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Find video protocols related to scientific articles indexed in Pubmed.
Rab5a is required for spindle length control and kinetochore-microtubule attachment during meiosis in oocytes.
FASEB J.
PUBLISHED: 05-31-2014
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Rab GTPases are highly conserved components of vesicle trafficking pathways. Rab5, as a master regulator of endocytic trafficking, has been shown to function in membrane tethering and docking. However, the function of Rab5 in meiosis has not been addressed. Here, we report elongated spindles and misaligned chromosomes, with kinetochore-microtubule misattachments, on specific depletion of Rab5a in mouse oocytes. Moreover, the localization and levels of centromere protein F (CENPF), a component of the nuclear matrix, are severely reduced at kinetochores in metaphase oocytes following Rab5a knockdown. Consistent with this finding, nuclear lamina disassembly in the transition from prophase arrest to meiosis I is also impaired in Rab5a-depleted oocytes. Notably, oocyte-specific ablation of CENPF phenocopies the meiotic defects resulting from Rab5a knockdown. In summary, our data support a model where Rab5a-positive vesicles, likely through interaction with nuclear lamina, modulate CENPF localization and levels at centromeres, consequently ensuring proper spindle length and kinetochore-microtubule attachment in meiotic oocytes.-Ma, R., Hou, X., Zhang, L., Sun, S.-C., Schedl, T., Moley, K., Wang, Q. Rab5a is required for spindle length control and kinetochore-microtubule attachment during meiosis in oocytes.
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Generation and purification of highly specific antibodies for detecting post-translationally modified proteins in vivo.
Nat Protoc
PUBLISHED: 01-23-2014
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Post-translational modifications alter protein structure, affecting activity, stability, localization and/or binding partners. Antibodies that specifically recognize post-translationally modified proteins have a number of uses including immunocytochemistry and immunoprecipitation of the modified protein to purify protein-protein and protein-nucleic acid complexes. However, antibodies directed at modified sites on individual proteins are often nonspecific. Here we describe a protocol to purify polyclonal antibodies that specifically detect the modified protein of interest. The approach uses iterative rounds of subtraction and affinity purification, using stringent washes to remove antibodies that recognize the unmodified protein and low sequence complexity epitopes containing the modified amino acid. Dot blot and western blot assays are used to assess antibody preparation specificity. The approach is designed to overcome the common occurrence that a single round of subtraction and affinity purification is not sufficient to obtain a modified protein-specific antibody preparation. One full round of antibody purification and specificity testing takes 6 d of discontinuous time.
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Sirt2 functions in spindle organization and chromosome alignment in mouse oocyte meiosis.
FASEB J.
PUBLISHED: 12-12-2013
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Sirtuins have been widely reported to be involved in multiple biological processes; however, their function in oocyte meiosis has not been. Here, by confocal scanning and quantitative analysis, we show that specific depletion of Sirt2 in mouse oocytes results in spindle defects and chromosome disorganization (35.5±8.7 vs. 9.6±3.8% control; P<0.05), with impaired microtubule-kinetochore interaction. Moreover, knockdown and overexpression experiments reveal that Sirt2 modulates the acetylation status of histone H4K16 and ?-tubulin in oocytes, which may in part mediate the defective phenotypes described above by influencing microtubule dynamics and kinetochore function. Finally, we find lower Sirt2 protein level in oocytes from aged mice by immunoblotting and that maternal age-associated meiotic defects can be ameliorated through overexpression of Sirt2 (33.2±5.1% old vs.12.7±5.2% old+Sirt2; P<0.05), providing support for the hypothesis that decreased Sirt2 is one of a number of factors contributing to oocyte age-dependent deficits. In summary, our data indicate a role for Sirt2 during oocyte meiosis and uncover a striking beneficial effect of increased Sirt2 expression on aged oocytes.-Zhang, L., Hou, X., Ma, R., Moley, K., Schedl, T., Wang, Q. Sirt2 functions in spindle organization and chromosome alignment in mouse oocyte meiosis.
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WormBase 2014: new views of curated biology.
Nucleic Acids Res.
PUBLISHED: 11-04-2013
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WormBase (http://www.wormbase.org/) is a highly curated resource dedicated to supporting research using the model organism Caenorhabditis elegans. With an electronic history predating the World Wide Web, WormBase contains information ranging from the sequence and phenotype of individual alleles to genome-wide studies generated using next-generation sequencing technologies. In recent years, we have expanded the contents to include data on additional nematodes of agricultural and medical significance, bringing the knowledge of C. elegans to bear on these systems and providing support for underserved research communities. Manual curation of the primary literature remains a central focus of the WormBase project, providing users with reliable, up-to-date and highly cross-linked information. In this update, we describe efforts to organize the original atomized and highly contextualized curated data into integrated syntheses of discrete biological topics. Next, we discuss our experiences coping with the vast increase in available genome sequences made possible through next-generation sequencing platforms. Finally, we describe some of the features and tools of the new WormBase Web site that help users better find and explore data of interest.
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Discovery of anthelmintic drug targets and drugs using chokepoints in nematode metabolic pathways.
PLoS Pathog.
PUBLISHED: 08-01-2013
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Parasitic roundworm infections plague more than 2 billion people (1/3 of humanity) and cause drastic losses in crops and livestock. New anthelmintic drugs are urgently needed as new drug resistance and environmental concerns arise. A "chokepoint reaction" is defined as a reaction that either consumes a unique substrate or produces a unique product. A chokepoint analysis provides a systematic method of identifying novel potential drug targets. Chokepoint enzymes were identified in the genomes of 10 nematode species, and the intersection and union of all chokepoint enzymes were found. By studying and experimentally testing available compounds known to target proteins orthologous to nematode chokepoint proteins in public databases, this study uncovers features of chokepoints that make them successful drug targets. Chemogenomic screening was performed on drug-like compounds from public drug databases to find existing compounds that target homologs of nematode chokepoints. The compounds were prioritized based on chemical properties frequently found in successful drugs and were experimentally tested using Caenorhabditis elegans. Several drugs that are already known anthelmintic drugs and novel candidate targets were identified. Seven of the compounds were tested in Caenorhabditis elegans and three yielded a detrimental phenotype. One of these three drug-like compounds, Perhexiline, also yielded a deleterious effect in Haemonchus contortus and Onchocerca lienalis, two nematodes with divergent forms of parasitism. Perhexiline, known to affect the fatty acid oxidation pathway in mammals, caused a reduction in oxygen consumption rates in C. elegans and genome-wide gene expression profiles provided an additional confirmation of its mode of action. Computational modeling of Perhexiline and its target provided structural insights regarding its binding mode and specificity. Our lists of prioritized drug targets and drug-like compounds have potential to expedite the discovery of new anthelmintic drugs with broad-spectrum efficacy.
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Stem cell proliferation versus meiotic fate decision in Caenorhabditis elegans.
Adv. Exp. Med. Biol.
PUBLISHED: 06-08-2013
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The C. elegans germ line has emerged as an important model for -understanding how a stem cell population is maintained throughout the life of the animal while still producing the gametes necessary for propagation of the species. The stem cell population in the adult hermaphrodite is relatively large, with stem cells giving rise to daughters that appear intrinsically equivalent; however, some of the daughters retain the proliferative fate while others enter meiotic prophase. While machinery exists for cells to progress through the mitotic cell cycle and machinery exists for cells to progress through meiotic prophase, central to understanding germ line development is identifying the genes and regulatory processes that determine whether the mitotic cell cycle or meiotic prophase machinery will be utilized; in other words, the genes that regulate the switch of germ cells from the proliferative stem cell fate to the meiotic development fate. Whether a germ cell self-renews or enters meiotic prophase is largely determined by its proximity to the distal tip cell (DTC), which is the somatic niche cell that caps the distal end of the gonad. Germ cells close to the DTC have high levels of GLP-1 Notch signaling, which promotes the proliferative fate, while cells further from the DTC have high activity levels of the GLD-1 and GLD-2 redundant RNA regulatory pathways, as well as a third uncharacterized pathway, each of which direct cells to enter meiotic prophase. Other factors and pathways modulate this core genetic pathway, or work in parallel to it, presumably to ensure that a tight balance is maintained between proliferation and meiotic entry.
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Introduction to germ cell development in Caenorhabditis elegans.
Adv. Exp. Med. Biol.
PUBLISHED: 06-08-2013
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A central feature of the continuum of life in sexually reproducing metazoans is the cycle of the germline from one generation to the next. This volume describes the cycle of the germline for Caenorhabditis elegans through chapters that are focused on distinct aspects or processes in germ cell development. Topics include sequential and dependent processes such as specification of germ cells as distinct from somatic cells, sex determination, stem cell proliferative fate versus meiotic development decision, recombination/progression through meiotic prophase, contemporaneous processes such as gametogenesis, meiotic development and apoptosis, and continuing the cycle into the next generation through fertilization and the oocyte-to-embryo transition. Throughout germ cell development, translational control and epigenetic mechanisms play prominent roles. These different aspects of germ cell development are seamlessly integrated under optimal conditions and are modified in the different reproductive strategies that are employed by C. elegans under harsh environmental conditions. In this chapter, we set the stage by providing a brief background on the C. elegans system and germ cell development, indicating processes in the cycle of the germline that are covered in each chapter.
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Toward an interactive article: integrating journals and biological databases.
BMC Bioinformatics
PUBLISHED: 05-19-2011
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Journal articles and databases are two major modes of communication in the biological sciences, and thus integrating these critical resources is of urgent importance to increase the pace of discovery. Projects focused on bridging the gap between journals and databases have been on the rise over the last five years and have resulted in the development of automated tools that can recognize entities within a document and link those entities to a relevant database. Unfortunately, automated tools cannot resolve ambiguities that arise from one term being used to signify entities that are quite distinct from one another. Instead, resolving these ambiguities requires some manual oversight. Finding the right balance between the speed and portability of automation and the accuracy and flexibility of manual effort is a crucial goal to making text markup a successful venture.
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Cyclin E and CDK-2 regulate proliferative cell fate and cell cycle progression in the C. elegans germline.
Development
PUBLISHED: 05-12-2011
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The C. elegans germline provides an excellent model for analyzing the regulation of stem cell activity and the decision to differentiate and undergo meiotic development. The distal end of the adult hermaphrodite germline contains the proliferative zone, which includes a population of mitotically cycling cells and cells in meiotic S phase, followed by entry into meiotic prophase. The proliferative fate is specified by somatic distal tip cell (DTC) niche-germline GLP-1 Notch signaling through repression of the redundant GLD-1 and GLD-2 pathways that promote entry into meiosis. Here, we describe characteristics of the proliferative zone, including cell cycle kinetics and population dynamics, as well as the role of specific cell cycle factors in both cell cycle progression and the decision between the proliferative and meiotic cell fate. Mitotic cell cycle progression occurs rapidly, continuously, with little or no time spent in G1, and with cyclin E (CYE-1) levels and activity high throughout the cell cycle. In addition to driving mitotic cell cycle progression, CYE-1 and CDK-2 also play an important role in proliferative fate specification. Genetic analysis indicates that CYE-1/CDK-2 promotes the proliferative fate downstream or in parallel to the GLD-1 and GLD-2 pathways, and is important under conditions of reduced GLP-1 signaling, possibly corresponding to mitotically cycling proliferative zone cells that are displaced from the DTC niche. Furthermore, we find that GLP-1 signaling regulates a third pathway, in addition to the GLD-1 and GLD-2 pathways and also independent of CYE-1/CDK-2, to promote the proliferative fate/inhibit meiotic entry.
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A high-resolution C. elegans essential gene network based on phenotypic profiling of a complex tissue.
Cell
PUBLISHED: 03-24-2011
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High-content screening for gene profiling has generally been limited to single cells. Here, we explore an alternative approach-profiling gene function by analyzing effects of gene knockdowns on the architecture of a complex tissue in a multicellular organism. We profile 554 essential C. elegans genes by imaging gonad architecture and scoring 94 phenotypic features. To generate a reference for evaluating methods for network construction, genes were manually partitioned into 102 phenotypic classes, predicting functions for uncharacterized genes across diverse cellular processes. Using this classification as a benchmark, we developed a robust computational method for constructing gene networks from high-content profiles based on a network context-dependent measure that ranks the significance of links between genes. Our analysis reveals that multi-parametric profiling in a complex tissue yields functional maps with a resolution similar to genetic interaction-based profiling in unicellular eukaryotes-pinpointing subunits of macromolecular complexes and components functioning in common cellular processes.
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MPK-1 ERK controls membrane organization in C. elegans oogenesis via a sex-determination module.
Dev. Cell
PUBLISHED: 03-01-2011
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Tissues that generate specialized cell types in a production line must coordinate developmental mechanisms with physiological demand, although how this occurs is largely unknown. In the Caenorhabditis elegans hermaphrodite, the developmental sex-determination cascade specifies gamete sex in the distal germline, while physiological sperm signaling activates MPK-1/ERK in the proximal germline to control plasma membrane biogenesis and organization during oogenesis. We discovered repeated utilization of a self-contained negative regulatory module, consisting of NOS-3 translational repressor, FEM-CUL-2 (E3 ubiquitin ligase), and TRA-1 (Gli transcriptional repressor), which acts both in sex determination and in physiological demand control of oogenesis, coordinating these processes. In the distal germline, where MPK-1 is not activated, TRA-1 represses the male fate as NOS-3 functions in translational repression leading to inactivation of the FEM-CUL-2 ubiquitin ligase. In the proximal germline, sperm-dependent physiological MPK-1 activation results in phosphorylation-based inactivation of NOS-3, FEM-CUL-2-mediated degradation of TRA-1 and the promotion of membrane organization during oogenesis.
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Cellular reprogramming: chromatin puts on the brake.
Curr. Biol.
PUBLISHED: 02-22-2011
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Directed reprogramming of differentiated cells allows the generation of specific cell types for therapeutics and can provide unexpected insights into development. A recent study demonstrates that efficient reprogramming of Caenorhabditis elegans germ cells into neurons can be achieved by knocking down a histone chaperone gene and ectopic expression of a terminal selector transcription factor.
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C. elegans star proteins, GLD-1 and ASD-2, regulate specific RNA targets to control development.
Adv. Exp. Med. Biol.
PUBLISHED: 12-31-2010
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A comprehensive understanding of the C. elegans STAR proteins GLD-1 and ASD-2 is emerging from a combination of studies. Those employing genetic analysis reveal in vivo function, others involving biochemical approaches pursue the identification of mRNA targets through which these proteins act. Lastly, mechanistic studies provide the molecular pathway of target mRNA regulation.
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Mitochondrial dysfunction and apoptosis in cumulus cells of type I diabetic mice.
PLoS ONE
PUBLISHED: 08-20-2010
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Impaired oocyte quality has been demonstrated in diabetic mice; however, the potential pathways by which maternal diabetes exerts its effects on the oocyte are poorly understood. Cumulus cells are in direct contact with the oocyte via gap junctions and provide essential nutrients to support oocyte development. In this study, we investigated the effects of maternal diabetes on the mitochondrial status in cumulus cells. We found an increased frequency of fragmented mitochondria, a decreased transmembrane potential and an aggregated distribution of mitochondria in cumulus cells from diabetic mice. Furthermore, while mitochondrial biogenesis in cumulus cells was induced by maternal diabetes, their metabolic function was disrupted as evidenced by lower ATP and citrate levels. Moreover, we present evidence suggesting that the mitochondrial impairments induced by maternal diabetes, at least in part, lead to cumulus cell apoptosis through the release of cytochrome c. Together the deleterious effects on cumulus cells may disrupt trophic and signaling interactions with the oocyte, contributing to oocyte incompetence and thus poor pregnancy outcomes in diabetic females.
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PRP-17 and the pre-mRNA splicing pathway are preferentially required for the proliferation versus meiotic development decision and germline sex determination in Caenorhabditis elegans.
Dev. Dyn.
PUBLISHED: 04-27-2010
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In C. elegans, the decision between germline stem cell proliferation and entry into meiosis is controlled by GLP-1 Notch signaling, which promotes proliferation through repression of the redundant GLD-1 and GLD-2 pathways that direct meiotic entry. We identify prp-17 as another gene functioning downstream of GLP-1 signaling that promotes meiotic entry, largely by acting on the GLD-1 pathway, and that also functions in female germline sex determination. PRP-17 is orthologous to the yeast and human pre-mRNA splicing factor PRP17/CDC40 and can rescue the temperature-sensitive lethality of yeast PRP17. This link to splicing led to an RNAi screen of predicted C. elegans splicing factors in sensitized genetic backgrounds. We found that many genes throughout the splicing cascade function in the proliferation/meiotic entry decision and germline sex determination indicating that splicing per se, rather than a novel function of a subset of splicing factors, is necessary for these processes.
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EOR-2 is an obligate binding partner of the BTB-zinc finger protein EOR-1 in Caenorhabditis elegans.
Genetics
PUBLISHED: 01-11-2010
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BTB-zinc finger transcription factors play many important roles in metazoan development. In these proteins, the BTB domain is critical for dimerization and for recruiting cofactors to target genes. Identification of these cofactors is important for understanding how BTB-zinc finger proteins influence transcription. Here we show that the novel but conserved protein EOR-2 is an obligate binding partner of the BTB-zinc finger protein EOR-1 in Caenorhabditis elegans. EOR-1 and EOR-2 function together to promote multiple Ras/ERK-dependent cell fates during development, and we show that EOR-1 is a robust substrate of ERK in vitro. A point mutation (L81F) in the EOR-1 BTB domain reduces both ERK phosphorylation and EOR-2 binding and eliminates all detectable biological function without affecting EOR-1 expression levels, localization, or dimerization. This point mutation lies near the predicted charged pocket region of the EOR-1 BTB dimer, a region that, in other BTB-zinc finger proteins, has been proposed to interact with corepressors or coactivators. We also show that a conserved zinc finger-like motif in EOR-2 is required for binding to EOR-1, that the interaction between EOR-1 and EOR-2 is direct, and that EOR-2 can bind to the human BTB-zinc finger protein PLZF. We propose that EOR-2 defines a new family of cofactors for BTB-zinc finger transcription factors that may have conserved roles in other organisms.
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A role for dynein in the inhibition of germ cell proliferative fate.
Mol. Cell. Biol.
PUBLISHED: 09-14-2009
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During normal development as well as in diseased states such as cancer, extracellular "niches" often provide cues to proximal cells and activate intracellular pathways. Activation of such signaling pathways in turn instructs cellular proliferation and differentiation. In the Caenorhabditis elegans gonad, GLP-1/Notch signaling instructs germ line stem cells to self-renew through mitotic cell division. As germ cells progressively move out of the niche, they differentiate by entering meiosis and eventually form gametes. In this model system, we uncovered an unexpected role for the dynein motor complex in promoting normal differentiation of proliferating germ cells. We demonstrate that dynein light chain 1 (DLC-1) and its partner, dynein heavy chain 1, inhibit the proliferative cell fate, in part through regulation of METT-10, a conserved putative methyltransferase. We show that DLC-1 physically interacts with METT-10 and promotes both its overall levels and nuclear accumulation. Our results add a new dimension to the processes controlled by the dynein motor complex, demonstrating that dynein can act as an antiproliferative factor.
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METT-10, a putative methyltransferase, inhibits germ cell proliferative fate in Caenorhabditis elegans.
Genetics
PUBLISHED: 07-13-2009
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Germ-line stem cells are unique because they either self-renew through mitosis or, at a certain frequency, switch to meiosis and produce gametes. The switch from proliferation to meiosis is tightly regulated, and aberrations in switching result in either too little or too much proliferation. To understand the genetic basis of this regulation, we characterized loss-of-function mutations and a novel tumorous allele of Caenorhabditis elegans mett-10, which encodes a conserved putative methyltransferase. We show that METT-10 is a nuclear protein that acts in the germ line to inhibit the specification of germ-cell proliferative fate. METT-10 also promotes vulva, somatic gonad, and embryo development and ensures meiotic development of those germ cells that do differentiate. In addition, phenotypic analysis of a mett-10 null allele reveals that METT-10 enables mitotic cell cycle progression. The finding that METT-10 functions to inhibit germ-cell proliferative fate, despite promoting mitotic cell cycle progression of those germ cells that do proliferate, separates the specification of proliferative fate from its execution.
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Maternal diabetes causes mitochondrial dysfunction and meiotic defects in murine oocytes.
Mol. Endocrinol.
PUBLISHED: 07-02-2009
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The adverse effects of maternal diabetes on embryo development and pregnancy outcomes have recently been shown to occur as early as the one-cell zygote stage. The hypothesis of this study was that maternally inherited mitochondria in oocytes from diabetic mice are abnormal and thus responsible in part for this latency of developmental compromise. In ovulated oocytes from diabetic mice, transmission electron microscopy revealed an alteration in mitochondrial ultrastructure, and the quantitative analysis of mitochondrial DNA copy number demonstrated an increase. The levels of ATP and tricarboxylic acid cycle metabolites in diabetic oocytes were markedly reduced compared with controls, suggesting a mitochondrial metabolic dysfunction. Abnormal distribution of mitochondria within maturing oocytes also was seen in diabetic mice. Furthermore, oocytes from diabetic mice displayed a higher frequency of spindle defects and chromosome misalignment in meiosis, resulting in increased aneuploidy rates in ovulated oocytes. Collectively, our results suggest that maternal diabetes results in oocyte defects that are transmitted to the fetus by two routes: first, meiotic spindle and chromatin defects result in nondisjunction leading to embryonic aneuploidy; second, structural and functional abnormalities of oocyte mitochondria, through maternal transmission, provide the embryo with a dysfunctional complement of mitochondria that may be propagated during embryogenesis.
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Multiple ERK substrates execute single biological processes in Caenorhabditis elegans germ-line development.
Proc. Natl. Acad. Sci. U.S.A.
PUBLISHED: 03-05-2009
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RAS-extracellular signal regulated kinase (ERK) signaling governs multiple aspects of cell fate specification, cellular transitions, and growth by regulating downstream substrates through phosphorylation. Understanding how perturbations to the ERK signaling pathway lead to developmental disorders and cancer hinges critically on identification of the substrates. Yet, only a limited number of substrates have been identified that function in vivo to execute ERK-regulated processes. The Caenorhabditis elegans germ line utilizes the well-conserved RAS-ERK signaling pathway in multiple different contexts. Here, we present an integrated functional genomic approach that identified 30 ERK substrates, each of which functions to regulate one or more of seven distinct biological processes during C. elegans germ-line development. Our results provide evidence for three themes that underlie the robustness and specificity of biological outcomes controlled by ERK signaling in C. elegans that are likely relevant to ERK signaling in other organisms: (i) multiple diverse ERK substrates function to control each individual biological process; (ii) different combinations of substrates function to control distinct biological processes; and (iii) regulatory feedback loops between ERK and its substrates help reinforce or attenuate ERK activation. Substrates identified here have conserved orthologs in humans, suggesting that insights from these studies will contribute to our understanding of human diseases involving deregulated ERK activity.
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High fat diet induced developmental defects in the mouse: oocyte meiotic aneuploidy and fetal growth retardation/brain defects.
PLoS ONE
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Maternal obesity is associated with poor outcomes across the reproductive spectrum including infertility, increased time to pregnancy, early pregnancy loss, fetal loss, congenital abnormalities and neonatal conditions. Furthermore, the proportion of reproductive-aged woman that are obese in the population is increasing sharply. From current studies it is not clear if the origin of the reproductive complications is attributable to problems that arise in the oocyte or the uterine environment.
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The 2012 Thomas Hunt Morgan medal: Kathryn V. Anderson.
Genetics
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The Genetics Society of America annually honors members who have made outstanding contributions to genetics. The Thomas Hunt Morgan Medal recognizes a lifetime contribution to the science of genetics. The Genetics Society of America Medal recognizes particularly outstanding contributions to the science of genetics over the past 31 years. The George W. Beadle Medal recognizes distinguished service to the field of genetics and the community of geneticists. The Elizabeth W. Jones Award for Excellence in Education recognizes individuals or groups who have had a significant, sustained impact on genetics education at any level, from kindergarten through graduate school and beyond. The Novitski Prize recognizes an extraordinary level of creativity and intellectual ingenuity in solving significant problems in biological research through the application of genetic methods. We are pleased to announce the 2012 awards.
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An intercellular pathway for glucose transport into mouse oocytes.
Am. J. Physiol. Endocrinol. Metab.
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Glucose is an essential nutrient for mammalian cells. Emerging evidence suggests that glucose within the oocyte regulates meiotic maturation. However, it remains controversial as to whether, and if so how, glucose enters oocytes within cumulus-oocyte complexes (COCs). We used a fluorescent glucose derivative (6-NBDG) to trace glucose transport within live mouse COCs and employed inhibitors of glucose transporters (GLUTs) and gap junction proteins to examine their distinct roles in glucose uptake by cumulus cells and the oocyte. We showed that fluorescent glucose enters both cumulus-enclosed and denuded oocytes. Treating COCs with GLUT inhibitors leads to simultaneous decreases in glucose uptake in cumulus cells and the surrounded oocyte but no effect on denuded oocytes. Pharmacological blockade of of gap junctions between the oocyte and cumulus cells significantly inhibited fluorescent glucose transport to oocytes. Moreover, we find that both in vivo hyperglycemic environment and in vitro high-glucose culture increase free glucose levels in oocytes via gap junctional channels. These findings reveal an intercellular pathway for glucose transport into oocytes: glucose is taken up by cumulus cells via the GLUT system and then transferred into the oocyte through gap junctions. This intercellular pathway may partly mediate the effects of high-glucose condition on oocyte quality.
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TEG-1 CD2BP2 regulates stem cell proliferation and sex determination in the C. elegans germ line and physically interacts with the UAF-1 U2AF65 splicing factor.
Dev. Dyn.
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For a stem cell population to exist over an extended period, a balance must be maintained between self-renewing (proliferating) and differentiating daughter cells. Within the Caenorhabditis elegans germ line, this balance is controlled by a genetic regulatory pathway, which includes the canonical Notch signaling pathway.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

How does it work?

We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.