Relevant bibliographies by topics / Meiosis

Academic literature on the topic 'Meiosis'

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Published: 4 June 2021
Last updated: 7 July 2024

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Journal articles on the topic "Meiosis"

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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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2

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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Dissertations / Theses on the topic "Meiosis"

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Canales, C. "Characterisation of extra sporogenous cells (ESP) : an avbidopsis gene required for another development." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365861.

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Phizicky, David V. (David Vincent). "Mechanisms preventing DNA replication between Meiosis I and Meiosis II." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/117786.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2018.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged student-submitted from PDF version of thesis.
Includes bibliographical references.
The vast majority of multicellular organisms reproduce using sexual reproduction, which requires the production of haploid gametes. These gametes are produced by meiosis, a specialized cell division during which one round of DNA replication is followed by two rounds of chromosome segregation, Meiosis I (MI) and Meiosis II (MII). This imbalance between rounds of DNA replication and chromosome segregation causes diploid cells to produce haploid gametes. In contrast, mitotically-dividing cells maintain ploidy by alternating between rounds of replication and segregation. It is unclear how meiosis accomplishes two sequential chromosome segregation events without an intervening round of DNA replication. In mitotic cells, both DNA replication and chromosome segregation are regulated by oscillations of cyclin-dependent kinase (CDK) activity. Both events initiate during G1 due to the associated low CDK-activity state, and both events are completed later in the cell cycle due to increased CDK activity. During meiosis, uncoupling replication and segregation presents a unique problem. After completion of MI, CDK activity decreases and then increases to drive MII chromosome segregation. However, DNA replication must remain inhibited between MI and MII. Given that an oscillation of CDK activity is sufficient for genome re-duplication in mitotic cells, I sought to understand how meiotic cells prevent DNA replication while resetting the chromosome segregation program. In this thesis, I show that meiotic cells inhibit two distinct steps of DNA replication: (1) loading of the replicative helicase onto replication origins, and (2) activation of the replicative helicase. CDK and the meiosis-specific kinase Ime2 cooperatively inhibit helicase loading during the meiotic divisions, and their simultaneous inhibition causes inappropriate helicase reloading. Further studies of Ime2 revealed two mechanisms by which it inhibits this process. First, I showed that Ime2-phosphorylation of the helicase directly inhibits its loading onto origins. Second, Ime2 cooperated with CDK to transcriptionally and proteolytically repress Cdc6, an essential helicase-loading protein. In addition, I found that meiotic cells use CDK and the polo-like kinase Cdc5 to promote degradation of Sld2, an essential helicase-activation protein. Together, these data demonstrate that multiple kinases inhibit both helicase loading and activation between MI and MII, thereby ensuring a reduction in ploidy.
by David V. Phizicky.
Ph. D.
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Marcet, Ortega Marina. "Surveillance mechanisms in mammalian meiosis." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/387429.

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Per tal de protegir les cèl·lules germinals de sofrir inestabilitat genòmica, diversos mecanismes de control s’encarreguen de que la progressió de la meiosis sigui correcte. En mamífers, els espermatòcits que presenten defectes de recombinació o de la formació de la vesícula sexual pateixen un bloqueig a l’estadi de paquitè. Estudis previs del nostre laboratori descriuen que la via complex MRE11-ATM-CHK2 activa l’arrest dependent de recombinació en presència de trencaments de doble cadena (DSBs) no reparats. L’objectiu d’aquest treball ha estat identificar si els membres de la família p53, els quals són possibles substrats de ATM i CHK2, participen en l’activació del arrest depenent de recombinació. En una aproximació genètica, hem obtingut ratolins doble mutants portadors d’una mutació de un membre de la família p53 (p53, Tap63 o p73) en un fons defectiu per Trip13. La mutació de Trip13 causa defectes de recombinació, el qual activa l’arrest depenent de recombinació en els espermatòcits a l’estadi de paquitè. Per tant, hem estudiat com l’absència d’algun membre de la família p53 afectava aquest fenotip d’arrest el espermatòcits Trip13mod/mod. Els nostres resultats demostren que tant la deficiència de p53 com Tap63, però no p73, permeten que els espermatòcits progressin més enllà i arribin a l’estadi de paquitè tardà tot i acumular nombrosos DSBs no reparats. Addicionalment, l’absència de p53 o Tap63 resulta en una disminució del nombre d’espermatòcits apoptòtics a l’estadi de paquitè primerenc. Així, els nostres resultats indiquen que p53 i TAp63 són responsables d’activar l’arrest dependent de recombinació en els espermatòcits de ratolí. Tot i així, els espermatòcits doble mutants encara presenten un bloqueig a l’estadi de paquitè. Per tal d’estudiar si els espermatòcits doble mutants arresten a causa de l’activació de l’arrest depenent de la correcta formació de la vesícula sexual, hem analitzat la funcionalitat del MSCI en els mutants Trip13. Per tant, el fet de saltar-se l’arrest dependent de recombinació ens ha permès elucidar el paper de TRIP13 en el silenciament meiòtic, de manera que al fallar la vesícula sexual es desencadena l’apoptosi i bloqueig dels mutants Trip13. Aquests resultats infereixen que el bloqueig depenent de recombinació i el depenent de la correcta formació de la vesícula sexual, són mecanismes que s’activen per mecanismes genèticament separats. A partir de l’observació que TRIP13 és necessari per implementar el silenciament del MSCI, he dut a terme un anàlisis exhaustiu de la transcripció en els mutants de Trip13. Els nostres resultats de marcatge de RNA amb EU i activació de la RNA polimerasa II fosforilada (S2) suggereixen que la expressió de RNA en els espermatòcits mutants per Trip13 es troba incrementada en els estadis inicials de la meiosis. Addicionalment, la seqüenciació del RNA ha permès observar que els gens dels cromosomes sexuals i gens pre-meiòtics es troben sobre expressats en els mutants de Trip13, suggerint que TRIP13 és necessari per mantenir l’expressió d’aquests gens a nivells baixos. En conjunt, els resultats presentats en aquest treball contribueixen a entendre com els mecanismes de control regulen diversos passes crucials de la progressió de la profase meiòtica en els espermatòcits de mamífer.
In order to protect germinal cells from genomic instability, surveillance mechanisms ensure that meiosis occurs properly. In mammals, spermatocytes that display recombination or sex body defects experience an arrest at pachytene stage. Previous studies from our lab described that the MRE11 complex-ATM-CHK2 pathway activates the recombination-dependent arrest in the presence of unrepaired double strand breaks (DSBs). In this work we aimed to identify if p53 family members, which are putative targets of ATM and CHK2, participate in the activation of the recombination-dependent arrest. As a genetic approach, we bred double mutant mice carrying a mutation of a member of the p53 family (p53, TAp63, p73) in a Trip13 defective background. Trip13 mutation causes recombination defects, which activate the recombination-dependent arrest in pachytene-stage spermatocytes. Thus, we studied how the absence of p53 family members affected the arrest phenotype of Trip13mod/mod spermatocytes. Our data showed that p53 and TAp63 deficiency, but not p73, allowed spermatocytes to progress further into late pachynema, despite accumulating numerous unrepaired DBSs. In addition, lack of p53 or TAp63 resulted in a decrease of apoptotic spermatocytes at early pachytene stage. Therefore, our results indicate that p53 and TAp63 are responsible to activate the recombination-dependent arrest in mouse spermatocytes. Even though, double mutant spermatocytes still arrested at pachytene stage. To study if double mutant spermatocytes were arresting due to the activation of the sex body deficient arrest we analyzed MSCI functionality in Trip13 mutants. Thus, by bypassing the recombination-dependent arrest has allowed us to elucidate a role for TRIP13 protein in meiotic silencing, which consequently triggers apoptosis in double mutants at late pachytene stage due to sex body impairment. These results infer that the recombination-dependent and the sex-body deficient arrest are activated by two genetically separated mechanisms. From the observation that TRIP13 is required to implement MSCI silencing, we performed an exhaustive analysis of transcription in Trip13 mutants. Our results suggested that RNA expression in Trip13 mutants was increased in early meiotic stage spermatocytes, assessed by EU-labeling RNA and phosphorylated(S2)-RNA polymerase II. Moreover, RNA sequencing data highlighted the observation that sex chromosome genes and pre-meiotic genes are overexpressed in Trip13 mutants, suggesting that TRIP13 is required to maintain the expression of these genes at low levels. Overall, the data presented in this work contributes to the understanding on how surveillance mechanisms control several crucial steps of meiotic prophase progression in mammalian spermatocytes.
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Fabig, Gunar. "Dynamic and ultrastructural characterization of chromosome segregation in C. elegans male meiosis." Technische Universität Dresden, 2018. https://tud.qucosa.de/id/qucosa%3A32727.

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The production of germ cells is an essential process in all sexually reproducing eukaryotes. During male meiosis, four haploid sperm cells are formed from one primary spermatocyte, thereby undergoing two consecutive cell divisions after only one round of chromosome duplication. This process was studied in the nematode Caenorhabditis elegans, as this model organism offers a number of experimental advantages to simultaneously analyze spindle dynamics and ultrastructure. The worm is easy to cultivate, completely sequenced and numerous mutants are available, the worm is small and thus ideal for light and electron microscopic investigations, and the transparent body allows live-cell imaging within living animals. Importantly, meiotic spindles in C. elegans males are organized by centrosomes and show a lagging X-chromosome, which is always segregated after the autosomes have been partitioned to the newly forming secondary spermatocytes. The aim of this thesis was to systematically investigate this characteristic feature of chromosome segregation in male meiotic spindles. For that, spindle dynamics in the first and second meiotic division was analyzed with fluorescence light microscopy. Furthermore, the spindle ultrastructure was investigated in spindles of various stages of meiosis I using electron tomography. Light microscopy revealed a shortening of the distance between centrosomes and chromosomes (anaphase A) and an increase in the pole-to-pole distance (anaphase B). Moreover, spindles in male meiosis I and II showed differences in certain aspects of spindle dynamics. In addition it was demonstrated that spindles in metaphase II in the presence of a single X-chromosome were shorter compared to spindles without the X-chromosome. In addition, it was found that the process of aging had an impact on spindle length in both metaphase I and II. By manipulating the number of unpaired chromosomes, it could be demonstrated that the lagging behavior of univalent chromosomes is caused by the incapability of pairing in meiotic prophase. After performing a quantitative analysis of the light microscopic data it was further shown that a dynamic microtubule bundle is connecting the X-chromosome to the spindle poles. Using laser microsurgery it could be demonstrated that this bundle exerts a pulling force to the univalent chromosome throughout anaphase. Unexpectedly, electron tomography showed that anaphase-type movements of the autosomes were not accompanied by a shortening of the kinetochore microtubules. Instead, three findings indicated a shortening of the centrosome-chromosome distance itself: (1) upon anaphase onset, tension is released on the beforehand stretched autosomes; (2) centrosomes shrink in preparation for meiosis II and (3) the attachment angle of end-on microtubules changes. Interestingly, microtubules connecting the X-chromosome to the spindle poles showed a high curvature around the kinetochore region of the X-chromosome, suggesting an involvement of motor proteins in the process of segregation. Taken together, this thesis gives the first detailed quantitative analysis of spindle dynamics and architecture during male meiosis in the nematode C. elegans. This wild-type data will serve as a basis for future mutant analyses and should help to further understand the complex dynamic and ultrastructural aspects of spindle organization in the meiotic divisions in C. elegans males.
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Connor, Colette. "Investigating the role of Cdc14 in the regulation of the meiosis I to meiosis II transition." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/21086.

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Meiosis is a specialized cell division that produces haploid gametes from a diploid progenitor cell. It consists of one round of DNA replication followed by two consecutive rounds of chromosome segregation. Homologous chromosomes segregate in meiosis I and sister chromatids segregate in meiosis II. Failure to correctly regulate meiosis can result in aneuploidy, where daughter cells inherit an incorrect number of chromosomes. Aneuploidy is usually poorly tolerated in eukaryotes, and is associated with infertility, miscarriages and birth defects. At the meiosis I to meiosis II transition, DNA replication does not occur between chromosome segregation steps despite the need for Spindle Pole Bodies (SPBs) to be re-licensed in order to build meiosis II spindles. The mechanisms that make this distinction are not yet known. In budding yeast, the protein phosphatase Cdc14 is essential for the progression of cells into meiosis II. Cdc14 is sequestered for the majority of the cell cycle in the nucleolus by the inhibitor Cfi1/Net, and is only released in anaphase. We have observed Cdc14 localizing to and interacting with SPB components when nucleolar sequestration is inhibited. Through fluorescence microscopy and EM analysis, we have determined that Cdc14 is required for the re-duplication of SPBs after meiosis I. Our data implies a role for Cdc14 in the phospho-regulation of SPB half-bridge component Sfi1. Cdc14 is therefore essential for the relicensing of SPB duplication, a crucial step necessary to ensure accurate chromosome segregation in meiosis.
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Igea, Fernández Ana. "CPEB4 replaces CPEB1 to complete meiosis." Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/22687.

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In vertebrate oocytes, meiotic progression is driven by the sequential translational activation of maternal messenger RNAs stored in the cytoplasm. This activation is mainly induced by the cytoplasmic elongation of their poly(A) tails, which is mediated by the cytoplasmic polyadenylation element (CPE) present in their 3’ untranslated regions (3´ UTRs). Sequential, phase-specific translation of these maternal mRNAs is required to complete the two meiotic divisions. Although the earlier polyadenylation events in prophase I and metaphase I are driven by the CPE-binding protein 1 (CPEB1), 90% of this protein is degraded by the anaphase promoting complex in the first meiotic division. The low levels of CPEB1 during interkinesis and in metaphase II raise the question of how the cytoplasmic polyadenylation required for the second meiotic division is achieved. In this work, we demonstrate that CPEB1 activates the translation of the maternal mRNA encoding CPEB4, which, in turn, recruits the cytoplasmic poly(A) polymerase GLD2 to “late” CPE-regulated mRNAs driving the transition from metaphase I to metaphase II, and, therefore, replacing CPEB1 for “late” meiosis polyadenylation.
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Çetin, Bülent. "Chromosome segregation in mitosis and meiosis." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669990.

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Rattani, Ahmed Anwer Ali. "Regulation of anaphase in mammalian meiosis." Thesis, University of Oxford, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.639733.

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Missegregation of chromosomes during meiosis leads to formation of aneuploid eggs. Estimates suggest that in humans, about 10-30% of fertilised eggs and one-third of all miscarriages are aneuploid. Accurate chromosome segregation depends on the coordination between stepwise cohesion resolution and attachments of homologous chromosomes through kinetochores to microtubules, emanating from opposite poles of the cell. The Spindle Assembly Checkpoint (SAC) monitors microtubule-kinetochore attachments and prevents resolution of cohesin complexes by inhibiting the ubiquitin ligase APC/Ccdc2o until all aberrant microtubule-kinetochore attachments have been rectified by an Aurora Kinase-dependent error correction machinery. During meiosis, these pathways work in seamless coordination to achieve balanced segregation of the genome at the first meiotic division. The cross-talk between different cell cycle pathways requires members with shared affiliations. During my DPhil studies, I worked on understanding the role of two such proteins, namely Bub1 (budding uninhibited by benzimidazoles 1) and Sgol2 (Shugoshin-like protein 2) in mouse oocytes. During the first meiotic division, Bub1 maintains the SAC, and through its kinase activity, Bub1 recruits Sgol2 to kinetochores to protect centromeric cohesion. This recruitment is essential for two rounds of chromosomes segregation in meiosis. Thus, Bub1localisation at kineto chores can coordinate the timing of anaphase with the centromeric cohesion protection.
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Winters, Tristan. "The role of STAG3 in mammalian meiosis." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2018. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-233399.

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The cohesin complex is essential for mitosis and meiosis. The specific meiotic roles of individual cohesin proteins are incompletely understood. We report in vivo functions of the only meiosis-specific STAG component of cohesin, STAG3. Newly generated STAG3-deficient mice of both sexes are sterile with meiotic arrest. In these mice, meiotic chromosome architecture is severely disrupted as no bona fide axial elements (AE) form and homologous chromosomes do not synapse. Axial element protein SYCP3 forms dot-like structures, many partially overlapping with centromeres. Asynapsis marker HORMAD1 is diffusely distributed throughout the chromatin, and SYCP1, which normally marks synapsed axes, is largely absent. Centromeric and telomeric sister chromatid cohesion are impaired. Centromere and telomere clustering occurs in the absence of STAG3, and telomere structure is not severely affected. Other cohesin proteins are present, localize throughout the STAG3-devoid chromatin, and form complexes with cohesin SMC1β. No other deficiency in a single meiosis-specific cohesin causes a phenotype as drastic as STAG3 deficiency. STAG3 emerges as the key STAG cohesin involved in major functions of meiotic cohesin.
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Fernandes, Joiselle Blanche. "Identification et caractérisation fonctionnelle de gènes contrôlant la fréquence de crossovers méiotiques." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS303/document.

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Les crossing-overs (CO) sont issus d’échange réciproque de matériel génétique entre les chromosomes homologues. Les COs produisent de la diversité génétique et sont essentiels chez la plupart des eucaryotes, pour la distribution équilibrée des chromosomes lors de la méiose. Malgré leur importance, et un large excès de précurseurs moléculaires, le nombre de CO est très limité dans la grande majorité des espèces (Typiquement 1 à 4 par paire de chromosomes). Cela suggère que les COs sont étroitement régulés, mais les mécanismes sous-jacents sont mal connus. Pour identifier les gènes qui limitent la formation des CO, l’équipe a mené un crible génétique chez Arabidopsis thaliana. Ces travaux ont mené à l’identification de plusieurs facteurs anti-CO, définissant trois voies : (i) L’hélicase FANCM et ses co-facteurs ; (ii) L’AAA-ATPase FIDGETIN-LIKE-1 (FIGL1) ; (iii) Le complexe RECQ4-Topoisomerase 3α-RMI1.Le premier objectif de ma thèse est d’explorer les relations entre ces trois voies en s’attachant aux questions suivantes ; (1) Jusqu’où peut-on augmenter la recombinaison en combinant les mutations dans FANCM, FIGL1 et RECQ4 ? Nous avons montré que la plus forte augmentation de recombinaison était obtenue dans recq4 figl1, atteignant 7,5 fois la fréquence du sauvage en moyenne sur le génome. (2) Quel est la distribution de ces extra-COs ? L’augmentation de recombinaison n’est pas homogène le long du génome : Les fréquences de CO augmente fortement des centromères vers les télomères, avec les plus hautes fréquences observées dans les régions distales. (3) La modification des fréquences de recombinaison est-elle identique lors des méioses mâles et femelle ? Chez le sauvage, la fréquence de recombinaison est plus élevée lors de la méiose mâle que femelle. Au contraire, la recombinaison femelle devient plus élevée que la recombinaison mâle chez les mutants recq4 et recq4 figl1. Ceci suggère que des contraintes qui s’appliquent sur la formation des CO lors de la méiose femelle sont relâchées chez ces mutants. En poursuivant le crible génétique, un nouveau mutant hyper-recombinant a été identifié. Le second objectif de ma thèse fut d’identifier et de caractériser fonctionnellement le gène correspondant. Une cartographie génétique et des études d’interactions protéine-protéine, ont mené à l’identification d’un facteur qui interagit directement avec FIGL1 et semble former un complexe conservé depuis les plantes jusqu’au mammifères. Nous avons baptisé cette protéine FLIP (Fidgetin-like-1 interacting protein). Les fréquences de recombinaisons sont augmentées dans flip-1, confirmant que FLIP1 limite la formation des COs. Des études d’épistasie ont montré que FLIP et FIGL1 agissent dans la même voie. De plus les protéines FIGL1/FLIP d’Arabidopsis ou humaine, interagissent avec RAD51 et DMC1, les deux protéines qui catalyse une étape clef de la recombinaison, l’invasion d’un ADN homologue. Finalement, dans flip comme dans figl1, la dynamique de DMC1 est modifiée. Nous proposons donc un modèle dans lequel le complexe FLIP-FIGL1 régule négativement l’activité de RAD51/DMC1 pour limiter la formation des COs. L’étude du complexe conservé FLIP-FIGL1 a mis en évidence un nouveau mode de régulation de la recombinaison, qui agit vraisemblablement à l’étape clé de l’échange de brin homologue. De plus, l’augmentation des CO sans précédent obtenues chez recq4 figl1 peut être d’un grand intérêt pour l’amélioration des plantes en permettant de diversité de nouvelles combinaisons alléliques
Meiotic crossovers (CO) are formed by reciprocal exchange of genetic material between the homologous chromosomes. CO generate genetic diversity and are essential for the proper segregation of chromosomes during meiosis in most eukaryotes. Despite their significance and a large excess of CO precursors, CO number is very low in vast majority of species (typically one to three per chromosome pair). This indicates that COs are tightly regulated but the underlying mechanisms of this limit remain elusive. In order to identify genes that limit COs, a genetic screen was performed in Arabidopsis thaliana. This led to the identification and characterization of several anti-CO factors belonging to three different pathways: (i) The FANCM helicase and its cofactors (ii) The AAA-ATPase FIDGETIN-LIKE-1 (FIGL1) (iii) The RECQ4 -Topoisomerase 3α-RMI1 complex. The first objective was to understand the functional relationship between these three pathways and to address following questions: (1) how far can we increase recombination when combining mutations in FANCM, FIGL1 and RECQ4? We show that the highest increase in recombination was obtained in figl1 recq4, reaching to 7.5 fold the wild type level, on average genome wide. (2) How is the distribution of recombination events genome wide in mutants? The increased CO frequency in the mutants was not uniform throughout the genome. CO frequency rises from the centromere to telomeres, with distal intervals having highest COs (3) is the recombination frequency increase same in both male and female? In Arabidopsis wild type, male has higher recombination than female meiosis. In contrast, in recq4 and recq4 figl1, female recombination was higher than male. This suggests that certain constraints that apply to CO formation in wild type females are relieved in the mutant. By continuing the same genetic screen, a novel anti-CO mutant was identified. The second objective was to identify and functionally characterize the corresponding gene. Genetic mapping and protein interaction studies led to the identification of a factor that directly interacts with FIGL1 and appears to form a conserved complex both in Arabidopsis and humans. Hence, the factor was named FLIP (Fidgetin-like-1 interacting protein). Recombination frequency is increased in flip, confirming that FLIP limit COs. Epistasis studies showed that FLIP and FIGL1 act in same pathway. Further, FIGL1/FLIP proteins of Arabidopsis and humans directly interact with the recombinases RAD51 and DMC1 which catalyze a crucial step of homologous recombination, the inter homolog strand invasion. In addition flip like figl1 modifies dynamics of DMC1. We thus propose a model wherein the FLIP-FIGL1 complex negatively regulates RAD51/DMC1 to limit CO formation. Studying the conserved FIGL1-FLIP complex led to the identification of a novel mode of regulation of recombination, that likely acts at the key step of homologous strand invasion. Further the unprecedented level of CO increase in recq4figl1 in hybrids could be of great interest for crop improvement, allowing the production of novel allele combinations
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Books on the topic "Meiosis"

1

B, Moens Peter, ed. Meiosis. Orlando: Academic Press, 1987.

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John, Bernard. Meiosis. Cambridge [England]: Cambridge University Press, 1990.

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Keeney, Scott, ed. Meiosis. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-527-5.

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Stuart, David T., ed. Meiosis. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6340-9.

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Keeney, Scott, ed. Meiosis. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-103-5.

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Ricardo, Benavente, and Volff Jean-Nicolas, eds. Meiosis. Basel: Karger, 2009.

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Meiosis. Dordrecht: Humana Press, 2009.

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John, B. Meiosis. Cambridge: Cambridge University Press, 1990.

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Pawlowski, Wojciech P., Mathilde Grelon, and Susan Armstrong, eds. Plant Meiosis. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-333-6.

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Pradillo, Mónica, and Stefan Heckmann, eds. Plant Meiosis. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4939-9818-0.

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Book chapters on the topic "Meiosis"

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Pryce, D. W., and R. J. McFarlane. "The Meiotic Recombination Hotspots of Schizosaccharomyces pombe." In Meiosis, 1–13. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000166614.

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Muyt, A. De, R. Mercier, C. Mézard, and M. Grelon. "Meiotic Recombination and Crossovers in Plants." In Meiosis, 14–25. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000166616.

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Martinez-Perez, E. "Meiosis in Cereal Crops: the Grasses are Back." In Meiosis, 26–42. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000166617.

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Zetka, M. "Homologue Pairing, Recombination and Segregation in Caenorhabditis elegans." In Meiosis, 43–55. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000166618.

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McKee, B. D. "Homolog Pairing and Segregation in Drosophila Meiosis." In Meiosis, 56–68. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000166619.

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Yang, F., and P. J. Wang. "The Mammalian Synaptonemal Complex: A Scaffold and Beyond." In Meiosis, 69–80. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000166620.

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Alsheimer, M. "The Dance Floor of Meiosis: Evolutionary Conservation of Nuclear Envelope Attachment and Dynamics of Meiotic Telomeres." In Meiosis, 81–93. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000166621.

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Suja, J. A., and J. L. Barbero. "Cohesin Complexes and Sister Chromatid Cohesion in Mammalian Meiosis." In Meiosis, 94–116. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000166622.

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Khil, P. P., and R. D. Camerini-Otero. "Variation in Patterns of Human Meiotic Recombination." In Meiosis, 117–27. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000166623.

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Garcia-Cruz, R., I. Roig, and M. Garcia Caldés. "Maternal Origin of the Human Aneuploidies. Are Homolog Synapsis and Recombination to Blame? Notes (Learned) from the Underbelly." In Meiosis, 128–36. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000166638.

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Conference papers on the topic "Meiosis"

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Wiriyasermkul, Nattavut, Veera Boobjing, and Pisit Chanvarasuth. "A Meiosis Genetic Algorithm." In 2010 Seventh International Conference on Information Technology: New Generations. IEEE, 2010. http://dx.doi.org/10.1109/itng.2010.152.

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"Chromatin and cytoskeleton reorganization in meiosis of wheat-rye substitution line (3R3B)." In Plant Genetics, Genomics, Bioinformatics, and Biotechnology. Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 2019. http://dx.doi.org/10.18699/plantgen2019-215.

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"3D-microscopy of prophase nucleus in the meiosis I of wheat-rye amphihaploids." In Plant Genetics, Genomics, Bioinformatics, and Biotechnology. Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 2019. http://dx.doi.org/10.18699/plantgen2019-106.

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Manaka, Thapelo, and Lydia Mavuru. "TEACHERS’ PREPAREDNESS AND EXPERIENCES IN TEACHING MEIOSIS TO GRADE 12 LEARNERS IN LIMPOPO PROVINCE." In International Conference on Education and New Developments 2020. inScience Press, 2020. http://dx.doi.org/10.36315/2020end032.

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Xiaoli Yang, Rong Ge, Yufei Yang, Hao Shen, Yingjie Li, and C. C. Tseng. "Interactive computer program for learning genetic principles of segregation and independent assortment through meiosis." In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5334401.

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Gabitova, Linara, Andrey Gorin, Diana Restifo, Dong-Hua Yang, David Cunningham, Gail E. Herman, and Igor A. Astsaturov. "Abstract 2448: Meiosis activating sterols counteract KRas-driven epithelial carcinogenesis via an LXR-dependent mechanism." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2448.

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"Retention and evolution of centromeric histone paralogs in rye: essential for the organization of chromosomes in rye meiosis." In Plant Genetics, Genomics, Bioinformatics, and Biotechnology (PlantGen2023). FRC Kazan Scientific Center RAS, Kazan, Russia;Institute of Cytology and Genetics SB RAS, Novosibirsk, Russia, 2023. http://dx.doi.org/10.18699/plantgen2023-21.

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Stuart, Maritza Regina, Patricia Maria Raulilno de Campos, Luíz Rafaelli Coutinho, Vania Ana Silveira Muniz, Daniela Soldera, and Ana Paula Madalena da Silva. "The role of the nurse in the care of children with down syndrome." In III SEVEN INTERNATIONAL MULTIDISCIPLINARY CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/seveniiimulti2023-228.

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Down syndrome is a genetic condition caused by trisomy 21 and which leads to inadequate chromosomal distribution during the meiosis phase. Down syndrome is not a disease. It consists of a natural genetic occurrence that happens for unknown reasons, in pregnancy, during the division of the cells of the embryo. It is a chromosomal alteration, when children are born endowed with three chromosomes (trisomy) 21, and not two as usual. This genetic alteration affects the development of the individual, determining some peculiar physical and cognitive characteristics. Faced with the positive diagnosis for down syndrome, family members, especially parents, receive a very large impact and have different reactions, often without knowing what to do, how to proceed, become disoriented, and develop various feelings such as fears, anguish, uncertainty, shame, insecurity, among others. In this sense, the role of the nursing professional is to guide this family, with a humanized approach, passing on to it the care inherent to the patient, and the knowledge about the syndrome. The nursing professional for being in charge of the care the family has in its attributions, especially the care, and in the families that receive this diagnosis its role is of paramount importance to the clarification and welcoming of these parents.
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Guthrie, Megan, Moli Williams, Ajay Valji, Robert Jones, Dale Vimalachandran, Daniel Palmer, Tim Cross, and Urszula McClurg. "P46 Meiotic proteins – liver cancer specific drug targets." In Abstracts of the British Association for the Study of the Liver Annual Meeting, 19–22 September 2023. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2023. http://dx.doi.org/10.1136/gutjnl-2023-basl.62.

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Stauffer, Weston T., Liangyu Zhang, and Abby Dernburg. "Diffusion through a liquid crystalline compartment regulates meiotic recombination." In Biophysics, Biology and Biophotonics IV: the Crossroads, edited by Adam Wax and Vadim Backman. SPIE, 2019. http://dx.doi.org/10.1117/12.2513378.

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Reports on the topic "Meiosis"

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Durham, Mary. Demonstrating Meiosis Using Manipulatable Chromosomes and Cells. Genetics Society of America Peer-Reviewed Education Portal (GSA PREP), May 2015. http://dx.doi.org/10.1534/gsaprep.2015.002.

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Singh, Anjali. Estimating the Chiasma Frequency in Diplotene-Diakinesis Stage. ConductScience, September 2020. http://dx.doi.org/10.55157/cs20200925.

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Chiasma is the point of crossing over or site where the exchange of genetic material takes place between two homologous, non-sister chromatids. The crossover occurs in the pachytene stage, however, it is observed in the diplotene stage of meiosis-I[2]. The cross-over between the two homologs also creates a new combination of parental genes, forming recombinants. The recombination of the genes causes variation in the population and exert a profound effect on genomic diversity and evolution. Meiotic recombination and variation in the population have been a concern for scientists to understand the impact and significance of crossing over in a population. Over time, various techniques, such as immunolocalization and electron microscopy of recombination nodules[2], were discovered for the analysis of meiotic recombination and quantification of crossing over. However, estimation of chiasma frequency is the traditional method followed widely to understand the phenomenon. Chiasma Frequency is defined as the estimation of the level of genetic recombination in a population. It is especially very effective to estimate the genetic recombination in organisms in which genetic analysis is impossible/difficult to perform[2]. So, this article is a layout of the origin of the concept of chiasmata, the factors affecting chiasma frequency, and its distribution in chromosomes. Also discussed, is the procedure for estimating chiasma frequency in plants as well as animals.
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Levy, Avraham, Clifford Weil, and Wojtek Pawlowski. Enhancing the Rate of Meiotic Crossing-Over for Plant Breeding. United States Department of Agriculture, January 2009. http://dx.doi.org/10.32747/2009.7696532.bard.

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Meiotic recombination contributes to the generation of biodiversity as well as to genome stability, ensuring the proper segregation of homo logs during meiosis. It is also an essential step in the process of plant breeding. It generates the diversity needed by the breeder for selection of novel varieties. In this project, we have collaborated towards the goals to identify and characterize key genes involved in meiotic recombination. In addition we have shown how some of these genes can be used, through loss of function, or through overexpression, to enhance homologous recombination in Arabidopsis and in maize. Our main achievements can be summarized as follows: 1- To establish a collection of mutants, in Arabidopsis and in maize for candidate genes. In Arabidopsis, insertion mutants were isolated in the following genes: AtMSHI, AtMSH4, AtMSH5, AtMLH3, AtPHSl, and mutants in the Mre11/Rad50/Nbs1 complex. In maize, the TILLING system was established and enabled to isolate mutants in candidate genes, such as Rad2l-4a, Sgo2, and Aml. In addition, we generated phs 1 mutant alleles as well as mutants in the Mre11/Rad50/Nbs1 complex. No mus8l mutants have been found thus far. 2- We showed that mutants in AtMLH3 have decreased rates of crossover, suggesting that overexpression of these genes may enhance crossover. Mutants in AtMSHlhad no effect and mutants in AtMSH4 and 5 showed sterility. Overexpression of these genes might also enhance crossover. The effect of other mutations on crossovers in maize is still being investigated. 3- We showed that overexpression of AtMLH1, RecG and RuvC under a meioticspecific promoter enhances meiotic crossover in Arabidopsis. The effect of PHSloverexpression on crossover is expected to be determined soon. 4- New tools have been developed and perfected to study the recombination genes effect on meiotic crossovers. This includes antibodies, cDNAs and fusion proteins.
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Pawlowski, Wojtek P., and Avraham A. Levy. What shapes the crossover landscape in maize and wheat and how can we modify it. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600025.bard.

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Meiotic recombination is a process in which homologous chromosomes engage in the exchange of DNA segments, creating gametes with new genetic makeup and progeny with new traits. The genetic diversity generated in this way is the main engine of crop improvement in sexually reproducing plants. Understanding regulation of this process, particularly the regulation of the rate and location of recombination events, and devising ways of modifying them, was the major motivation of this project. The project was carried out in maize and wheat, two leading crops, in which any advance in the breeder’s toolbox can have a huge impact on food production. Preliminary work done in the USA and Israeli labs had established a strong basis to address these questions. The USA lab pioneered the ability to map sites where recombination is initiated via the induction of double-strand breaks in chromosomal DNA. It has a long experience in cytological analysis of meiosis. The Israeli lab has expertise in high resolution mapping of crossover sites and has done pioneering work on the importance of epigenetic modifications for crossover distribution. It has identified genes that limit the rates of recombination. Our working hypothesis was that an integrative analysis of double-strand breaks, crossovers, and epigenetic data will increase our understanding of how meiotic recombination is regulated and will enhance our ability to manipulate it. The specific objectives of the project were: To analyze the connection between double-strand breaks, crossover, and epigenetic marks in maize and wheat. Protocols developed for double-strand breaks mapping in maize were applied to wheat. A detailed analysis of existing and new data in maize was conducted to map crossovers at high resolution and search for DNA sequence motifs underlying crossover hotspots. Epigenetic modifications along maize chromosomes were analyzed as well. Finally, a computational analysis tested various hypotheses on the importance of chromatin structure and specific epigenetic modifications in determining the locations of double-strand breaks and crossovers along chromosomes. Transient knockdowns of meiotic genes that suppress homologous recombination were carried out in wheat using Virus-Induced Gene Silencing. The target genes were orthologs of FANCM, DDM1, MET1, RECQ4, and XRCC2.
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Hood-DeGrenier, Jennifer. Active Learning Workshops for Teaching Key Topics in Introductory Cell and Molecular Biology: Structure of DNA/RNA, Structure of Proteins, and Cell Division via Mitosis and Meiosis. Genetics Society of America Peer-Reviewed Education Portal (GSA PREP), December 2015. http://dx.doi.org/10.1534/gsaprep.2015.004.

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Gregory p. Copenhaver. Regulation of Meiotic Recombination. Office of Scientific and Technical Information (OSTI), November 2011. http://dx.doi.org/10.2172/1028811.

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Dray, Eloise, Myun Hwa Dunlop, Liisa Kauppi, Joseph San San Filippo, Claudia Wiese, Miaw-Sheue Tsai, Sead Begovic, et al. Molecular Basis for Enhancement of the Meiotic DMCI Recombinase by RAD51AP1. Office of Scientific and Technical Information (OSTI), November 2010. http://dx.doi.org/10.2172/1011037.

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Izhar, Shamay, Maureen Hanson, and Nurit Firon. Expression of the Mitochondrial Locus Associated with Cytoplasmic Male Sterility in Petunia. United States Department of Agriculture, February 1996. http://dx.doi.org/10.32747/1996.7604933.bard.

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The main goal of the proposed research was to continue the mutual investigations into the molecular basis of CMS and male fertility restoration [MRF], with the ultimate goal of understanding these phenomena in higher plants. The experiments focused on: (1) dissecting apart the complex CMS - specific mitochondrial S-Pcf locus, in order to distinguish its essential parts which cause sterility from other parts and study its molecular evolution. (2) Studying the expression of the various regions of the S-Pcf locus in fertile and sterile lines and comparing the structure and ultrastructure of sterile and fertile tissues. (3) Determine whether alteration in respiration is genetically associated with CMS. Our mutual investigations further substantiated the association between the S-Pcf locus and CMS by the findings that the fertile phenotype of a population of unstable petunia somatic hybrids which contain the S-Pcf locus, is due to the presence of multiple muclear fertility restoration genes in this group of progenies. The information obtained by our studies indicate that homologous recombination played a major role in the molecular evolution of the S-Pcf locus and the CMS trait and in the generation of mitochondrial mutations in general. Our data suggest that the CMS cytoplasm evolved by introduction of a urs-s containing sublimon into the main mitochondrial genome via homologous recombination. We have also found that the first mutation detected so far in S-Pcf is a consequence of a homologous recombination mechanism involving part of the cox2 coding sequence. In all the cases studied by us, at the molecular level, we found that fusion of two different cells caused mitochondrial DNA recombination followed by sorting out of a specific mtDNA population or sequences. This sequence of events suggested as a mechanism for the generation of novel mitochondrial genomes and the creation of new traits. The present research also provides data concerning the expression of the recombined and complex CMS-specific S-Pcf locus as compared with the expression of additional mitochondrial proteins as well as comparative histological and ultrastructural studies of CMS and fertile Petunia. Evidence is provided for differential localization of mitochondrially encoded proteins in situ at the tissue level. The similar localization patterns of Pcf and atpA may indicate that Pcf product could interfere with the functioning of the mitochondrial ATPase in a tissue undergoing meiosis and microsporogenesis. Studies of respiration in CMS and fertile Petunia lines indicate that they differe in the partitioning of electron transport through the cytochrome oxidase and alternative oxidase pathways. The data indicate that the electron flux through the two oxidase pathways differs between mitochondria from fertile and sterile Petunia lines at certain redox states of the ubiquinone pool. In summary, extensive data concerning the CMS-specific S-Pcf locus of Petunia at the DNA and protein levels as well as information concerning different biochemical activity in CMS as compared to male fertile lines have been accumulated during the three years of this project. In addition, the involvement of the homologous recombination mechanism in the evolution of mt encoded traits is emphasized.
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9

Arnaoudova, Yanina, Boyan Arnaoudov, and Nasya Tomlekova. Meiotic Behaviour of Pollen Mother Cells in Eight Genotypes of Pepper ( Capsicum annuum L.) under Water Deficit. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, November 2021. http://dx.doi.org/10.7546/crabs.2021.11.18.

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10

Hirota, Marina, Carlos A. Nobre, Ane Alencar, Julia Areiera, Francisco de Assis Costa, Bernardo Flores, Clarissa Gandour, et al. Policy Brief: Um Chamado de Ação Global para Evitar os ‘Pontos de Não-Retorno da Floresta Amazônica. Sustainable Development Solutions Network (SDSN), November 2022. http://dx.doi.org/10.55161/wmsa6060.

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Territórios Indígenas (TIs) na Amazônia protegem aproximadamente 24.5 gigatoneladas de carbono (GtC) acima do solo, atuam como barreiras significativas contra o desmatamento e a degradação florestal, e funcionam como importantes amortecedores contra as mudanças climáticas. TIs demarcadas apresentam desmatamento significativamente menor do que terras não reconhecidas oficialmente, demonstrando a importância de se demarcar TIs tanto para proteger os meios de subsistência e as culturas dos povos nativos da Amazônia, quanto para conservar suas florestas e rios.
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