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Results: 1 to 10 of 23

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The gene family that cheats Mendel.
Shropshire JD, Rokas A
(2017) Elife 6:
MeSH Terms: Alleles, Meiosis, Poisons, Schizosaccharomyces, Spores, Fungal
Show Abstract · Added March 21, 2018
Some alleles of the gene family can increase their chances of spreading by using poisons to kill other alleles, and antidotes to save themselves.
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5 MeSH Terms
Loss of col8a1a function during zebrafish embryogenesis results in congenital vertebral malformations.
Gray RS, Wilm TP, Smith J, Bagnat M, Dale RM, Topczewski J, Johnson SL, Solnica-Krezel L
(2014) Dev Biol 386: 72-85
MeSH Terms: Alleles, Animals, Collagen Type VIII, Crosses, Genetic, Gene Expression Regulation, Developmental, In Situ Hybridization, Meiosis, Microscopy, Confocal, Microscopy, Electron, Transmission, Mutation, Notochord, Osteoblasts, Protein-Lysine 6-Oxidase, Spine, Time Factors, Zebrafish
Show Abstract · Added March 20, 2014
Congenital vertebral malformations (CVM) occur in 1 in 1000 live births and in many cases can cause spinal deformities, such as scoliosis, and result in disability and distress of affected individuals. Many severe forms of the disease, such as spondylocostal dystostosis, are recessive monogenic traits affecting somitogenesis, however the etiologies of the majority of CVM cases remain undetermined. Here we demonstrate that morphological defects of the notochord in zebrafish can generate congenital-type spine defects. We characterize three recessive zebrafish leviathan/col8a1a mutant alleles ((m531, vu41, vu105)) that disrupt collagen type VIII alpha1a (col8a1a), and cause folding of the embryonic notochord and consequently adult vertebral column malformations. Furthermore, we provide evidence that a transient loss of col8a1a function or inhibition of Lysyl oxidases with drugs during embryogenesis was sufficient to generate vertebral fusions and scoliosis in the adult spine. Using periodic imaging of individual zebrafish, we correlate focal notochord defects of the embryo with vertebral malformations (VM) in the adult. Finally, we show that bends and kinks in the notochord can lead to aberrant apposition of osteoblasts normally confined to well-segmented areas of the developing vertebral bodies. Our results afford a novel mechanism for the formation of VM, independent of defects of somitogenesis, resulting from aberrant bone deposition at regions of misshapen notochord tissue.
Copyright © 2013 Elsevier Inc. All rights reserved.
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16 MeSH Terms
The Arabidopsis SYN3 cohesin protein is important for early meiotic events.
Yuan L, Yang X, Ellis JL, Fisher NM, Makaroff CA
(2012) Plant J 71: 147-60
MeSH Terms: Arabidopsis, Arabidopsis Proteins, Cell Cycle Proteins, Chromosome Pairing, Gene Expression Regulation, Developmental, Gene Expression Regulation, Plant, Germ Cells, Plant, Meiosis, Plants, Genetically Modified, Promoter Regions, Genetic, RNA Interference
Show Abstract · Added January 25, 2016
α-Kleisins are core components of meiotic and mitotic cohesin complexes. Arabidopsis contains four genes that encode α-kleisin proteins: SYN1, SYN2, SYN3 and SYN4. SYN1, a REC8 ortholog, is essential for meiosis, while SYN2 and SYN4 appear to be SCC1 orthologs and function in mitosis. SYN3 is essential for megagametogenesis and is enriched in the nucleolus of meiotic and mitotic cells. In this study the role of SYN3 during meiosis was investigated by characterization of plants that express SYN3-RNAi constructs from either meiotic DMC1, native SYN3, or inducible PX7 promoters. Reduction of SYN3 caused defects in homologous chromosome synapsis and synaptonemal complex (SC) formation during male and female meiosis. Consistent with this observation, relatively little signal for the SC component ZYP1 was detected on the chromosomes of SYN3-RNAi plants. ZYP1 transcript levels were relatively normal, but several transcripts for genes that encode proteins involved in meiotic recombination were altered, which suggested that a reduction in SYN3 may inhibit meiotic progression by alteration of meiotic gene expression.
© 2012 The Authors. The Plant Journal © 2012 Blackwell Publishing Ltd.
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11 MeSH Terms
Poor correlations in the levels of pathogenic mitochondrial DNA mutations in polar bodies versus oocytes and blastomeres in humans.
Gigarel N, Hesters L, Samuels DC, Monnot S, Burlet P, Kerbrat V, Lamazou F, Benachi A, Frydman R, Feingold J, Rotig A, Munnich A, Bonnefont JP, Frydman N, Steffann J
(2011) Am J Hum Genet 88: 494-8
MeSH Terms: Blastomeres, DNA, Mitochondrial, Embryonic Development, Female, Humans, MELAS Syndrome, MERRF Syndrome, Male, Meiosis, Mutation, Oocytes, Oogenesis, Pregnancy, Preimplantation Diagnosis
Show Abstract · Added December 12, 2013
Because the mtDNA amount remains stable in the early embryo until uterine implantation, early human development is completely dependent on the mtDNA pool of the mature oocyte. Both quantitative and qualitative mtDNA defects therefore may negatively impact oocyte competence or early embryonic development. However, nothing is known about segregation of mutant and wild-type mtDNA molecules during human meiosis. To investigate this point, we compared the mutant levels in 51 first polar bodies (PBs) and their counterpart (oocytes, blastomeres, or whole embryos), at risk of having (1) the "MELAS" m.3243A>G mutation in MT-TL1 (n = 30), (2) the "MERRF" m.8344A>G mutation in MT-TK (n = 15), and (3) the m.9185T>G mutation located in MT-ATP6 (n = 6). Seven out of 51 of the PBs were mutation free and had homoplasmic wild-type counterparts. In the heteroplasmic PBs, measurement of the mutant load was a rough estimate of the counterpart mutation level (R(2) = 0.52), and high mutant-load differentials between the two populations were occasionally observed (ranging from -34% to +34%). The mutant-load differentials between the PB and its counterpart were higher in highly mutated PBs, suggestive of a selection process acting against highly mutated cells during gametogenesis or early embryonic development. Finally, individual discrepancies in mutant loads between PBs and their counterparts make PB-based preconception diagnosis unreliable for the prevention of mtDNA disorder transmission. Such differences were not observed in animal models, and they emphasize the need to conduct thorough studies on mtDNA segregation in humans.
Copyright © 2011 The American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.
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14 MeSH Terms
State of the APC/C: organization, function, and structure.
McLean JR, Chaix D, Ohi MD, Gould KL
(2011) Crit Rev Biochem Mol Biol 46: 118-36
MeSH Terms: Anaphase-Promoting Complex-Cyclosome, Animals, Catalysis, Cell Cycle Proteins, Cell Nucleus, Humans, Meiosis, Microscopy, Electron, Mitosis, Models, Biological, Spindle Apparatus, Ubiquitin-Protein Ligase Complexes, Ubiquitin-Protein Ligases
Show Abstract · Added March 5, 2014
The ubiquitin-proteasome protein degradation system is involved in many essential cellular processes including cell cycle regulation, cell differentiation, and the unfolded protein response. The anaphase-promoting complex/cyclosome (APC/C), an evolutionarily conserved E3 ubiquitin ligase, was discovered 15 years ago because of its pivotal role in cyclin degradation and mitotic progression. Since then, we have learned that the APC/C is a very large, complex E3 ligase composed of 13 subunits, yielding a molecular machine of approximately 1 MDa. The intricate regulation of the APC/C is mediated by the Cdc20 family of activators, pseudosubstrate inhibitors, protein kinases and phosphatases and the spindle assembly checkpoint. The large size, complexity, and dynamic nature of the APC/C represent significant obstacles toward high-resolution structural techniques; however, over the last decade, there have been a number of lower resolution APC/C structures determined using single particle electron microscopy. These structures, when combined with data generated from numerous genetic and biochemical studies, have begun to shed light on how APC/C activity is regulated. Here, we discuss the most recent developments in the APC/C field concerning structure, substrate recognition, and catalysis.
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13 MeSH Terms
A spatial and temporal map of C. elegans gene expression.
Spencer WC, Zeller G, Watson JD, Henz SR, Watkins KL, McWhirter RD, Petersen S, Sreedharan VT, Widmer C, Jo J, Reinke V, Petrella L, Strome S, Von Stetina SE, Katz M, Shaham S, Rätsch G, Miller DM
(2011) Genome Res 21: 325-41
MeSH Terms: Animals, Caenorhabditis elegans, Computational Biology, Databases, Genetic, Gene Expression Profiling, Gene Expression Regulation, Developmental, Male, Meiosis, Molecular Sequence Data, Oogenesis, Open Reading Frames, Transcription, Genetic, Untranslated Regions, X Chromosome Inactivation
Show Abstract · Added February 21, 2014
The C. elegans genome has been completely sequenced, and the developmental anatomy of this model organism is described at single-cell resolution. Here we utilize strategies that exploit this precisely defined architecture to link gene expression to cell type. We obtained RNAs from specific cells and from each developmental stage using tissue-specific promoters to mark cells for isolation by FACS or for mRNA extraction by the mRNA-tagging method. We then generated gene expression profiles of more than 30 different cells and developmental stages using tiling arrays. Machine-learning-based analysis detected transcripts corresponding to established gene models and revealed novel transcriptionally active regions (TARs) in noncoding domains that comprise at least 10% of the total C. elegans genome. Our results show that about 75% of transcripts with detectable expression are differentially expressed among developmental stages and across cell types. Examination of known tissue- and cell-specific transcripts validates these data sets and suggests that newly identified TARs may exercise cell-specific functions. Additionally, we used self-organizing maps to define groups of coregulated transcripts and applied regulatory element analysis to identify known transcription factor- and miRNA-binding sites, as well as novel motifs that likely function to control subsets of these genes. By using cell-specific, whole-genome profiling strategies, we have detected a large number of novel transcripts and produced high-resolution gene expression maps that provide a basis for establishing the roles of individual genes in cellular differentiation.
1 Communities
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14 MeSH Terms
A novel predicted bromodomain-related protein affects coordination between meiosis and spermiogenesis in Drosophila and is required for male meiotic cytokinesis.
Bergner LM, Hickman FE, Wood KH, Wakeman CM, Stone HH, Campbell TJ, Lightcap SB, Favors SM, Aldridge AC, Hales KG
(2010) DNA Cell Biol 29: 487-98
MeSH Terms: Amino Acid Sequence, Animals, Chromosomal Proteins, Non-Histone, Cloning, Molecular, Conserved Sequence, Cytokinesis, Drosophila Proteins, Drosophila melanogaster, Female, Genes, Insect, Infertility, Male, Insect Proteins, Male, Meiosis, Mitochondria, Molecular Sequence Data, Mutation, Protein Structure, Tertiary, Spermatogenesis, Testis
Show Abstract · Added August 14, 2014
Temporal coordination of meiosis with spermatid morphogenesis is crucial for successful generation of mature sperm cells. We identified a recessive male sterile Drosophila melanogaster mutant, mitoshell, in which events of spermatid morphogenesis are initiated too early, before meiotic onset. Premature mitochondrial aggregation and fusion lead to an aberrant mitochondrial shell around premeiotic nuclei. Despite successful meiotic karyokinesis, improper mitochondrial localization in mitoshell testes is associated with defective astral central spindles and a lack of contractile rings, leading to meiotic cytokinesis failure. We mapped and cloned the mitoshell gene and found that it encodes a novel protein with a bromodomain-related region. It is conserved in some insect lineages. Bromodomains typically bind to histone acetyl-lysine residues and therefore are often associated with chromatin. The Mitoshell bromodomain-related region is predicted to have an alpha helical structure similar to that of bromodomains, but not all the crucial residues in the ligand-binding loops are conserved. We speculate that Mitoshell may participate in transcriptional regulation of spermatogenesis-specific genes, though perhaps with different ligand specificity compared to traditional bromodomains.
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20 MeSH Terms
Fast microtubule dynamics in meiotic spindles measured by single molecule imaging: evidence that the spindle environment does not stabilize microtubules.
Needleman DJ, Groen A, Ohi R, Maresca T, Mirny L, Mitchison T
(2010) Mol Biol Cell 21: 323-33
MeSH Terms: Animals, Biopolymers, Cell Extracts, Cyclopropanes, Kinetics, Meiosis, Microtubules, Molecular Imaging, Ovum, Photobleaching, Pyridines, Thiazoles, Time Factors, Tubulin, Xenopus laevis
Show Abstract · Added March 5, 2014
Metaphase spindles are steady-state ensembles of microtubules that turn over rapidly and slide poleward in some systems. Since the discovery of dynamic instability in the mid-1980s, models for spindle morphogenesis have proposed that microtubules are stabilized by the spindle environment. We used single molecule imaging to measure tubulin turnover in spindles, and nonspindle assemblies, in Xenopus laevis egg extracts. We observed many events where tubulin molecules spend only a few seconds in polymer and thus are difficult to reconcile with standard models of polymerization dynamics. Our data can be quantitatively explained by a simple, phenomenological model-with only one adjustable parameter-in which the growing and shrinking of microtubule ends is approximated as a biased random walk. Microtubule turnover kinetics did not vary with position in the spindle and were the same in spindles and nonspindle ensembles nucleated by Tetrahymena pellicles. These results argue that the high density of microtubules in spindles compared with bulk cytoplasm is caused by local enhancement of nucleation and not by local stabilization. It follows that the key to understanding spindle morphogenesis will be to elucidate how nucleation is spatially controlled.
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15 MeSH Terms
Asunder is a critical regulator of dynein-dynactin localization during Drosophila spermatogenesis.
Anderson MA, Jodoin JN, Lee E, Hales KG, Hays TS, Lee LA
(2009) Mol Biol Cell 20: 2709-21
MeSH Terms: Animals, Animals, Genetically Modified, Cell Cycle Proteins, Cell Nucleus, Chromosome Segregation, Drosophila Proteins, Drosophila melanogaster, Dynactin Complex, Dyneins, Fertility, Green Fluorescent Proteins, HeLa Cells, Humans, Immunoblotting, Infertility, Male, Male, Meiosis, Microscopy, Fluorescence, Microtubule-Associated Proteins, Mutation, Reverse Transcriptase Polymerase Chain Reaction, Spermatids, Spermatocytes, Spermatogenesis, Spindle Apparatus, Transfection
Show Abstract · Added March 5, 2014
Spermatogenesis uses mitotic and meiotic cell cycles coordinated with growth and differentiation programs to generate functional sperm. Our analysis of a Drosophila mutant has revealed that asunder (asun), which encodes a conserved protein, is an essential regulator of spermatogenesis. asun spermatocytes arrest during prophase of meiosis I. Strikingly, arrested spermatocytes contain free centrosomes that fail to stably associate with the nucleus. Spermatocytes that overcome arrest exhibit severe defects in meiotic spindle assembly, chromosome segregation, and cytokinesis. Furthermore, the centriole-derived basal body is detached from the nucleus in asun postmeiotic spermatids, resulting in abnormalities later in spermatogenesis. We find that asun spermatocytes and spermatids exhibit drastic reduction of perinuclear dynein-dynactin, a microtubule motor complex. We propose a model in which asun coordinates spermatogenesis by promoting dynein-dynactin recruitment to the nuclear surface, a poorly understood process required for nucleus-centrosome coupling at M phase entry and fidelity of meiotic divisions.
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26 MeSH Terms
alpha-Endosulfine is a conserved protein required for oocyte meiotic maturation in Drosophila.
Von Stetina JR, Tranguch S, Dey SK, Lee LA, Cha B, Drummond-Barbosa D
(2008) Development 135: 3697-706
MeSH Terms: Amino Acid Sequence, Animals, Animals, Genetically Modified, Biological Evolution, CDC2 Protein Kinase, Cell Differentiation, Conserved Sequence, Drosophila Proteins, Drosophila melanogaster, Female, Humans, Meiosis, Molecular Sequence Data, Mutation, Nuclear Envelope, Oocytes, Peptides, Protein Binding, Protein-Serine-Threonine Kinases, Sequence Alignment, Ubiquitin-Protein Ligases
Show Abstract · Added March 5, 2014
Meiosis is coupled to gamete development and must be well regulated to prevent aneuploidy. During meiotic maturation, Drosophila oocytes progress from prophase I to metaphase I. The molecular factors controlling meiotic maturation timing, however, are poorly understood. We show that Drosophila alpha-endosulfine (endos) plays a key role in this process. endos mutant oocytes have a prolonged prophase I and fail to progress to metaphase I. This phenotype is similar to that of mutants of cdc2 (synonymous with cdk1) and of twine, the meiotic homolog of cdc25, which is required for Cdk1 activation. We found that Twine and Polo kinase levels are reduced in endos mutants, and identified Early girl (Elgi), a predicted E3 ubiquitin ligase, as a strong Endos-binding protein. In elgi mutant oocytes, the transition into metaphase I occurs prematurely, but Polo and Twine levels are unaffected. These results suggest that Endos controls meiotic maturation by regulating Twine and Polo levels, and, independently, by antagonizing Elgi. Finally, germline-specific expression of the human alpha-endosulfine ENSA rescues the endos mutant meiotic defects and infertility, and alpha-endosulfine is expressed in mouse oocytes, suggesting potential conservation of its meiotic function.
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21 MeSH Terms