Relevant bibliographies by topics / Meiotic inhibition

Academic literature on the topic 'Meiotic inhibition'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Meiotic inhibition"

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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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Wang, Xia, Jason E. Swain, Mathieu Bollen, Xiao-Tie Liu, Dana A. Ohl, and Gary D. Smith. "Endogenous regulators of protein phosphatase-1 during mouse oocyte development and meiosis." Reproduction 128, no. 5 (November 2004): 493–502. http://dx.doi.org/10.1530/rep.1.00173.

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Reversible phosphorylation, involving protein kinases and phosphatases (PP), is important in regulating oocyte meiosis. Okadaic acid (OA) inhibition of PP1 and/or PP2A stimulates oocyte germinal vesicle breakdown (GVB). In oocytes, PP1 is localized in the cytoplasm and nucleus, yet endogenous regulation of oocyte PP1 has not been investigated. The objectives of the study were to identify intra-oocyte mechanisms regulating PP1 during acquisition of OA-sensitive meiotic competence and meiotic resumption. Immunohistochemical studies revealed that GVB-incompetent oocytes contained equivalent cytoplasmic and nuclear PP1. Upon development of OA-sensitive meiotic competence, PP1 displayed differential intracellular localization with significantly greater nuclear staining with distinct nucleolar rimming compared with cytoplasmic staining. Germinal vesicle-intact oocytes contained neither nuclear inhibitor of PP1, nor PP1 cytoplasmic inhibitor-1 transcripts or proteins. Reverse transcription-PCR with PP1 cytoplasmic inhibitor-2 (I2) primers and oocyte RNA amplified a predicted 330-bp product with the identical sequence to mouse liver I2. Oocytes contained a heat-stable PP1 inhibitor with biochemical properties of I2. Phosphorylation of PP1 at Thr320 by cyclin dependent kinase-1 (CDK1) causes PP1 inactivation. Germinal vesicle-intact oocytes did not contain phospho-Thr320-PP1. Upon GVB, PP1 became phosphorylated at Thr320 and this phosphorylation did not occur if GVB was blocked with the CDK1 inhibitor, roscovitine (ROSC). Inhibition of oocyte GVB with ROSC was reversible and coincided with PP1 phosphorylation at Thr320. Increased oocyte staining of nuclear PP1 compared with cytoplasmic staining at a chronological stage when oocytes gain meiotic competence, and phosphorylation and inhibition of PP1 by CDK1 at or around GVB appear to be important mechanisms in regulating oocyte PP1 activity and meiosis. In addition, these studies provide further support for PP1 being the OA-sensitive PP important in the regulation of the acquisition of meiotic competence, nuclear events during meiotic arrest, and GVB.
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Chen, Hanchen, Chengpeng He, Chongyang Wang, Xuanpeng Wang, Fengyin Ruan, Junjie Yan, Ping Yin, Yingxiang Wang, and Shunping Yan. "RAD51 supports DMC1 by inhibiting the SMC5/6 complex during meiosis." Plant Cell 33, no. 8 (May 16, 2021): 2869–82. http://dx.doi.org/10.1093/plcell/koab136.

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Abstract Meiosis is a fundamental process for sexual reproduction in most eukaryotes and the evolutionarily conserved recombinases RADiation sensitive51 (RAD51) and Disrupted Meiotic cDNA1 (DMC1) are essential for meiosis and thus fertility. The mitotic function of RAD51 is clear, but the meiotic function of RAD51 remains largely unknown. Here we show that RAD51 functions as an interacting protein to restrain the Structural Maintenance of Chromosomes5/6 (SMC5/6) complex from inhibiting DMC1. We unexpectedly found that loss of the SMC5/6 partially suppresses the rad51 knockout mutant in terms of sterility, pollen inviability, and meiotic chromosome fragmentation in a DMC1-dependent manner in Arabidopsis thaliana. Biochemical and cytological studies revealed that the DMC1 localization in meiotic chromosomes is inhibited by the SMC5/6 complex, which is attenuated by RAD51 through physical interactions. This study not only identified the long-sought-after function of RAD51 in meiosis but also discovered the inhibition of SMC5/6 on DMC1 as a control mechanism during meiotic recombination.
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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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Marangos, Petros, Emmy W. Verschuren, Ruby Chen, Peter K. Jackson, and John Carroll. "Prophase I arrest and progression to metaphase I in mouse oocytes are controlled by Emi1-dependent regulation of APCCdh1." Journal of Cell Biology 176, no. 1 (December 26, 2006): 65–75. http://dx.doi.org/10.1083/jcb.200607070.

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Mammalian oocytes are arrested in prophase of the first meiotic division. Progression into the first meiotic division is driven by an increase in the activity of maturation-promoting factor (MPF). In mouse oocytes, we find that early mitotic inhibitor 1 (Emi1), an inhibitor of the anaphase-promoting complex (APC) that is responsible for cyclin B destruction and inactivation of MPF, is present at prophase I and undergoes Skp1–Cul1–F-box/βTrCP-mediated destruction immediately after germinal vesicle breakdown (GVBD). Exogenous Emi1 or the inhibition of Emi1 destruction in prophase-arrested oocytes leads to a stabilization of cyclin B1–GFP that is sufficient to trigger GVBD. In contrast, the depletion of Emi1 using morpholino oligonucleotides increases cyclin B1–GFP destruction, resulting in an attenuation of MPF activation and a delay of entry into the first meiotic division. Finally, we show that Emi1-dependent effects on meiosis I require the presence of Cdh1. These observations reveal a novel mechanism for the control of entry into the first meiotic division: an Emi1-dependent inhibition of APCCdh1.
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Cairo, Albert, Anna Vargova, Neha Shukla, Claudio Capitao, Pavlina Mikulkova, Sona Valuchova, Jana Pecinkova, Petra Bulankova, and Karel Riha. "Meiotic exit in Arabidopsis is driven by P-body–mediated inhibition of translation." Science 377, no. 6606 (August 5, 2022): 629–34. http://dx.doi.org/10.1126/science.abo0904.

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Meiosis, at the transition between diploid and haploid life cycle phases, is accompanied by reprograming of cell division machinery and followed by a transition back to mitosis. We show that, in Arabidopsis , this transition is driven by inhibition of translation, achieved by a mechanism that involves processing bodies (P-bodies). During the second meiotic division, the meiosis-specific protein THREE-DIVISION MUTANT 1 (TDM1) is incorporated into P-bodies through interaction with SUPPRESSOR WITH MORPHOGENETIC EFFECTS ON GENITALIA 7 (SMG7). TDM1 attracts eIF4F, the main translation initiation complex, temporarily sequestering it in P-bodies and inhibiting translation. The failure of tdm1 mutants to terminate meiosis can be overcome by chemical inhibition of translation. We propose that TDM1-containing P-bodies down-regulate expression of meiotic transcripts to facilitate transition of cell fates to postmeiotic gametophyte differentiation.
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Cao, Zubing, Tengteng Xu, Xu Tong, Dandan Zhang, Chengxue Liu, Yiqing Wang, Di Gao, et al. "HASPIN kinase mediates histone deacetylation to regulate oocyte meiotic maturation in pigs." Reproduction 157, no. 6 (June 2019): 501–10. http://dx.doi.org/10.1530/rep-18-0447.

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HASPIN kinase-catalyzed phosphorylation of histone H3 on threonine 3 (H3T3p) directs the activity and localization of chromosomal passenger complex (CPC) and spindle assembly checkpoint (SAC) to regulate chromosome condensation and segregation in both mitosis and meiosis. However, the function of HASPIN kinase in the meiotic maturation of porcine oocytes is not yet known. Here, we found that HASPIN mRNA is constantly expressed in porcine oocyte maturation and subsequent early embryo development. H3T3p is highly enriched on chromosomes at germinal vesicle breakdown (GVBD) stage and thereafter maintains a low level in progression through metaphase I (MI) to metaphase II (MII). Correspondingly, H3T3p was completely abolished in oocytes treated with an inhibitor of HASPIN kinase. Functionally, inhibition of HASPIN activity led to a significant reduction in the rate of oocyte meiotic maturation and the limited cumulus expansion. Additionally, HASPIN inhibition caused both spindle disorganization and chromosome misalignment in oocytes at MI and MII stage. Importantly, HASPIN inhibition severely prevented deacetylation of several highly conserved lysine (K) residues of histone H3 and H4 including H3K9, H3K14, H4K5, H4K8, H4K12 and H4K16 on the metaphase chromosomes during oocyte meiotic maturation. Taken together, these results demonstrate that HASPIN kinase regulates porcine oocyte meiotic maturation via modulating histone deacetylation.
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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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Zhang, Jin, Lihua Ren, Yang Zou, Lianshuang Zhang, Jialiu Wei, Yanbo Li, Ji Wang, Zhiwei Sun, and Xianqing Zhou. "Silica nanoparticles induce start inhibition of meiosis and cell cycle arrest via down-regulating meiotic relevant factors." Toxicology Research 5, no. 5 (2016): 1453–64. http://dx.doi.org/10.1039/c6tx00236f.

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Silica nanoparticles induced cell cycle arrest and proliferation inhibition by down-regulating the expressions of meiotic regulatory factors through causing DNA damages resulting from oxidative stress, leading to the inhibition of the start and process of meiosis.
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Varadarajan, Ramya, Joseph Ayeni, Zhigang Jin, Ellen Homola, and Shelagh D. Campbell. "Myt1 inhibition of Cyclin A/Cdk1 is essential for fusome integrity and premeiotic centriole engagement in Drosophila spermatocytes." Molecular Biology of the Cell 27, no. 13 (July 2016): 2051–63. http://dx.doi.org/10.1091/mbc.e16-02-0104.

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Regulation of cell cycle arrest in premeiotic G2 phase coordinates germ cell maturation and meiotic cell division with hormonal and developmental signals by mechanisms that control Cyclin B synthesis and inhibitory phosphorylation of the M-phase kinase, Cdk1. In this study, we investigated how inhibitory phosphorylation of Cdk1 by Myt1 kinase regulates premeiotic G2 phase of Drosophila male meiosis. Immature spermatocytes lacking Myt1 activity exhibit two distinct defects: disrupted intercellular bridges (fusomes) and premature centriole disengagement. As a result, the myt1 mutant spermatocytes enter meiosis with multipolar spindles. These myt1 defects can be suppressed by depletion of Cyclin A activity or ectopic expression of Wee1 (a partially redundant Cdk1 inhibitory kinase) and phenocopied by expression of a Cdk1F mutant defective for inhibitory phosphorylation. We therefore conclude that Myt1 inhibition of Cyclin A/Cdk1 is essential for normal fusome behavior and centriole engagement during premeiotic G2 arrest of Drosophila male meiosis. The novel meiotic functions we discovered for Myt1 kinase are spatially and temporally distinct from previously described functions of Myt1 as an inhibitor of Cyclin B/Cdk1 to regulate G2/MI timing.
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Dissertations / Theses on the topic "Meiotic inhibition"

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Batsiokis, Madeline. "Bovine in vitro embryo production (IVP): assessment of two new approaches to improve the efficiency of embryo production." Thesis, 2020. http://hdl.handle.net/2440/123985.

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Books on the topic "Meiotic inhibition"

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Haseltine. Meiotic Inhibition. John Wiley & Sons, 1988.

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Florence, Haseltine, First Neal L, and Center for Population Research (National Institute of Child Health and Human Development), eds. Meiotic inhibition: Molecular control of meiosis : proceedings of a symposium held at the National Institutes of Health, Bethesda, Maryland, January 1987. New York: A.R. Liss, 1988.

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Book chapters on the topic "Meiotic inhibition"

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Pinel, Dominic, and Vincent J. J. Martin. "Meiotic Recombination-Based Genome Shuffling ofSaccharomyces CerevisiaeandSchefferomyces Stiptisfor Increased Inhibitor Tolerance to Lignocellulosic Substrate Toxicity." In Engineering Complex Phenotypes in Industrial Strains, 233–50. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118433034.ch9.

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MacLaughlin, David T., Tatsuo Kuroda, Elizabeth A. Catlin, and Patricia K. Donahoe. "Mullerian Inhibiting Substance Activity in the Development of the Reproductive Tract and Lung in the Fetus and Control of Oocyte Meiosis in the Adult." In Growth Factors in Reproduction, 151–66. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4612-3162-2_11.

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Reports on the topic "Meiotic inhibition"

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Weiss, David, and Neil Olszewski. Manipulation of GA Levels and GA Signal Transduction in Anthers to Generate Male Sterility. United States Department of Agriculture, 2000. http://dx.doi.org/10.32747/2000.7580678.bard.

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The original objectives of the research were: i. To study the role of GA in anther development, ii. To manipulate GA and/or GA signal transduction levels in the anthers in order to generate male sterility. iii. To characterize the GA signal transduction repressor, SPY. Previous studies have suggested that gibberellins (GAs) are required for normal anther development. In this work, we studied the role of GA in the regulation of anther development in petunia. When plants were treated with the GA-biosynthesis inhibitor paclobutrazol, anther development was arrested. Microscopic analysis of these anthers revealed that paclobutrazol inhibits post-meiotic developmental processes. The treated anthers contained pollen grains but the connective tissue and tapetum cells were degenerated. The expression of the GA-induced gene, GIP, can be used in petunia as a molecular marker to: study GA responses. Analyses of GIP expression during anther development revealed that the gene is induced only after microsporogenesis. This observation further suggests a role for GA in the regulation of post-meiotic processes during petunia anther development. Spy acts as a negative regulator of gibberellin (GA) action in Arabidopsis. We cloned the petunia Spy homologue, PhSPY, and showed that it can complement the spy-3 mutation in Arabidopsis. Overexpression of Spy in transgenic petunia plants affected various GA-regulated processes, including seed germination, shoot elongation, flower initiation, flower development and the expression of a GA- induced gene, GIP. In addition, anther development was inhibited in the transgenic plants following microsporogenesis. The N-terminus of Spy contains tetratricopeptide repeats (TPR). TPR motifs participate in protein-protein interactions, suggesting that Spy is part of a multiprotein complex. To test this hypothesis, we over-expressed the SPY's TPR region without the catalytic domain in transgenic petunia and generated a dominant- negative Spy mutant. The transgenic seeds were able to germinate on paclobutrazol, suggesting an enhanced GA signal. Overexpression of PhSPY in wild type Arabidopsis did not affect plant stature, morphology or flowering time. Consistent with Spy being an O-GlcNAc transferase (OGT), Spy expressed in insect cells was shown to O-GlcNAc modify itself. Consistent with O-GlcNAc modification playing a role in GA signaling, spy mutants had a reduction in the GlcNAc modification of several proteins. After treatment of the GA deficient, gal mutant, with GA3 the GlcNAc modification of proteins of the same size as those affected in spy mutants exhibited a reduction in GlcNAcylation. GA-induced GlcNAcase may be responsible for this de-GlcNAcylation because, treatment of gal with GA rapidly induced an increase in GlcNAcase activity. Several Arabidopsis proteins that interact with the TPR domain of Spy were identified using yeast two-hybrids screens. One of these proteins was GIGANTEA (GI). Consistent with GI and Spy functioning as a complex in the plant the spy-4 was epistatic to gi. These experiments also demonstrated that, in addition to its role in GA signaling, Spy functions in the light signaling pathways controlling hypocotyl elongation and photoperiodic induction of flowering. A second Arabidopsis OGT, SECRET AGENT (SCA), was discovered. Like SPY, SCA O-GlcNAc modifies itself. Although sca mutants do not exhibit dramatic phenotypes, spy/sca double mutants exhibit male and female gamete and embryo lethality, indicating that Spy and SCA have overlapping functions. These results suggest that O-GlcNAc modification is an essential modification in plants that has a role in multiple signaling pathways.
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