Oocyte Aneuploidy—More Tools to Tackle an Old Problem
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Mutational Inactivation of STAG2 Causes Aneuploidy in Human Cancer
REPORTS mean difference for all rubric score elements was ing becomes a more commonly supported facet 18. C. L. Townsend, E. Heit, Mem. Cognit. 39, 204 (2011). rejected. Univariate statistical tests of the observed of STEM graduate education then students’ in- 19. D. F. Feldon, M. Maher, B. Timmerman, Science 329, 282 (2010). mean differences between the teaching-and- structional training and experiences would alle- 20. B. Timmerman et al., Assess. Eval. High. Educ. 36,509 research and research-only conditions indicated viate persistent concerns that current programs (2011). significant results for the rubric score elements underprepare future STEM faculty to perform 21. No outcome differences were detected as a function of “testability of hypotheses” [mean difference = their teaching responsibilities (28, 29). the type of teaching experience (TA or GK-12) within the P sample population participating in both research and 0.272, = 0.006; CI = (.106, 0.526)] with the null teaching. hypothesis rejected in 99.3% of generated data References and Notes 22. Materials and methods are available as supporting samples (Fig. 1) and “research/experimental de- 1. W. A. Anderson et al., Science 331, 152 (2011). material on Science Online. ” P 2. J. A. Bianchini, D. J. Whitney, T. D. Breton, B. A. Hilton-Brown, 23. R. L. Johnson, J. Penny, B. Gordon, Appl. Meas. Educ. 13, sign [mean difference = 0.317, = 0.002; CI = Sci. Educ. 86, 42 (2001). (.106, 0.522)] with the null hypothesis rejected in 121 (2000). 3. C. E. Brawner, R. M. Felder, R. Allen, R. Brent, 24. R. J. A. Little, J. -
A Gene Expression Resource Generated by Genome-Wide Lacz
© 2015. Published by The Company of Biologists Ltd | Disease Models & Mechanisms (2015) 8, 1467-1478 doi:10.1242/dmm.021238 RESOURCE ARTICLE A gene expression resource generated by genome-wide lacZ profiling in the mouse Elizabeth Tuck1,**, Jeanne Estabel1,*,**, Anika Oellrich1, Anna Karin Maguire1, Hibret A. Adissu2, Luke Souter1, Emma Siragher1, Charlotte Lillistone1, Angela L. Green1, Hannah Wardle-Jones1, Damian M. Carragher1,‡, Natasha A. Karp1, Damian Smedley1, Niels C. Adams1,§, Sanger Institute Mouse Genetics Project1,‡‡, James N. Bussell1, David J. Adams1, Ramiro Ramırez-Soliś 1, Karen P. Steel1,¶, Antonella Galli1 and Jacqueline K. White1,§§ ABSTRACT composite of RNA-based expression data sets. Strong agreement was observed, indicating a high degree of specificity in our data. Knowledge of the expression profile of a gene is a critical piece of Furthermore, there were 1207 observations of expression of a information required to build an understanding of the normal and particular gene in an anatomical structure where Bgee had no essential functions of that gene and any role it may play in the data, indicating a large amount of novelty in our data set. development or progression of disease. High-throughput, large- Examples of expression data corroborating and extending scale efforts are on-going internationally to characterise reporter- genotype-phenotype associations and supporting disease gene tagged knockout mouse lines. As part of that effort, we report an candidacy are presented to demonstrate the potential of this open access adult mouse expression resource, in which the powerful resource. expression profile of 424 genes has been assessed in up to 47 different organs, tissues and sub-structures using a lacZ reporter KEY WORDS: Gene expression, lacZ reporter, Mouse, Resource gene. -
DCAF1 Ubiquitin E3 Ligase Directs Protein Phosphatase 2A Degradation to Control Oocyte Meiotic Maturation
ARTICLE Received 28 Jan 2015 | Accepted 7 Jul 2015 | Published 18 Aug 2015 DOI: 10.1038/ncomms9017 OPEN CRL4–DCAF1 ubiquitin E3 ligase directs protein phosphatase 2A degradation to control oocyte meiotic maturation Chao Yu1, Shu-Yan Ji1,*, Qian-Qian Sha1,*, Qing-Yuan Sun2 & Heng-Yu Fan1 Oocyte meiosis is a specialized cell cycle that gives rise to fertilizable haploid gametes and is precisely controlled in various dimensions. We recently found that E3 ubiquitin ligase CRL4 is required for female fertility by regulating DNA hydroxymethylation to maintain oocyte survival and to promote zygotic genome reprogramming. However, not all phenotypes of CRL4-deleted oocytes could be explained by this mechanism. Here we show that CRL4 controls oocyte meiotic maturation by proteasomal degradation of protein phosphatase 2A scaffold subunit, PP2A-A. Oocyte-specific deletion of DDB1 or DCAF1 (also called VPRBP) results in delayed meiotic resumption and failure to complete meiosis I along with PP2A-A accumulation. DCAF1 directly binds to and results in the poly-ubiquitination of PP2A-A. Moreover, combined deletion of Ppp2r1a rescues the meiotic defects caused by DDB1/DCAF1 deficiency. These results provide in vivo evidence that CRL4-directed PP2A-A degradation is physiologically essential for regulating oocyte meiosis and female fertility. 1 Life Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China. 2 State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China. * These authors contributed equally to this work. Correspondence and requests for materials should be addressed to H.-Y.F. (email: [email protected]). -
Reconstructing Cell Cycle Pseudo Time-Series Via Single-Cell Transcriptome Data—Supplement
School of Natural Sciences and Mathematics Reconstructing Cell Cycle Pseudo Time-Series Via Single-Cell Transcriptome Data—Supplement UT Dallas Author(s): Michael Q. Zhang Rights: CC BY 4.0 (Attribution) ©2017 The Authors Citation: Liu, Zehua, Huazhe Lou, Kaikun Xie, Hao Wang, et al. 2017. "Reconstructing cell cycle pseudo time-series via single-cell transcriptome data." Nature Communications 8, doi:10.1038/s41467-017-00039-z This document is being made freely available by the Eugene McDermott Library of the University of Texas at Dallas with permission of the copyright owner. All rights are reserved under United States copyright law unless specified otherwise. File name: Supplementary Information Description: Supplementary figures, supplementary tables, supplementary notes, supplementary methods and supplementary references. CCNE1 CCNE1 CCNE1 CCNE1 36 40 32 34 32 35 30 32 28 30 30 28 28 26 24 25 Normalized Expression Normalized Expression Normalized Expression Normalized Expression 26 G1 S G2/M G1 S G2/M G1 S G2/M G1 S G2/M Cell Cycle Stage Cell Cycle Stage Cell Cycle Stage Cell Cycle Stage CCNE1 CCNE1 CCNE1 CCNE1 40 32 40 40 35 30 38 30 30 28 36 25 26 20 20 34 Normalized Expression Normalized Expression Normalized Expression 24 Normalized Expression G1 S G2/M G1 S G2/M G1 S G2/M G1 S G2/M Cell Cycle Stage Cell Cycle Stage Cell Cycle Stage Cell Cycle Stage Supplementary Figure 1 | High stochasticity of single-cell gene expression means, as demonstrated by relative expression levels of gene Ccne1 using the mESC-SMARTer data. For every panel, 20 sample cells were randomly selected for each of the three stages, followed by plotting the mean expression levels at each stage. -
Multivariate Analysis Reveals Genetic Associations of the Resting Default
Multivariate analysis reveals genetic associations of PNAS PLUS the resting default mode network in psychotic bipolar disorder and schizophrenia Shashwath A. Medaa,1, Gualberto Ruañob,c, Andreas Windemuthb, Kasey O’Neila, Clifton Berwisea, Sabra M. Dunna, Leah E. Boccaccioa, Balaji Narayanana, Mohan Kocherlab, Emma Sprootena, Matcheri S. Keshavand, Carol A. Tammingae, John A. Sweeneye, Brett A. Clementzf, Vince D. Calhoung,h,i, and Godfrey D. Pearlsona,h,j aOlin Neuropsychiatry Research Center, Institute of Living at Hartford Hospital, Hartford, CT 06102; bGenomas Inc., Hartford, CT 06102; cGenetics Research Center, Hartford Hospital, Hartford, CT 06102; dDepartment of Psychiatry, Beth Israel Deaconess Hospital, Harvard Medical School, Boston, MA 02215; eDepartment of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX 75390; fDepartment of Psychology, University of Georgia, Athens, GA 30602; gThe Mind Research Network, Albuquerque, NM 87106; Departments of hPsychiatry and jNeurobiology, Yale University, New Haven, CT 06520; and iDepartment of Electrical and Computer Engineering, The University of New Mexico, Albuquerque, NM 87106 Edited by Robert Desimone, Massachusetts Institute of Technology, Cambridge, MA, and approved April 4, 2014 (received for review July 15, 2013) The brain’s default mode network (DMN) is highly heritable and is Although risk for psychotic illnesses is driven in small part by compromised in a variety of psychiatric disorders. However, ge- highly penetrant, often private mutations such as copy number netic control over the DMN in schizophrenia (SZ) and psychotic variants, substantial risk also is likely conferred by multiple genes bipolar disorder (PBP) is largely unknown. Study subjects (n = of small effect sizes interacting together (7). According to the 1,305) underwent a resting-state functional MRI scan and were “common disease common variant” (CDCV) model, one would analyzed by a two-stage approach. -
TITLE PAGE Oxidative Stress and Response to Thymidylate Synthase
Downloaded from molpharm.aspetjournals.org at ASPET Journals on October 2, 2021 -Targeted -Targeted 1 , University of of , University SC K.W.B., South Columbia, (U.O., Carolina, This article has not been copyedited and formatted. The final version may differ from this version. This article has not been copyedited and formatted. The final version may differ from this version. This article has not been copyedited and formatted. The final version may differ from this version. This article has not been copyedited and formatted. The final version may differ from this version. This article has not been copyedited and formatted. The final version may differ from this version. This article has not been copyedited and formatted. The final version may differ from this version. This article has not been copyedited and formatted. The final version may differ from this version. This article has not been copyedited and formatted. The final version may differ from this version. This article has not been copyedited and formatted. The final version may differ from this version. This article has not been copyedited and formatted. The final version may differ from this version. This article has not been copyedited and formatted. The final version may differ from this version. This article has not been copyedited and formatted. The final version may differ from this version. This article has not been copyedited and formatted. The final version may differ from this version. This article has not been copyedited and formatted. The final version may differ from this version. This article has not been copyedited and formatted. -
Podocin Inactivation in Mature Kidneys Causes Focal Segmental Glomerulosclerosis and Nephrotic Syndrome
BASIC RESEARCH www.jasn.org Podocin Inactivation in Mature Kidneys Causes Focal Segmental Glomerulosclerosis and Nephrotic Syndrome Ge´raldine Mollet,*† Julien Ratelade,*† Olivia Boyer,*†‡ Andrea Onetti Muda,*§ ʈ Ludivine Morisset,*† Tiphaine Aguirre Lavin,*† David Kitzis,*† Margaret J. Dallman, ʈ Laurence Bugeon, Norbert Hubner,¶ Marie-Claire Gubler,*† Corinne Antignac,*†** and Ernie L. Esquivel*† *INSERM, U574, Hoˆpital Necker-Enfants Malades, Paris, France; †Faculte´deMe´ decine Rene´ Descartes, Universite´ Paris Descartes, Paris, France; ‡Pediatric Nephrology Department and **Department of Genetics, Hoˆpital Necker- Enfants Malades, Assistance Publique-Hoˆpitaux de Paris, Paris, France; §Department of Pathology, Campus ʈ Biomedico University, Rome, Italy; Department of Biological Sciences, Imperial College London, London, England; and ¶Max-Delbruck Center for Molecular Medicine, Berlin, Germany ABSTRACT Podocin is a critical component of the glomerular slit diaphragm, and genetic mutations lead to both familial and sporadic forms of steroid-resistant nephrotic syndrome. In mice, constitutive absence of podocin leads to rapidly progressive renal disease characterized by mesangiolysis and/or mesangial sclerosis and nephrotic syndrome. Using established Cre-loxP technology, we inactivated podocin in the adult mouse kidney in a podocyte-specific manner. Progressive loss of podocin in the glomerulus recapitu- lated albuminuria, hypercholesterolemia, hypertension, and renal failure seen in nephrotic syndrome in humans. Lesions of FSGS appeared -
Exomechip-Wide Analysis of 95 626 Individuals Identifies 10 Novel Loci Associated with QT and JT Intervals
1 humans ◼ Circulation: Dan E. January 2018 Creative Commons Creative genome arrhythmias, cardiac arrhythmias, cardiac ◼ License, which permits PhD et al death, sudden, cardiac death, sudden, cardiac genetics The full author list is available on page 7. to: Correspondence Arking, PhD, Johns Hopkins School of Medicine, 733 N. Broadway, MD 21205. MRB 459, Baltimore, E-mail [email protected] Key Words: ◼ ◼ © 2018 The Authors. Genomic and Precision Medicine is published on behalf of the American Heart Association, Inc., Kluwer Health, Inc. This by Wolters is an open access article under the terms of the Attribution Non-Commercial- NoDerivs use, distribution, and reproduction that the in any medium, provided cited, original work is properly and no the use is noncommercial, modifications or adaptations are made. Nathan A. Bihlmeyer, Nathan A. Bihlmeyer, 626 626 individuals 626 individuals 449 variants, both common 449 variants, both common 884 European ancestry individuals, 884 European We performed an ExomeChip-wide analysis performed an ExomeChip-wide analysis We Editorial by Bos and Pereira See 2018;11:e001758. DOI: 10.1161/CIRCGEN.117.001758 QT interval, measured through a standard ECG, captures ECG, captures a standard through QT interval, measured Our analyses show a role for myocyte internal Our analyses show a role structure 341 genes from the Illumina Infinium HumanExome 341 genes from e, in 17 om 23 cohorts (comprised 83 Circ Genom Precis Med. and rar CONCLUSIONS: in modulating QT interval duration, adding to and interconnections of potassium, sodium, and calcium ion regulation, known roles previous anticipate that these discoveries will We as well as autonomic control. -
SGOL2 Antibody (Center) Affinity Purified Rabbit Polyclonal Antibody (Pab) Catalog # Ap20106c
10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 SGOL2 Antibody (Center) Affinity Purified Rabbit Polyclonal Antibody (Pab) Catalog # AP20106c Specification SGOL2 Antibody (Center) - Product Information Application WB,E Primary Accession Q562F6 Other Accession NP_689737.3 Reactivity Human Host Rabbit Clonality Polyclonal Isotype Rabbit Ig Calculated MW 144739 Antigen Region 391-419 SGOL2 Antibody (Center) - Additional Information Gene ID 151246 Other Names Shugoshin-like 2, Shugoshin-2, Sgo2, Tripin, SGOL2 Antibody (Center) (Cat. #AP20106c) SGOL2 western blot analysis in U-937 cell line lysates (35ug/lane).This demonstrates the Target/Specificity SGOL2 antibody detected the SGOL2 protein This SGOL2 antibody is generated from (arrow). rabbits immunized with a KLH conjugated synthetic peptide between 391-419 amino acids from the Central region of human SGOL2 Antibody (Center) - Background SGOL2. Cooperates with PPP2CA to protect Dilution centromeric cohesin from separase-mediated WB~~1:1000 cleavage in oocytes specifically during meiosis I. Has a crucial role in protecting REC8 at Format centromeres from cleavage by separase. Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This During meiosis, protects centromeric cohesion antibody is purified through a protein A complexes until metaphase II/anaphase II column, followed by peptide affinity transition, preventing premature release of purification. meiosis-specific REC8 cohesin complexes from anaphase I centromeres. Is thus essential for Storage an accurate gametogenesis. May act by Maintain refrigerated at 2-8°C for up to 2 targeting PPP2CA to centromeres, thus leading weeks. For long term storage store at -20°C to cohesin dephosphorylation (By similarity). -
The Genetic Program of Pancreatic Beta-Cell Replication in Vivo
Page 1 of 65 Diabetes The genetic program of pancreatic beta-cell replication in vivo Agnes Klochendler1, Inbal Caspi2, Noa Corem1, Maya Moran3, Oriel Friedlich1, Sharona Elgavish4, Yuval Nevo4, Aharon Helman1, Benjamin Glaser5, Amir Eden3, Shalev Itzkovitz2, Yuval Dor1,* 1Department of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel 2Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel. 3Department of Cell and Developmental Biology, The Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel 4Info-CORE, Bioinformatics Unit of the I-CORE Computation Center, The Hebrew University and Hadassah, The Institute for Medical Research Israel- Canada, The Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel 5Endocrinology and Metabolism Service, Department of Internal Medicine, Hadassah-Hebrew University Medical Center, Jerusalem 91120, Israel *Correspondence: [email protected] Running title: The genetic program of pancreatic β-cell replication 1 Diabetes Publish Ahead of Print, published online March 18, 2016 Diabetes Page 2 of 65 Abstract The molecular program underlying infrequent replication of pancreatic beta- cells remains largely inaccessible. Using transgenic mice expressing GFP in cycling cells we sorted live, replicating beta-cells and determined their transcriptome. Replicating beta-cells upregulate hundreds of proliferation- related genes, along with many novel putative cell cycle components. Strikingly, genes involved in beta-cell functions, namely glucose sensing and insulin secretion were repressed. Further studies using single molecule RNA in situ hybridization revealed that in fact, replicating beta-cells double the amount of RNA for most genes, but this upregulation excludes genes involved in beta-cell function. -
Transdifferentiation of Human Mesenchymal Stem Cells
Transdifferentiation of Human Mesenchymal Stem Cells Dissertation zur Erlangung des naturwissenschaftlichen Doktorgrades der Julius-Maximilians-Universität Würzburg vorgelegt von Tatjana Schilling aus San Miguel de Tucuman, Argentinien Würzburg, 2007 Eingereicht am: Mitglieder der Promotionskommission: Vorsitzender: Prof. Dr. Martin J. Müller Gutachter: PD Dr. Norbert Schütze Gutachter: Prof. Dr. Georg Krohne Tag des Promotionskolloquiums: Doktorurkunde ausgehändigt am: Hiermit erkläre ich ehrenwörtlich, dass ich die vorliegende Dissertation selbstständig angefertigt und keine anderen als die von mir angegebenen Hilfsmittel und Quellen verwendet habe. Des Weiteren erkläre ich, dass diese Arbeit weder in gleicher noch in ähnlicher Form in einem Prüfungsverfahren vorgelegen hat und ich noch keinen Promotionsversuch unternommen habe. Gerbrunn, 4. Mai 2007 Tatjana Schilling Table of contents i Table of contents 1 Summary ........................................................................................................................ 1 1.1 Summary.................................................................................................................... 1 1.2 Zusammenfassung..................................................................................................... 2 2 Introduction.................................................................................................................... 4 2.1 Osteoporosis and the fatty degeneration of the bone marrow..................................... 4 2.2 Adipose and bone -
Oryctolagus Cuniculus)
Genome Gene Expression Profiling Analysis Reveals Fur Development in Rex Rabbits (Oryctolagus cuniculus) Journal: Genome Manuscript ID gen-2017-0003.R2 Manuscript Type: Article Date Submitted by the Author: 31-Jul-2017 Complete List of Authors: Zhao, Bohao; Yangzhou University Chen, Yang; Yangzhou University Yan, Xiaorong ; Yangzhou University Hao, Ye; YangzhouDraft University Zhu, Jie; Yangzhou University Weng, Qiiaoqing; Zhejiang Yuyao Xinnong Rabbit Industry Co., Ltd. Wu, Xinsheng; Yangzhou University, College of Animal Science and Technology Is the invited manuscript for consideration in a Special This submission is not invited Issue? : Keyword: Chinchilla rex rabbit, fur development, key gene, transcriptome https://mc06.manuscriptcentral.com/genome-pubs Page 1 of 138 Genome 1 Gene Expression Profiling Analysis Reveals Fur Development in Rex 2 Rabbits ( Oryctolagus cuniculus ) 3 BoHao Zhao 1, Yang Chen 1, XiaoRong Yan 1, Ye Hao 1, Jie Zhu 1, QiaoQing Weng 2, and 4 XinSheng Wu 1* 5 1 The Key Laboratory of Animal Genetics & Breeding and Molecular Design of Jiangsu Province, 6 College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, P.R. 7 China. ; 8 2 Zhejiang Yuyao Xinnong Rabbit Industry Co., Ltd., Yuyao, Zhejiang 315400, China 9 *Corresponding author E-mail: [email protected] 10 Draft 1 https://mc06.manuscriptcentral.com/genome-pubs Genome Page 2 of 138 11 Abstract 12 Fur is an important economic trait in rabbits. The identification of genes that 13 influence fur development and knowledge regarding the actions of these genes 14 provides useful tools for improving fur quality. However, the mechanism of fur 15 development is unclear. To obtain candidate genes related to fur development, the 16 transcriptomes of tissues from backs and bellies of Chinchilla rex rabbits were 17 compared.