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Yoshinori Watanabe - One of the best experts on this subject based on the ideXlab platform.
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analysis of schizosaccharomyces pombe Meiosis
CSH Protocols, 2017Co-Authors: Yoshinori Watanabe, Masayuki Yamamoto, Akira Yamashita, Takeshi SakunoAbstract:Meiosis is a specialized cell cycle that generates haploid gametes from diploid cells. The fission yeast Schizosaccharomyces pombe is one of the best model organisms for studying the regulatory mechanisms of Meiosis. S. pombe cells, which normally grow in the haploid state, diploidize by conjugation and initiate Meiosis when starved for nutrients, especially nitrogen. Following two rounds of chromosome segregation, spore formation takes place. The switch from mitosis to Meiosis is controlled by a kinase, Pat1, and an RNA-binding protein, Mei2. Mei2 is also a key factor for Meiosis-specific gene expression. Studies on S. pombe have offered insights into cell cycle regulation and chromosome segregation during Meiosis. Here we outline the current understanding of the molecular mechanisms regulating the initiation and progression of Meiosis, and introduce methods for the study of Meiosis in fission yeast.
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selective elimination of messenger rna prevents an incidence of untimely Meiosis
Nature, 2006Co-Authors: Yuriko Harigaya, Yuji Chikashige, Yoshinori Watanabe, Hirotsugu Tanaka, Soichiro Yamanaka, Kayoko Tanaka, Chihiro Tsutsumi, Yasushi HiraokaAbstract:Much remains unknown about the molecular regulation of Meiosis. Here we show that Meiosis-specific transcripts are selectively removed if expressed during vegetative growth in fission yeast. These messenger RNAs contain a cis-acting region—which we call the DSR—that confers this removal via binding to a YTH-family protein Mmi1. Loss of Mmi1 function severely impairs cell growth owing to the untimely expression of meiotic transcripts. Microarray analysis reveals that at least a dozen such Meiosis-specific transcripts are eliminated by the DSR–Mmi1 system. Mmi1 remains in the form of multiple nuclear foci during vegetative growth. At meiotic prophase these foci precipitate to a single focus, which coincides with the dot formed by the master Meiosis-regulator Mei2. A meiotic arrest due to the loss of the Mei2 dot is released by a reduction in Mmi1 activity. We propose that Mei2 turns off the DSR–Mmi1 system by sequestering Mmi1 to the dot and thereby secures stable expression of Meiosis-specific transcripts. All eukaryotic cells have the potential to undergo Meiosis — the type of cell division that reduces the chromosome number to produce reproductive cells or gametes — yet most never initiate it. So the discovery of a complex system to control Meiosis, rather than a simple 'start now' instruction, seems surprising. It involves selective elimination of any Meiosis-specific messenger RNAs that are generated in growing yeast cells. This may be a fail-safe mechanism against any unnecessary meiotic gene expression that could cause havoc in cells using the 'other' cell division mechanism, mitosis, to divide and multiply with a full set of chromosomes. A newly discovered control system regulates the eliminations of Meiosis-specific transcripts during mitosis, but allows their expression in Meiosis.
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pre meiotic s phase is linked to reductional chromosome segregation and recombination
Nature, 2001Co-Authors: Yoshinori Watanabe, Masayuki Yamamoto, Shihori Yokobayashi, Paul NurseAbstract:Meiosis is initiated from G1 of the cell cycle and is characterized by a pre-meiotic S phase followed by two successive nuclear divisions. The first of these, Meiosis I, differs from mitosis in having a reductional pattern of chromosome segregation. Here we show that Meiosis can be initiated from G2 in fission yeast cells by ectopically activating the Meiosis-inducing network. The subsequent Meiosis I occurs without a pre-meiotic S phase and with decreased recombination, and exhibits a mitotic pattern of equational chromosome segregation. The subsequent Meiosis II results in random chromosome segregation. This behaviour is similar to that observed in cells lacking the meiotic cohesin Rec8 (refs 3, 4), which becomes associated with chromosomes at G1/S phase, including the inner centromere, a region that is probably critical for sister-centromere orientation. If the expression of Rec8 is delayed to S phase/G2, then the centromeres behave equationally. We propose that the presence of Rec8 in chromatin is required at the pre-meiotic S phase to construct centromeres that behave reductionally and chromosome arms capable of a high level of recombination, and that this explains why Meiosis is initiated from G1 of the cell cycle.
Masayuki Yamamoto - One of the best experts on this subject based on the ideXlab platform.
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analysis of schizosaccharomyces pombe Meiosis
CSH Protocols, 2017Co-Authors: Yoshinori Watanabe, Masayuki Yamamoto, Akira Yamashita, Takeshi SakunoAbstract:Meiosis is a specialized cell cycle that generates haploid gametes from diploid cells. The fission yeast Schizosaccharomyces pombe is one of the best model organisms for studying the regulatory mechanisms of Meiosis. S. pombe cells, which normally grow in the haploid state, diploidize by conjugation and initiate Meiosis when starved for nutrients, especially nitrogen. Following two rounds of chromosome segregation, spore formation takes place. The switch from mitosis to Meiosis is controlled by a kinase, Pat1, and an RNA-binding protein, Mei2. Mei2 is also a key factor for Meiosis-specific gene expression. Studies on S. pombe have offered insights into cell cycle regulation and chromosome segregation during Meiosis. Here we outline the current understanding of the molecular mechanisms regulating the initiation and progression of Meiosis, and introduce methods for the study of Meiosis in fission yeast.
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pre meiotic s phase is linked to reductional chromosome segregation and recombination
Nature, 2001Co-Authors: Yoshinori Watanabe, Masayuki Yamamoto, Shihori Yokobayashi, Paul NurseAbstract:Meiosis is initiated from G1 of the cell cycle and is characterized by a pre-meiotic S phase followed by two successive nuclear divisions. The first of these, Meiosis I, differs from mitosis in having a reductional pattern of chromosome segregation. Here we show that Meiosis can be initiated from G2 in fission yeast cells by ectopically activating the Meiosis-inducing network. The subsequent Meiosis I occurs without a pre-meiotic S phase and with decreased recombination, and exhibits a mitotic pattern of equational chromosome segregation. The subsequent Meiosis II results in random chromosome segregation. This behaviour is similar to that observed in cells lacking the meiotic cohesin Rec8 (refs 3, 4), which becomes associated with chromosomes at G1/S phase, including the inner centromere, a region that is probably critical for sister-centromere orientation. If the expression of Rec8 is delayed to S phase/G2, then the centromeres behave equationally. We propose that the presence of Rec8 in chromatin is required at the pre-meiotic S phase to construct centromeres that behave reductionally and chromosome arms capable of a high level of recombination, and that this explains why Meiosis is initiated from G1 of the cell cycle.
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Regulation of Meiosis in Fission Yeast
Cell structure and function, 1996Co-Authors: Masayuki YamamotoAbstract:The fission yeast Schizosaccharomyces pombe initiates sexual development under starved conditions. Nutritional starvation decreases the level of intracellular cAMP. This decrease induces expression of the stell gene, which encodes a key transcription factor for genes required for mating and Meiosis. Mutational analyses of S. pombe genes encoding components of the cAMP cascade have shown that S. pombe cells stay in the mitotic cell cycle as long as the level of cAMP-dependent protein kinase activity is high, but are committed to mating and Meiosis if this activity is lowered. To initiate Meiosis in S. pombe, a protein kinase encoded by pat1 (also called ran1) should be inactivated. This inactivation results from deprivation of nutrients via a cascade of expression of genes including ste11. The mei2 gene encodes a factor indispensable for the initiation of Meiosis, and its expression is regulated directly by Ste11. If Pat1 kinase is intact, it blocks Mei2 function. Mei2 is required at two distinct stages of Meiosis, once prior to premeiotic DNA synthesis and then prior to the first meiotic division (Meiosis I). Mei2 is an RNA-binding protein, and forms a complex with a specific RNA species to promote Meiosis I. This RNA species, named meiRNA, is polyadenylated but is unlikely to encode a protein product. It is essential for Meiosis I, but not for either cell growth or premeiotic DNA synthesis. These observations unequivocally demonstrate that RNA plays a critical role in the control of Meiosis.
Katja Wassmann - One of the best experts on this subject based on the ideXlab platform.
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Kinetochore individualization in Meiosis I is required for centromeric cohesin removal in Meiosis II.
The EMBO journal, 2021Co-Authors: Yulia Gryaznova, Sandra A. Touati, Damien Cladiere, Leonor Keating, Warif El Yakoubi, Eulalie Buffin, Katja WassmannAbstract:Partitioning of the genome in Meiosis occurs through two highly specialized cell divisions, named Meiosis I and Meiosis II. Step-wise cohesin removal is required for chromosome segregation in Meiosis I, and sister chromatid segregation in Meiosis II. In Meiosis I, mono-oriented sister kinetochores appear as fused together when examined by high-resolution confocal microscopy, whereas they are clearly separated in Meiosis II, when attachments are bipolar. It has been proposed that bipolar tension applied by the spindle is responsible for the physical separation of sister kinetochores, removal of cohesin protection, and chromatid separation in Meiosis II. We show here that this is not the case, and initial separation of sister kinetochores occurs already in anaphase I independently of bipolar spindle forces applied on sister kinetochores, in mouse oocytes. This kinetochore individualization depends on separase cleavage activity. Crucially, without kinetochore individualization in Meiosis I, bivalents when present in Meiosis II oocytes separate into chromosomes and not sister chromatids. This shows that whether centromeric cohesin is removed or not is determined by the kinetochore structure prior to Meiosis II.
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Kinetochore individualization in Meiosis I is required for centromeric cohesin removal in Meiosis II
2020Co-Authors: Yulia Gryaznova, Damien Cladiere, Leonor Keating, Warif El Yakoubi, Eulalie Buffin, Sandra Touati, Katja WassmannAbstract:Partitioning of the genome in Meiosis occurs through two highly specialized cell divisions, named Meiosis I and II. Step-wise cohesin removal is required for chromosome segregation in Meiosis I, and sister chromatid segregation in Meiosis II. In Meiosis I, mono-oriented sister kinetochores appear as fused together when examined by high resolution confocal microscopy, whereas they are clearly separated in Meiosis II, when attachments are bipolar. It has been proposed that bipolar tension applied by the spindle is responsible for the physical separation of sister kinetochores, removal of cohesin protection and chromatid separation in Meiosis II. We show here that this is not the case, and initial separation of sister kinetochores occurs already in anaphase I, when attachments are still monopolar, and independently of pericentromeric Sgo2 removal. This kinetochore individualization occurs also independently of spindle forces applied on sister kinetochores, but importantly, depends on cleavage activity of Separase. Crucially, without kinetochore individualization by Separase in Meiosis I, oocytes separate bivalents into chromosomes and not sister chromatids in Meiosis II, showing that whether centromeric cohesin is removed or not is determined by the kinetochore structure prior to Meiosis II.
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Sister chromatid segregation in Meiosis II: Deprotection through phosphorylation
Cell Cycle, 2013Co-Authors: Katja WassmannAbstract:Meiotic divisions (Meiosis I and II) are specialized cell divisions to generate haploid gametes. The first meiotic division with the separation of chromosomes is named reductional division. The second division, which takes place immediately after Meiosis I without intervening S-phase, is equational, with the separation of sister chromatids, similar to mitosis. This meiotic segregation pattern requires the two-step removal of the cohesin complex holding sister chromatids together: cohesin is removed from chromosome arms that have been subjected to homologous recombination in Meiosis I and from the centromere region in Meiosis II. Cohesin in the centromere region is protected from removal in Meiosis I, but this protection has to be removeddeprotectedfor sister chromatid segregation in Meiosis II. Whereas the mechanisms of cohesin protection are quite well understood, the mechanisms of deprotection have been largely unknown until recently. In this review I summarize our current knowledge on cohesin deprotection.
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The PP2A Inhibitor I2PP2A Is Essential for Sister Chromatid Segregation in Oocyte Meiosis II
Current Biology - CB, 2013Co-Authors: Jean-philippe Chambon, Sandra A. Touati, Stephane Berneau, Damien Cladiere, Celine Hebras, Rachel Groeme, Alex Mcdougall, Katja WassmannAbstract:Haploid gametes are generated through two consecutive meiotic divisions, with the segregation of chromosome pairs in Meiosis 1 and sister chromatids in Meiosis II. Separase-mediated stepwise removal of cohesion, first from chromosome arms and later from the centromere region, is a prerequisite for maintaining sister chromatids together until their separation in Meiosis II [1]. In all model organisms, centromeric cohesin is protected from separase-dependent removal in Meiosis 1 through the activity of PP2A-B56 phosphatase, which is recruited to centromeres by shugoshin/MEI-S332 (Sgo) [2-5]. How this protection of centromeric cohesin is removed in Meiosis 11 is not entirely clear; we find that all the PP2A subunits remain colocalized with the cohesin subunit Rec8 at the centromere of metaphase II chromosomes. Here, we show that sister chromatid separation in oocytes depends on a PP2A inhibitor, namely I2PP2A. I2PP2A colocalizes with the PP2A enzyme at centromeres at metaphase 11, independently of bipolar attachment. When I2PP2A is depleted, sister chromatids fail to segregate during Meiosis II. Our findings demonstrate that in oocytes I2PP2A is essential for faithful sister chromatid segregation by mediating deprotection of centromeric cohesin in Meiosis II.
Nori Kurata - One of the best experts on this subject based on the ideXlab platform.
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the novel gene homologous pairing aberration in rice Meiosis1 of rice encodes a putative coiled coil protein required for homologous chromosome pairing in Meiosis
The Plant Cell, 2004Co-Authors: Ken-ichi Nonomura, Mutsuko Nakano, Mitsugu Eiguchi, Nori Kurata, Toshiyuki Fukuda, Akio Miyao, Hirohiko HirochikaAbstract:We have identified and characterized a novel gene, PAIR1 (HOMOLOGOUS PAIRING ABERRATION IN RICE Meiosis1), required for homologous chromosome pairing and cytokinesis in male and female meiocytes of rice (Oryza sativa). The pair1 mutation, tagged by the endogenous retrotransposon Tos17, exhibited Meiosis-specific defects and resulted in complete sterility in male and female gametes. The PAIR1 gene encodes a 492–amino acid protein, which contains putative coiled-coil motifs in the middle, two basic regions at both termini, and a potential nuclear localization signal at the C terminus. Expression of the PAIR1 gene was detected in the early stages of flower development, in which the majority of the sporocytes had not entered Meiosis. During prophase I of the pair1 meiocyte, all the chromosomes became entangled to form a compact sphere adhered to a nucleolus, and homologous pairing failed. At anaphase I and telophase I, chromosome nondisjunction and degenerated spindle formation resulted in multiple uneven spore production. However, chromosomal fragmentation frequent in plant meiotic mutants was never observed in all of the pair1 meiocytes. These observations clarify that the PAIR1 protein plays an essential role in establishment of homologous chromosome pairing in rice Meiosis.
Terry J Hassold - One of the best experts on this subject based on the ideXlab platform.
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Counting cross-overs: characterizing meiotic recombination in mammals
Human molecular genetics, 2000Co-Authors: Terry J Hassold, Stephanie L. Sherman, Patricia A. HuntAbstract:Until recently, most of our understanding of meiotic recombination has come from studies of lower eukaryotes. However, over the past few years several components of the mammalian meiotic recombination pathway have been identified, and new molecular and cytological approaches to the analysis of mammalian Meiosis have been developed. In this review, we discuss recent advances in three areas: the application of new techniques to study genome-wide levels of recombination in individual meioses; studies analyzing temporal aspects of the mammalian recombination pathway; and studies linking the genesis of human trisomies to alterations in meiotic exchange patterns.
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centromeric genotyping and direct analysis of nondisjunction in humans down syndrome
Chromosoma, 1998Co-Authors: Joseph She, Stephanie L Sherma, Terry J HassoldAbstract:In species with chiasmate meioses, alterations in genetic recombination are an important correlate of nondisjunction. In general, these alterations fall into one of two categories: either homologous chromosomes fail to pair and/or recombine at Meiosis I, or they are united by chiasmata that are suboptimally positioned. Recent studies of human nondisjunction suggest that these relationships apply to our species as well. However, methodological limitations in human genetic mapping have made it difficult to determine whether the important determinant(s) in human nondisjunction is absent recombination, altered recombination, or both. In the present report, we describe somatic cell hybrid studies of chromosome 21 nondisjunction aimed at overcoming this limitation. By using hybrids to “capture” individual chromosomes 21 of the proband and parent of origin of trisomy, it is possible to identify complementary recombinant meiotic products, and thereby to uncover crossovers that cannot be detected by conventional mapping methods. In the present report, we summarize studies of 23 cases. Our results indicate that recombination in proximal 21q is infrequent in trisomy-generating meioses and that, in a proportion of the meioses, recombination does not occur anywhere on 21q. Thus, our observations indicate that failure to recombine is responsible for a proportion of trisomy 21 cases.
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recombination and maternal age dependent nondisjunction molecular studies of trisomy 16
American Journal of Human Genetics, 1995Co-Authors: Terry J Hassold, M Merrill, K Adkins, Sallie Freema, Stephanie L ShermaAbstract:Trisomy 16 is the most common human trisomy, occurring in {ge} 1% of all clinically recognized pregnancies. It is thought to be completely dependent on maternal age and thus provides a useful model for studying the association of increasing maternal age and nondisjunction. We have been conducting a study to determine the parent and meiotic stage of origin of trisorny 16 and the possible association of nondisjunction and aberrant recombination. In the present report, we summarize our observations on 62 spontaneous abortions with trisomy 16. All trisomies were maternally derived, and in virtually all the error occurred at Meiosis I. In studies of genetic recombination, we observed a highly significant reduction in recombination in the trisomy-generating meioses by comparison with normal female meioses. However, most cases of trisomy 16 had at least one detectable crossover between the nondisjoined chromosomes, indicating that it is reduced-and not absent-recombination that is the important predisposing factor. Additionally, our data indicate an altered distribution of crossing-over in trisomy 16, as we rarely observed crossovers in the proximal long and short arms. Thus, it may be that, at least for trisomy 16, the association between maternal age and trisomy is due to diminished recombination, particularly inmore » the proximal regions of the chromosome. 34 refs., 2 figs., 2 tabs.« less
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non disjunction of chromosome 21 in maternal Meiosis i evidence for a maternal age dependent mechanism involving reduced recombination
Human Molecular Genetics, 1994Co-Authors: Stephanie L. Sherman, Michael B. Petersen, Sallie B Freeman, Dorothy Pettay, Lisa Taft, Jane Hersey, Merete Frantzen, Margareta Mikkelsen, Terry J HassoldAbstract:Over 300 cases of trisomy 21 were analyzed to characterize the causes of maternal non-disjunction and to evaluate the basis for maternal age-dependent trisomy 21. We confirmed the observation that recombination along 21q is reduced among non-disjoined chromosomes 21 and further demonstrated that the alterations in recombination are restricted to Meiosis I origin. Analysis of the crossover distribution indicates that reduction in recombination is not due simply to failure of pairing and/or absence of recombination in a proportion of cases. Instead, we observed an increase in both zero- and one-exchange events among trisomy 21-generating meioses suggesting that an overall reduction in recombination may be the underlying cause of non-disjunction. Lastly, we observed an age-related reduction in recombination among the Meiosis I cases, with older women having less recombination along 21q than younger women. Thus, reduced genetic recombination may be responsible, at least in part, for the association between advancing maternal age and trisomy 21.
