and recombination, two-step meiosis), its secondary modifications (in polyploids or asexuals, inverted meiosis), its importance in punctuating life cycles (meiotic arrests, epigenetic resetting, meiotic asymmetry, meiotic fairness) and features associated with recombination (disjunction constraints, heterochiasmy, crossover interference and hotspots). We present the various evolutionary scenarios and selective pressures that have been proposed to account for these features, and we highlight that their evolutionary significance often remains largely mysterious. Resolving these mysteries will likely provide decisive steps towards understanding why sex and recombination are found in the majority of eukaryotes. This article is part of the themed issue ‘Weird sex: the underappreciated diversity of sexual reproduction’.
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Endow, Sharyn A., and Donald J. Komma. "Spindle Dynamics during Meiosis in Drosophila Oocytes." Journal of Cell Biology 137, no. 6 (June 16, 1997): 1321–36. http://dx.doi.org/10.1083/jcb.137.6.1321.
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Mature oocytes of Drosophila are arrested in metaphase of meiosis I. Upon activation by ovulation or fertilization, oocytes undergo a series of rapid changes that have not been directly visualized previously. We report here the use of the Nonclaret disjunctional (Ncd) microtubule motor protein fused to the green fluorescent protein (GFP) to monitor changes in the meiotic spindle of live oocytes after activation in vitro. Meiotic spindles of metaphase-arrested oocytes are relatively stable, however, meiotic spindles of in vitro–activated oocytes are highly dynamic: the spindles elongate, rotate around their long axis, and undergo an acute pivoting movement to reorient perpendicular to the oocyte surface. Many oocytes spontaneously complete the meiotic divisions, permitting visualization of progression from meiosis I to II. The movements of the spindle after oocyte activation provide new information about the dynamic changes in the spindle that occur upon re-entry into meiosis and completion of the meiotic divisions. Spindles in live oocytes mutant for a lossof-function ncd allele fused to gfp were also imaged. The genesis of spindle defects in the live mutant oocytes provides new insights into the mechanism of Ncd function in the spindle during the meiotic divisions.
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Sandhu, Rima, Aniketa Sinha, and Ben Montpetit. "The SR-protein Npl3 is an essential component of the meiotic splicing regulatory network in Saccharomyces cerevisiae." Nucleic Acids Research 49, no. 5 (February 12, 2021): 2552–68. http://dx.doi.org/10.1093/nar/gkab071.
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Abstract The meiotic gene expression program in Saccharomyces cerevisiae involves regulated splicing of meiosis-specific genes via multiple splicing activators (e.g. Mer1, Nam8, Tgs1). Here, we show that the SR protein Npl3 is required for meiotic splicing regulation and is essential for proper execution of the meiotic cell cycle. The loss of Npl3, though not required for viability in mitosis, caused intron retention in meiosis-specific transcripts, inefficient meiotic double strand break processing and an arrest of the meiotic cell cycle. The targets of Npl3 overlapped in some cases with other splicing regulators, while also having unique target transcripts that were not shared. In the absence of Npl3, splicing defects for three transcripts (MER2, HOP2 and SAE3) were rescued by conversion of non-consensus splice sites to the consensus sequence. Methylation of Npl3 was further found to be required for splicing Mer1-dependent transcripts, indicating transcript-specific mechanisms by which Npl3 supports splicing. Together these data identify an essential function for the budding yeast SR protein Npl3 in meiosis as part of the meiotic splicing regulatory network.
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Bilodeau-Goeseels, S. "Review: The regulation of meiotic maturation in bovine oocytes." Canadian Journal of Animal Science 88, no. 3 (September 1, 2008): 343–49. http://dx.doi.org/10.4141/cjas08002.
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Meiotic maturation in mammalian oocytes is initiated during fetal development, arrested for several years in some cases, then completed at the time of ovulation. Although the mechanisms involved in oocyte meiotic arrest and meiotic resumption are not fully understood, new players and roles have recently been identified. This paper reviews the role of follicle cells, as well as the role of the cyclic adenosine 3', 5'-monophosphate (cAMP) pathway, in the maintenance of meiotic arrest. Potential mechanisms by which luteinizing hormone (LH) signals meiotic resumption are also reviewed. New findings on the role of adenosine monophosphate-activated kinase (PRKA), as well as the effects of culture medium composition on meiosis in vitro, are also discussed. From a practical perspective, improved understanding of the mechanisms involved in the control of meiosis will facilitate better control of the process in vitro resulting in increased developmental competence and increased efficiency of in vitro embryo production procedures. Key words: Bovine, oocyte, meiosis, cAMP
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Chen, Hanchen, Chengpeng He, Chongyang Wang, Xuanpeng Wang, Fengyin Ruan, Junjie Yan, Ping Yin, Yingxiang Wang, and Shunping Yan. "RAD51 supports DMC1 by inhibiting the SMC5/6 complex during meiosis." Plant Cell 33, no. 8 (May 16, 2021): 2869–82. http://dx.doi.org/10.1093/plcell/koab136.
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Abstract Meiosis is a fundamental process for sexual reproduction in most eukaryotes and the evolutionarily conserved recombinases RADiation sensitive51 (RAD51) and Disrupted Meiotic cDNA1 (DMC1) are essential for meiosis and thus fertility. The mitotic function of RAD51 is clear, but the meiotic function of RAD51 remains largely unknown. Here we show that RAD51 functions as an interacting protein to restrain the Structural Maintenance of Chromosomes5/6 (SMC5/6) complex from inhibiting DMC1. We unexpectedly found that loss of the SMC5/6 partially suppresses the rad51 knockout mutant in terms of sterility, pollen inviability, and meiotic chromosome fragmentation in a DMC1-dependent manner in Arabidopsis thaliana. Biochemical and cytological studies revealed that the DMC1 localization in meiotic chromosomes is inhibited by the SMC5/6 complex, which is attenuated by RAD51 through physical interactions. This study not only identified the long-sought-after function of RAD51 in meiosis but also discovered the inhibition of SMC5/6 on DMC1 as a control mechanism during meiotic recombination.
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Smith, H. E., and A. P. Mitchell. "A transcriptional cascade governs entry into meiosis in Saccharomyces cerevisiae." Molecular and Cellular Biology 9, no. 5 (May 1989): 2142–52. http://dx.doi.org/10.1128/mcb.9.5.2142.
Full textAbstract:
Two signals activate meiosis in yeast: starvation and expression of the a1 and alpha 2 products of the mating-type locus. Prior studies suggest that these signals stimulate expression of an activator of meiosis, the IME1 (inducer of meiosis) product. We have cloned a gene, IME2, with properties similar to those of IME1: both genes are required for meiosis, and both RNAs are induced in meiotic cells. Elevated dosage of IME1 or IME2 stimulates the meiotic recombination pathway without starvation; thus, the IME products may be part of the switch that activates meiosis. IME1 was found to be required for IME2 expression, and a multicopy IME2 plasmid permitted meiosis in an ime1 deletion mutant. Accordingly, we propose that the IME1 product stimulates meiosis mainly through activation of IME2 expression.
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Smith, H. E., and A. P. Mitchell. "A transcriptional cascade governs entry into meiosis in Saccharomyces cerevisiae." Molecular and Cellular Biology 9, no. 5 (May 1989): 2142–52. http://dx.doi.org/10.1128/mcb.9.5.2142-2152.1989.
Full textAbstract:
Two signals activate meiosis in yeast: starvation and expression of the a1 and alpha 2 products of the mating-type locus. Prior studies suggest that these signals stimulate expression of an activator of meiosis, the IME1 (inducer of meiosis) product. We have cloned a gene, IME2, with properties similar to those of IME1: both genes are required for meiosis, and both RNAs are induced in meiotic cells. Elevated dosage of IME1 or IME2 stimulates the meiotic recombination pathway without starvation; thus, the IME products may be part of the switch that activates meiosis. IME1 was found to be required for IME2 expression, and a multicopy IME2 plasmid permitted meiosis in an ime1 deletion mutant. Accordingly, we propose that the IME1 product stimulates meiosis mainly through activation of IME2 expression.
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Fan, Xueying, Ioannis Moustakas, Vanessa Torrens-Juaneda, Qijing Lei, Geert Hamer, Leoni A. Louwe, Gonneke S. K. Pilgram, et al. "Transcriptional progression during meiotic prophase I reveals sex-specific features and X chromosome dynamics in human fetal female germline." PLOS Genetics 17, no. 9 (September 9, 2021): e1009773. http://dx.doi.org/10.1371/journal.pgen.1009773.
Full textAbstract:
During gametogenesis in mammals, meiosis ensures the production of haploid gametes. The timing and length of meiosis to produce female and male gametes differ considerably. In contrast to males, meiotic prophase I in females initiates during development. Hence, the knowledge regarding progression through meiotic prophase I is mainly focused on human male spermatogenesis and female oocyte maturation during adulthood. Therefore, it remains unclear how the different stages of meiotic prophase I between human oogenesis and spermatogenesis compare. Analysis of single-cell transcriptomics data from human fetal germ cells (FGC) allowed us to identify the molecular signatures of female meiotic prophase I stages leptotene, zygotene, pachytene and diplotene. We have compared those between male and female germ cells in similar stages of meiotic prophase I and revealed conserved and specific features between sexes. We identified not only key players involved in the process of meiosis, but also highlighted the molecular components that could be responsible for changes in cellular morphology that occur during this developmental period, when the female FGC acquire their typical (sex-specific) oocyte shape as well as sex-differences in the regulation of DNA methylation. Analysis of X-linked expression between sexes during meiotic prophase I suggested a transient X-linked enrichment during female pachytene, that contrasts with the meiotic sex chromosome inactivation in males. Our study of the events that take place during meiotic prophase I provide a better understanding not only of female meiosis during development, but also highlights biomarkers that can be used to study infertility and offers insights in germline sex dimorphism in humans.
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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.
Full textAbstract:
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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Smirnova, Natalya A., Peter J. Romanienko, Pavel P. Khil, and R. Daniel Camerini-Otero. "Gene expression profiles of Spo11−/− mouse testes with spermatocytes arrested in meiotic prophase I." Reproduction 132, no. 1 (July 2006): 67–77. http://dx.doi.org/10.1530/rep.1.00997.
Full textAbstract:
Spo11, a meiosis-specific protein, introduces double-strand breaks on chromosomal DNA and initiates meiotic recombination in a wide variety of organisms. Mouse null Spo11 spermatocytes fail to synapse chromosomes and progress beyond the zygotene stage of meiosis. We analyzed gene expression profiles in Spo11−/ −adult and juvenile wild-type testis to describe genes expressed before and after the meiotic arrest resulting from the knocking out of Spo11. These genes were characterized using the Gene Ontology data base. To focus on genes involved in meiosis, we performed comparative gene expression analysis of Spo11−/ −and wild-type testes from 15-day mice, when spermatocytes have just entered pachytene. We found that the knockout of Spo11 causes dramatic changes in the level of expression of genes that participate in meiotic recombination (Hop2, Brca2, Mnd1, FancG) and in the meiotic checkpoint (cyclin B2, Cks2), but does not affect genes encoding protein components of the synaptonemal complex. Finally, we discovered unknown genes that are affected by the disruption of the Spo11 gene and therefore may be specifically involved in meiosis and spermatogenesis.
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Lin, T. Y., S. Viswanathan, C. Wood, P. G. Wilson, N. Wolf, and M. T. Fuller. "Coordinate developmental control of the meiotic cell cycle and spermatid differentiation in Drosophila males." Development 122, no. 4 (April 1, 1996): 1331–41. http://dx.doi.org/10.1242/dev.122.4.1331.
Full textAbstract:
Wild-type function of four Drosophila genes, spermatocyte arrest, cannonball, always early and meiosis I arrest, is required both for cell-cycle progression through the G2/M transition of meiosis I in males and for onset of spermatid differentiation. In males mutant for any one of these meiotic arrest genes, mature primary spermatocytes with partially condensed chromosomes accumulate and postmeiotic cells are lacking. The arrest in cell-cycle progression occurs prior to degradation of cyclin A protein. The block in spermatogenesis in these mutants is not simply a secondary consequence of meiotic cell-cycle arrest, as spermatid differentiation proceeds in males mutant for the cell cycle activating phosphatase twine. Instead, the arrest of both meiosis and spermiogenesis suggests a control point that may serve to coordinate the male meiotic cell cycle with the spermatid differentiation program. The phenotype of the Drosophila meiotic arrest mutants is strikingly similar to the histopathological features of meiosis I maturation arrest infertility in human males, suggesting that the control point may be conserved from flies to man.