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1
Zhang, Qian, Wenzhe Zhang, Xinyi Wu, Hanni Ke, Yingying Qin, Shidou Zhao, and Ting Guo. "Homozygous missense variant in MEIOSIN causes premature ovarian insufficiency." Human Reproduction 38, Supplement_2 (November 1, 2023): ii47—ii56. http://dx.doi.org/10.1093/humrep/dead084.
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Abstract STUDY QUESTION Are variants of genes involved in meiosis initiation responsible for premature ovarian insufficiency (POI)? SUMMARY ANSWER A MEIOSIN variant participates in the pathogenesis of human POI by impairing meiosis due to insufficient transcriptional activation of essential meiotic genes. WHAT IS KNOWN ALREADY Meiosis is the key event for the establishment of the ovarian reserve, and several gene defects impairing meiotic homologous recombination have been found to contribute to the pathogenesis of POI. Although STRA8 and MEIOISN variants have been found to associate with POI in a recent study, the condition of other meiosis initiation genes is unknown and direct evidence of variants participating in the pathogenesis of POI is still lacking. STUDY DESIGN, SIZE, DURATION This was a retrospective genetic study. An in-house whole exome sequencing (WES) database of 1030 idiopathic POI patients was screened for variations of meiosis initiation genes. PARTICIPANTS/MATERIALS, SETTING, METHODS Homozygous or compound heterozygous variations of genes involved in meiosis initiation were screened in the in-house WES database. The pathogenicity of the variation was verified by in vitro experiments, including protein structure prediction and dual-luciferase reporter assay. The effect of the variant on ovarian function and meiosis was demonstrated through histological analyses in a point mutation mouse model. MAIN RESULTS AND THE ROLE OF CHANCE One homozygous variant in MEIOSIN (c.1735C>T, p.R579W) and one in STRA8 (c.258 + 1G>A), which initiates meiosis via the retinoic acid-dependent pathway, were identified in a patient with idiopathic POI respectively. The STRA8 variation has been reported in the recently published work. For the MEIOSIN variation, the dual-luciferase reporter assay revealed that the variant adversely affected the transcriptional function of MEIOSIN in upregulating meiotic genes. Furthermore, knock-in mice with the homologous mutation confirmed that the variation impacted the meiotic prophase I program and accelerated oocyte depletion. Moreover, the variant p.R579W localizing in the high-mobility group (HMG) box domain disrupted the nuclear localization of the MEIOSIN protein but was dispensable for the cell-cycle switch of oocytes, suggesting a unique role of the MEIOSIN HMG box domain in meiosis initiation. LIMITATIONS, REASONS FOR CAUTION Further studies are needed to explore the role of other meiosis initiation genes in the pathogenesis of POI. WIDER IMPLICATIONS OF THE FINDINGS The MEIOSIN variant was verified to cause POI by impaired transcriptional regulation of meiotic genes and was inherited by a recessive mode. The function of HMG box domain in MEIOSIN protein was also expanded by this study. Although causative variations in meiotic initiation genes are rare in POI, our study confirmed the pathogenicity of a MEIOSIN variant and elucidated another mechanism of human infertility. STUDY FUNDING/COMPETING INTEREST(s) This work was supported by the National Key Research & Developmental Program of China (2022YFC2703800, 2022YFC2703000), National Natural Science Foundation for Distinguished Young Scholars (82125014), National Natural Science Foundation of China (32070847, 32170867, 82071609), Basic Science Center Program of NSFC (31988101), Natural Science Foundation of Shandong Province for Grand Basic Projects (ZR2021ZD33), Natural Science Foundation of Shandong Province for Excellent Young Scholars (ZR2022YQ69), Taishan Scholars Program for Young Experts of Shandong Province (tsqn202211371), and Qilu Young Scholars Program of Shandong University. The authors declare no conflict of interest. TRIAL REGISTRATION NUMBER N/A.
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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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Ross, Lyle O., Susannah Rankin, Michèle F. Shuster, and Dean S. Dawson. "Effects of Homology, Size and Exchange on the Meiotic Segregation of Model Chromosomes in Saccharomyces cerevisiae." Genetics 142, no. 1 (January 1, 1996): 79–89. http://dx.doi.org/10.1093/genetics/142.1.79.
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In most eukaryotic organisms, chiasmata, the connections formed between homologous chromosomes as a consequence of crossing over, are important for ensuring that the homologues move away from each other at meiosis I. Some organisms have the capacity to partition the rare homologues that have failed to experience reciprocal recombination. The yeast Saccharomyces cerevisiae is able to correctly partition achiasmate homologues with low fidelity by a mechanism that is largely unknown. It is possible to test which parameters affect the ability of achiasmate chromosomes to segregate by constructing strains that will have three achiasmate chromosomes at the time of meiosis. The meiotic partitioning of these chromosomes can be monitored to determine which ones segregate away from each other at meiosis I. This approach was used to test the influence of homologous yeast DNA sequences, recombination intiation sites, chromosome size and crossing over on the meiotic segregation of the model chromosomes. Chrome some size had no effect on achiasmate segregation. The influence of homologous yeast sequences on the segregation of noncrossover model chromosomes was negligible. In meioses in which two of the three model chromosomes experienced a crossover, they nearly always disjoined at meiosis I.
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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.
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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.
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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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Uranishi, Kousuke, Masataka Hirasaki, Yuka Kitamura, Yosuke Mizuno, Masazumi Nishimoto, Ayumu Suzuki, and Akihiko Okuda. "Two DNA Binding Domains of MGA Act in Combination to Suppress Ectopic Activation of Meiosis-Related Genes in Mouse Embryonic Stem Cells." Stem Cells 39, no. 11 (July 14, 2021): 1435–46. http://dx.doi.org/10.1002/stem.3433.
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Abstract Although the physiological meaning of the high potential of mouse embryonic stem cells (ESCs) for meiotic entry is not understood, a rigid safeguarding system is required to prevent ectopic onset of meiosis. PRC1.6, a non-canonical PRC1, is known for its suppression of precocious and ectopic meiotic onset in germ cells and ESCs, respectively. MGA, a scaffolding component of PRC1.6, bears two distinct DNA-binding domains termed bHLHZ and T-box. However, it is unclear how this feature contributes to the functions of PRC1.6. Here, we demonstrated that both domains repress distinct sets of genes in murine ESCs, but substantial numbers of meiosis-related genes are included in both gene sets. In addition, our data demonstrated that bHLHZ is crucially involved in repressing the expression of Meiosin, which plays essential roles in meiotic entry with Stra8, revealing at least part of the molecular mechanisms that link negative and positive regulation of meiotic onset.
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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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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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Paliulis, Leocadia V., and R. Bruce Nicklas. "The Reduction of Chromosome Number in Meiosis Is Determined by Properties Built into the Chromosomes." Journal of Cell Biology 150, no. 6 (September 18, 2000): 1223–32. http://dx.doi.org/10.1083/jcb.150.6.1223.
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In meiosis I, two chromatids move to each spindle pole. Then, in meiosis II, the two are distributed, one to each future gamete. This requires that meiosis I chromosomes attach to the spindle differently than meiosis II chromosomes and that they regulate chromosome cohesion differently. We investigated whether the information that dictates the division type of the chromosome comes from the whole cell, the spindle, or the chromosome itself. Also, we determined when chromosomes can switch from meiosis I behavior to meiosis II behavior. We used a micromanipulation needle to fuse grasshopper spermatocytes in meiosis I to spermatocytes in meiosis II, and to move chromosomes from one spindle to the other. Chromosomes placed on spindles of a different meiotic division always behaved as they would have on their native spindle; e.g., a meiosis I chromosome attached to a meiosis II spindle in its normal fashion and sister chromatids moved together to the same spindle pole. We also showed that meiosis I chromosomes become competent meiosis II chromosomes in anaphase of meiosis I, but not before. The patterns for attachment to the spindle and regulation of cohesion are built into the chromosome itself. These results suggest that regulation of chromosome cohesion may be linked to differences in the arrangement of kinetochores in the two meiotic divisions.
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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.
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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.
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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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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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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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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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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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Sakuno, Takeshi, and Yasushi Hiraoka. "Rec8 Cohesin: A Structural Platform for Shaping the Meiotic Chromosomes." Genes 13, no. 2 (January 22, 2022): 200. http://dx.doi.org/10.3390/genes13020200.
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Meiosis is critically different from mitosis in that during meiosis, pairing and segregation of homologous chromosomes occur. During meiosis, the morphology of sister chromatids changes drastically, forming a prominent axial structure in the synaptonemal complex. The meiosis-specific cohesin complex plays a central role in the regulation of the processes required for recombination. In particular, the Rec8 subunit of the meiotic cohesin complex, which is conserved in a wide range of eukaryotes, has been analyzed for its function in modulating chromosomal architecture during the pairing and recombination of homologous chromosomes in meiosis. Here, we review the current understanding of Rec8 cohesin as a structural platform for meiotic chromosomes.
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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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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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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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Fujiwara, Yasuhiro, Mary Ann Handel, and Yuki Okada. "R-Loop Formation in Meiosis: Roles in Meiotic Transcription-Associated DNA Damage." Epigenomes 6, no. 3 (August 24, 2022): 26. http://dx.doi.org/10.3390/epigenomes6030026.
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Meiosis is specialized cell division during gametogenesis that produces genetically unique gametes via homologous recombination. Meiotic homologous recombination entails repairing programmed 200–300 DNA double-strand breaks generated during the early prophase. To avoid interference between meiotic gene transcription and homologous recombination, mammalian meiosis is thought to employ a strategy of exclusively transcribing meiotic or post-meiotic genes before their use. Recent studies have shown that R-loops, three-stranded DNA/RNA hybrid nucleotide structures formed during transcription, play a crucial role in transcription and genome integrity. Although our knowledge about the function of R-loops during meiosis is limited, recent findings in mouse models have suggested that they play crucial roles in meiosis. Given that defective formation of an R-loop can cause abnormal transcription and transcription-coupled DNA damage, the precise regulatory network of R-loops may be essential in vivo for the faithful progression of mammalian meiosis and gametogenesis.
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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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Loidl, Josef, and Knud Nairz. "Karyotype Variability in Yeast Caused by Nonallelic Recombination in Haploid Meiosis." Genetics 146, no. 1 (May 1, 1997): 79–88. http://dx.doi.org/10.1093/genetics/146.1.79.
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Chromosomes of altered size were found in the meiotic products of a haploid Saccharomyces cerevisiae strain by pulsed field gel electrophoretic separation of whole chromosomes. About 7% of haploid meioses produced chromosomes that differed by ≥10 kb from their wild-type counterparts. Chromosomes most often became enlarged or shortened due to recombination events between sister chromatids at nonallelic sequences. By this mechanism chromosome III acquired tandem arrays of up to eight extra copies of the ∼100 kb MAT-HMR segment during repeated rounds of haploid meioses. Enlarged chromosomes III were unstable and changed their size during meiosis more often than remaining unchanged. Altered chromosomes appeared also as the products of intrachromatid recombination and of reciprocal translocations caused by ectopic recombination between nonhomologous chromosomes. In diploid meiosis, chromosomes of altered size occurred at least 10 times less frequently, whereas in mitotic cultures cells with altered karyotypes were virtually absent. The results show that various forms of ectopic recombination are promoted by the absence of allelic homologies.
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Sou, Ieng Fong, Rebecca M. Pryce, Wee-Wei Tee, and Urszula Lucja McClurg. "Meiosis initiation: a story of two sexes in all creatures great and small." Biochemical Journal 478, no. 20 (October 28, 2021): 3791–805. http://dx.doi.org/10.1042/bcj20210412.
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Meiosis facilitates diversity across individuals and serves as a major driver of evolution. However, understanding how meiosis begins is complicated by fundamental differences that exist between sexes and species. Fundamental meiotic research is further hampered by a current lack of human meiotic cells lines. Consequently, much of what we know relies on data from model organisms. However, contextualising findings from yeast, worms, flies and mice can be challenging, due to marked differences in both nomenclature and the relative timing of meiosis. In this review, we set out to combine current knowledge of signalling and transcriptional pathways that control meiosis initiation across the sexes in a variety of organisms. Furthermore, we highlight the emerging links between meiosis initiation and oncogenesis, which might explain the frequent re-expression of normally silent meiotic genes in a variety of human cancers.
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Tsubouchi, Hideo. "The Hop2-Mnd1 Complex and Its Regulation of Homologous Recombination." Biomolecules 13, no. 4 (April 10, 2023): 662. http://dx.doi.org/10.3390/biom13040662.
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Homologous recombination (HR) is essential for meiosis in most sexually reproducing organisms, where it is induced upon entry into meiotic prophase. Meiotic HR is conducted by the collaborative effort of proteins responsible for DNA double-strand break repair and those produced specifically during meiosis. The Hop2-Mnd1 complex was originally identified as a meiosis-specific factor that is indispensable for successful meiosis in budding yeast. Later, it was found that Hop2-Mnd1 is conserved from yeasts to humans, playing essential roles in meiosis. Accumulating evidence suggests that Hop2-Mnd1 promotes RecA-like recombinases towards homology search/strand exchange. This review summarizes studies on the mechanism of the Hop2-Mnd1 complex in promoting HR and beyond.
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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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McCarroll, R. M., and R. E. Esposito. "SPO13 negatively regulates the progression of mitotic and meiotic nuclear division in Saccharomyces cerevisiae." Genetics 138, no. 1 (September 1, 1994): 47–60. http://dx.doi.org/10.1093/genetics/138.1.47.
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Abstract The meiosis-specific yeast gene SPO13 has been previously shown to be required to obtain two successive divisions in meiosis. We report here that vegetative expression of this gene causes a CDC28-dependent cell-cycle arrest at mitosis. Overexpression of SPO13 during meiosis causes a transient block to completion of the meiosis I division and suppresses the inability of cdc28ts strains to execute meiosis II. The spo13 defect can be partially suppressed by conditions that slow progression of the first meiotic division. Based on the results presented below, we propose that SPO13 acts as a meiotic timing function by transiently blocking progression through the meiosis I division, thereby allowing (1) coordination of the first division with assembly of the reductional segregation apparatus, and (2) subsequent entry into a second round of segregation to separate replicated sister chromatids without an intervening S-phase.
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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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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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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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Farini, Donatella, and Massimo De Felici. "The Beginning of Meiosis in Mammalian Female Germ Cells: A Never-Ending Story of Intrinsic and Extrinsic Factors." International Journal of Molecular Sciences 23, no. 20 (October 20, 2022): 12571. http://dx.doi.org/10.3390/ijms232012571.
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Meiosis is the unique division of germ cells resulting in the recombination of the maternal and paternal genomes and the production of haploid gametes. In mammals, it begins during the fetal life in females and during puberty in males. In both cases, entering meiosis requires a timely switch from the mitotic to the meiotic cell cycle and the transition from a potential pluripotent status to meiotic differentiation. Revealing the molecular mechanisms underlying these interrelated processes represents the essence in understanding the beginning of meiosis. Meiosis facilitates diversity across individuals and acts as a fundamental driver of evolution. Major differences between sexes and among species complicate the understanding of how meiosis begins. Basic meiotic research is further hindered by a current lack of meiotic cell lines. This has been recently partly overcome with the use of primordial-germ-cell-like cells (PGCLCs) generated from pluripotent stem cells. Much of what we know about this process depends on data from model organisms, namely, the mouse; in mice, the process, however, appears to differ in many aspects from that in humans. Identifying the mechanisms and molecules controlling germ cells to enter meiosis has represented and still represents a major challenge for reproductive medicine. In fact, the proper execution of meiosis is essential for fertility, for maintaining the integrity of the genome, and for ensuring the normal development of the offspring. The main clinical consequences of meiotic defects are infertility and, probably, increased susceptibility to some types of germ-cell tumors. In the present work, we report and discuss data mainly concerning the beginning of meiosis in mammalian female germ cells, referring to such process in males only when pertinent. After a brief account of this process in mice and humans and an historical chronicle of the major hypotheses and progress in this topic, the most recent results are reviewed and discussed.
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Park, Zachory M., Abigail J. Sporer, Katherine Kraft, Krystal K. Lum, Edith Blackman, Ethan Belnap, Christopher M. Yellman, and Mark D. Rose. "Kar4, the yeast homolog of METTL14, is required for mRNA m6A methylation and meiosis." PLOS Genetics 19, no. 8 (August 21, 2023): e1010896. http://dx.doi.org/10.1371/journal.pgen.1010896.
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KAR4, the yeast homolog of the mammalian mRNA N6A-methyltransferase complex component METTL14, is required for two disparate developmental programs in Saccharomyces cerevisiae: mating and meiosis. To understand KAR4’s role in yeast mating and meiosis, we used a genetic screen to isolate 25 function-specific mutant alleles, which map to non-overlapping surfaces on a predicted structure of the Kar4 protein (Kar4p). Most of the mating-specific alleles (Mat-) abolish Kar4p’s interaction with the transcription factor Ste12p, indicating that Kar4p’s mating function is through Ste12p. In yeast, the mRNA methyltransferase complex was previously defined as comprising Ime4p (Kar4p’s paralog and the homolog of mammalian METTL3), Mum2p (homolog of mammalian WTAP), and Slz1p (MIS), but not Kar4p. During meiosis, Kar4p interacts with Ime4p, Mum2p, and Slz1p. Moreover, cells lacking Kar4p have highly reduced levels of mRNA methylation during meiosis indicating that Kar4p is a key member of the methyltransferase complex, as it is in humans. Analysis of kar4Δ/Δ and 7 meiosis-specific alleles (Mei-) revealed that Kar4p is required early in meiosis, before initiation of S-phase and meiotic recombination. High copy expression of the meiotic transcriptional activator IME1 rescued the defect of these Mei- alleles. Surprisingly, Kar4p was also found to be required at a second step for the completion of meiosis and sporulation. Over-expression of IME1 in kar4Δ/Δ permits pre-meiotic S-phase, but most cells remained arrested with a monopolar spindle. Analysis of the function-specific mutants revealed that roughly half became blocked after premeiotic DNA synthesis and did not sporulate (Spo-). Loss of Kar4p’s Spo function was suppressed by overexpression of RIM4, a meiotic translational regulator. Overexpression of IME1 and RIM4 together allowed sporulation of kar4Δ/Δ cells. Taken together, these data suggest that Kar4p regulates meiosis at multiple steps, presumably reflecting requirements for methylation in different stages of meiotic gene expression.
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Llano, Elena, and Alberto M. Pendás. "Synaptonemal Complex in Human Biology and Disease." Cells 12, no. 13 (June 25, 2023): 1718. http://dx.doi.org/10.3390/cells12131718.
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The synaptonemal complex (SC) is a meiosis-specific multiprotein complex that forms between homologous chromosomes during prophase of meiosis I. Upon assembly, the SC mediates the synapses of the homologous chromosomes, leading to the formation of bivalents, and physically supports the formation of programmed double-strand breaks (DSBs) and their subsequent repair and maturation into crossovers (COs), which are essential for genome haploidization. Defects in the assembly of the SC or in the function of the associated meiotic recombination machinery can lead to meiotic arrest and human infertility. The majority of proteins and complexes involved in these processes are exclusively expressed during meiosis or harbor meiosis-specific subunits, although some have dual functions in somatic DNA repair and meiosis. Consistent with their functions, aberrant expression and malfunctioning of these genes have been associated with cancer development. In this review, we focus on the significance of the SC and their meiotic-associated proteins in human fertility, as well as how human genetic variants encoding for these proteins affect the meiotic process and contribute to infertility and cancer development.
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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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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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Havekes, Francis W. J., J. Hans de Jong, and Christa Heyting. "Comparative analysis of female and male meiosis in three meiotic mutants of tomato." Genome 40, no. 6 (December 1, 1997): 879–86. http://dx.doi.org/10.1139/g97-814.
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Female meiosis was analysed in squash preparations of ovules from three meiotic mutants and wild-type plants of tomato. In the completely asynaptic mutant as6, chromosome pairing and chiasma formation were virtually absent in both sexes. In the partially asynaptic mutant asb, with intermediate levels of chromosome pairing at pachytene, there were a higher number of chiasmate chromosome arms in female meiosis than in male meiosis, whereas in the desynaptic mutant as5 there were normal levels of chromosome pairing at pachytene and a similar reduction in chiasma frequency in the two sexes. In wild-type tomato, we found slightly higher numbers of chiasmate chromosome arms in female meiosis than in male meiosis. We propose that the higher female chiasma frequencies in mutant asb and wild-type tomato result from a longer duration of female meiotic prophase. This would allow chromosomes more time to pair and recombine. It is possible that a longer duration of prophase I does not affect mutants as5 and as6, either because the meiotic defect acts before the pairing process begins (in as6) or because it acts at a later stage and involves chiasma maintenance (in as5).Key words: female meiosis, tomato, chiasma, mutant.
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Zeng, Xuemei, and William S. Saunders. "The Saccharomyces cerevisiae Centromere Protein Slk19p Is Required for Two Successive Divisions During Meiosis." Genetics 155, no. 2 (June 1, 2000): 577–87. http://dx.doi.org/10.1093/genetics/155.2.577.
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Abstract Meiotic cell division includes two separate and distinct types of chromosome segregation. In the first segregational event the sister chromatids remain attached at the centromere; in the second the chromatids are separated. The factors that control the order of chromosome segregation during meiosis have not yet been identified but are thought to be confined to the centromere region. We showed that the centromere protein Slk19p is required for the proper execution of meiosis in Saccharomyces cerevisiae. In its absence diploid cells skip meiosis I and execute meiosis II division. Inhibiting recombination does not correct this phenotype. Surprisingly, the initiation of recombination is apparently required for meiosis II division. Thus Slk19p appears to be part of the mechanism by which the centromere controls the order of meiotic divisions.
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Lo, Hsiao-Chi, Lihong Wan, Adam Rosebrock, Bruce Futcher, and Nancy M. Hollingsworth. "Cdc7-Dbf4 Regulates NDT80 Transcription as Well as Reductional Segregation during Budding Yeast Meiosis." Molecular Biology of the Cell 19, no. 11 (November 2008): 4956–67. http://dx.doi.org/10.1091/mbc.e08-07-0755.
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In budding yeast, as in other eukaryotes, the Cdc7 protein kinase is important for initiation of DNA synthesis in vegetative cells. In addition, Cdc7 has crucial meiotic functions: it facilitates premeiotic DNA replication, and it is essential for the initiation of recombination. This work uses a chemical genetic approach to demonstrate that Cdc7 kinase has additional roles in meiosis. First, Cdc7 allows expression of NDT80, a meiosis-specific transcriptional activator required for the induction of genes involved in exit from pachytene, meiotic progression, and spore formation. Second, Cdc7 is necessary for recruitment of monopolin to sister kinetochores, and it is necessary for the reductional segregation occurring at meiosis I. The use of the same kinase to regulate several distinct meiosis-specific processes may be important for the coordination of these processes during meiosis.
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Sharon, G., and G. Simchen. "Mixed segregation of chromosomes during single-division meiosis of Saccharomyces cerevisiae." Genetics 125, no. 3 (July 1, 1990): 475–85. http://dx.doi.org/10.1093/genetics/125.3.475.
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Abstract Normal meiosis consists of two consecutive cell divisions in which all the chromosomes behave in a concerted manner. Yeast cells homozygous for the mutation cdc5, however, may be directed through a single meiotic division of a novel type. Dyad analysis of a cdc5/cdc5 strain with centromere-linked markers on four different chromosomes has shown that, in these meioses, some chromosomes within a given cell segregate reductionally whereas others segregate equationally. The choice between the two types of segregation in these meioses is made individually by each chromosome pair. Different chromosome pairs exhibit different segregation tendencies. Similar results were obtained for cells homozygous for cdc14.
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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.
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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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Sears, D. D., J. H. Hegemann, J. H. Shero, and P. Hieter. "Cis-acting determinants affecting centromere function, sister-chromatid cohesion and reciprocal recombination during meiosis in Saccharomyces cerevisiae." Genetics 139, no. 3 (March 1, 1995): 1159–73. http://dx.doi.org/10.1093/genetics/139.3.1159.
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Abstract We have employed a system that utilizes homologous pairs of human DNA-derived yeast artificial chromosomes (YACs) as marker chromosomes to assess the specific role(s) of conserved centromere DNA elements (CDEI, CDEII and CDEIII) in meiotic chromosome disjunction fidelity. Thirteen different centromere (CEN) mutations were tested for their effects on meiotic centromere function. YACs containing a wild-type CEN DNA sequence segregate with high fidelity in meiosis I (99% normal segregation) and in meiosis II (96% normal segregation). YACs containing a 31-bp deletion mutation in centromere DNA element II (CDEII delta 31) in either a heterocentric (mutant/wild type), homocentric (mutant/mutant) or monosomic (mutant/--) YAC pair configuration exhibited high levels (16-28%) of precocious sister-chromatid segregation (PSS) and increased levels (1-6%) of nondisjunction meiosis I (NDI). YACs containing this mutation also exhibit high levels (21%) of meiosis II nondisjunction. Interestingly, significant alterations in homolog recombination frequency were observed in the exceptional PSS class of tetrads, suggesting unusual interactions between prematurely separated sister chromatids and their homologous nonsister chromatids. We also have assessed the meiotic segregation effects of rare gene conversion events occurring at sites located immediately adjacent to or distantly from the centromere region. Proximal gene conversion events were associated with extremely high levels (60%) of meiosis I segregation errors (including both PSS and NDI), whereas distal events had no apparent effect. Taken together, our results indicate a critical role for CDEII in meiosis and underscore the importance of maintaining sister-chromatid cohesion for proper recombination in meiotic prophase and for proper disjunction in meiosis I.
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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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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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Tyc, Katarzyna M., Rajiv C. McCoy, Karen Schindler, and Jinchuan Xing. "Mathematical modeling of human oocyte aneuploidy." Proceedings of the National Academy of Sciences 117, no. 19 (April 29, 2020): 10455–64. http://dx.doi.org/10.1073/pnas.1912853117.
Full textAbstract:
Aneuploidy is the leading contributor to pregnancy loss, congenital anomalies, and in vitro fertilization (IVF) failure in humans. Although most aneuploid conceptions are thought to originate from meiotic division errors in the female germline, quantitative studies that link the observed phenotypes to underlying error mechanisms are lacking. In this study, we developed a mathematical modeling framework to quantify the contribution of different mechanisms of erroneous chromosome segregation to the production of aneuploid eggs. Our model considers the probabilities of all possible chromosome gain/loss outcomes that arise from meiotic errors, such as nondisjunction (NDJ) in meiosis I and meiosis II, and premature separation of sister chromatids (PSSC) and reverse segregation (RS) in meiosis I. To understand the contributions of different meiotic errors, we fit our model to aneuploidy data from 11,157 blastocyst-stage embryos. Our best-fitting model captures several known features of female meiosis, for instance, the maternal age effect on PSSC. More importantly, our model reveals previously undescribed patterns, including an increased frequency of meiosis II errors among eggs affected by errors in meiosis I. This observation suggests that the occurrence of NDJ in meiosis II is associated with the ploidy status of an egg. We further demonstrate that the model can be used to identify IVF patients who produce an extreme number of aneuploid embryos. The dynamic nature of our mathematical model makes it a powerful tool both for understanding the relative contributions of mechanisms of chromosome missegregation in human female meiosis and for predicting the outcomes of assisted reproduction.
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Mitchell, A. P., and K. S. Bowdish. "Selection for early meiotic mutants in yeast." Genetics 131, no. 1 (May 1, 1992): 65–72. http://dx.doi.org/10.1093/genetics/131.1.65.
Full textAbstract:
Abstract In the yeast Saccharomyces cerevisiae, only a/alpha cells can enter meiosis; a and alpha cells cannot. Because a/alpha cells are typically diploid and a and alpha cells are typically haploid, this cell type restriction ensures that only diploid cells enter meiosis. Entry into meiosis is accompanied by an increase in expression of the IME1 gene; the IME1 product (IME1) then activates IME2 and other meiotic genes. We have found that IME1 expression is toxic to starved haploid cells, presumably because IME1 directs them into meiosis. IME1 toxicity is greater in rad52 mutants, in which meiotic recombination causes lethal damage. Suppressors of IME1 toxicity include recessive mutations in two genes, RIM11 and RIM16 (Regulator of Inducer of Meiosis), that are required for IME1 to activate IME2 expression. RIM11 maps near CIN4 on chromosome XIII.
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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.
Full textAbstract:
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.