Chromosome 10
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Searching the Genomes of Inbred Mouse Strains for Incompatibilities That Reproductively Isolate Their Wild Relatives
Journal of Heredity 2007:98(2):115–122 ª The American Genetic Association. 2007. All rights reserved. doi:10.1093/jhered/esl064 For permissions, please email: [email protected]. Advance Access publication January 5, 2007 Searching the Genomes of Inbred Mouse Strains for Incompatibilities That Reproductively Isolate Their Wild Relatives BRET A. PAYSEUR AND MICHAEL PLACE From the Laboratory of Genetics, University of Wisconsin, Madison, WI 53706. Address correspondence to the author at the address above, or e-mail: [email protected]. Abstract Identification of the genes that underlie reproductive isolation provides important insights into the process of speciation. According to the Dobzhansky–Muller model, these genes suffer disrupted interactions in hybrids due to independent di- vergence in separate populations. In hybrid populations, natural selection acts to remove the deleterious heterospecific com- binations that cause these functional disruptions. When selection is strong, this process can maintain multilocus associations, primarily between conspecific alleles, providing a signature that can be used to locate incompatibilities. We applied this logic to populations of house mice that were formed by hybridization involving two species that show partial reproductive isolation, Mus domesticus and Mus musculus. Using molecular markers likely to be informative about species ancestry, we scanned the genomes of 1) classical inbred strains and 2) recombinant inbred lines for pairs of loci that showed extreme linkage disequi- libria. By using the same set of markers, we identified a list of locus pairs that displayed similar patterns in both scans. These genomic regions may contain genes that contribute to reproductive isolation between M. domesticus and M. -
Construction of Stable Mouse Arti Cial Chromosome from Native Mouse
Construction of Stable Mouse Articial Chromosome from Native Mouse Chromosome 10 for Generation of Transchromosomic Mice Satoshi Abe Tottori University Kazuhisa Honma Trans Chromosomics, Inc Akane Okada Tottori University Kanako Kazuki Tottori University Hiroshi Tanaka Trans Chromosomics, Inc Takeshi Endo Trans Chromosomics, Inc Kayoko Morimoto Trans Chromosomics, Inc Takashi Moriwaki Tottori University Shusei Hamamichi Tottori University Yuji Nakayama Tottori University Teruhiko Suzuki Tokyo Metropolitan Institute of Medical Science Shoko Takehara Trans Chromosomics, Inc Mitsuo Oshimura Tottori University Yasuhiro Kazuki ( [email protected] ) Tottori University Research Article Page 1/21 Keywords: mouse articial chromosome (MAC), microcell-mediated chromosome transfer (MMCT), chromosome engineering, transchromosomic (Tc) mouse, humanized model mouse Posted Date: July 9th, 2021 DOI: https://doi.org/10.21203/rs.3.rs-675300/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 2/21 Abstract Mammalian articial chromosomes derived from native chromosomes have been applied to biomedical research and development by generating cell sources and transchromosomic (Tc) animals. Human articial chromosome (HAC) is a precedent chromosomal vector which achieved generation of valuable humanized animal models for fully human antibody production and human pharmacokinetics. While humanized Tc animals created by HAC vector have attained signicant contributions, there was a potential issue to be addressed regarding stability in mouse tissues, especially highly proliferating hematopoietic cells. Mouse articial chromosome (MAC) vectors derived from native mouse chromosome 11 demonstrated improved stability, and they were utilized for humanized Tc mouse production as a standard vector. In mouse, however, stability of MAC vector derived from native mouse chromosome other than mouse chromosome 11 remains to be evaluated. -
Synovial Sarcoma: Recent Discoveries As a Roadmap to New Avenues for Therapy
Published OnlineFirst January 22, 2015; DOI: 10.1158/2159-8290.CD-14-1246 REVIEW Synovial Sarcoma: Recent Discoveries as a Roadmap to New Avenues for Therapy Torsten O. Nielsen 1 , Neal M. Poulin 1 , and Marc Ladanyi 2 ABSTRACT Oncogenesis in synovial sarcoma is driven by the chromosomal translocation t(X,18; p11,q11), which generates an in-frame fusion of the SWI/SNF subunit SS18 to the C-terminal repression domains of SSX1 or SSX2. Proteomic studies have identifi ed an integral role of SS18–SSX in the SWI/SNF complex, and provide new evidence for mistargeting of polycomb repression in synovial sarcoma. Two recent in vivo studies are highlighted, providing additional support for the importance of WNT signaling in synovial sarcoma: One used a conditional mouse model in which knock- out of β-catenin prevents tumor formation, and the other used a small-molecule inhibitor of β-catenin in xenograft models. Signifi cance: Synovial sarcoma appears to arise from still poorly characterized immature mesenchymal progenitor cells through the action of its primary oncogenic driver, the SS18–SSX fusion gene, which encodes a multifaceted disruptor of epigenetic control. The effects of SS18–SSX on polycomb-mediated gene repression and SWI/SNF chromatin remodeling have recently come into focus and may offer new insights into the basic function of these processes. A central role for deregulation of WNT–β-catenin sig- naling in synovial sarcoma has also been strengthened by recent in vivo studies. These new insights into the the biology of synovial sarcoma are guiding novel preclinical and clinical studies in this aggressive cancer. -
MLLT10 (AF10) Antibody (Center) Purified Rabbit Polyclonal Antibody (Pab) Catalog # Ap1906b
苏州工业园区双圩路9号1幢 邮 编 ： 215000 电 话 ： 0512-88856768 MLLT10 (AF10) Antibody (Center) Purified Rabbit Polyclonal Antibody (Pab) Catalog # AP1906b Specification MLLT10 (AF10) Antibody (Center) - Product info Application WB, IF Primary Accession P55197 Reactivity Human Host Rabbit Clonality Polyclonal Isotype Rabbit Ig MLLT10 (AF10) Antibody (Center) - Additional info Gene ID 8028 Other Names Protein AF-10, ALL1-fused gene from chromosome 10 protein, MLLT10, AF10 Western blot analysis of MLLT10 (Cat. Target/Specificity #AP1906b) in K562 cell line lysates This MLLT10 (AF10) antibody is generated from rabbits (35ug/lane). MLLT10 (arrow) was immunized with a KLH conjugated synthetic peptide between detected using the purified Pab.(2ug/ml) 294-323 amino acids from the Central region of human MLLT10 (AF10). Dilution WB~~1:1000 IF~~1:10~50 Format Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS. Storage Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. Precautions MLLT10 (AF10) Antibody (Center) is for research use only and Fluorescent confocal image of Hela cell not for use in diagnostic or therapeutic procedures. stained with MLLT10 (AF10) Antibody (Center)(Cat#AP1906b).HeLa cells were fixed with 4% PFA (20 min), MLLT10 (AF10) Antibody (Center) - Protein Information permeabilized with Triton X-100 (0.1%, 10 min), then incubated with MLLT10 Name MLLT10 (HGNC:16063) primary antibody (1:25, 1 h at 37℃). For secondary antibody, Alexa Fluor® 488 Function conjugated donkey anti-rabbit antibody Probably involved in transcriptional regulation. -
Hormonal Regulation of TSEI-Repressed Genes:Evidence
MOLECULAR AND CELLULAR BIOLOGY, JUlY 1989, p. 2837-2846 Vol. 9, No. 7 0270-7306/89/072837-10$02.00/0 Copyright C) 1989, American Society for Microbiology Hormonal Regulation of TSEI-Repressed Genes: Evidence for Multiple Genetic Controls in Extinction MATHEW J. THAYER AND R. E. K. FOURNIER* Department of Molecul(ar Medicine, Fred Hiutchinson Cancer Research Center, 1124 Columbia Street, Seattle, Washington 98104 Received 9 January 1989/Accepted 26 March 1989 Somatic cell hybrids formed by fusing hepatoma cells with fibroblasts generally fail to express liver functions, a phenomenon termed extinction. Previous studies demonstrated that extinction of the genes encoding tyrosine aminotransferase, phosphoenolpyruvate carboxykinase, and argininosuccinate synthetase is mediated by a specific genetic locus (TSEI) that maps to mouse chromosome 11 and human chromosome 17. In this report, we show that full repression of these genes requires a genetic factor in addition to TSE1. This conclusion is based on the observation that residual gene activity was apparent in monochromosomal hybrids retaining human TSEI but not in complex hybrids retaining many fibroblast chromosomes. Furthermore, TSE1- repressed genes were hormone inducible, whereas fully extinguished genes were not. Analysis of hybrid segregants indicated that genetic loci required for the complete repression phenotype were distinct from TSE1. Tissue-specific gene expression in mammalian cells is ing that single fibroblast chromosome are extinguished for primarily regulated at the level of transcription (8). A par- both serum albumin and alcohol dehydrogenase gene activ- ticular gene may account for a large fraction of total tran- ity (A. C. Chin and R. E. K. Fournier, submitted for publi- scription in one cell type yet be virtually silent in other cell cation). -
134 Mb (Almost the Same As the Size of Chromosome 10). It Is ~4–4.5% of the Total Human Genome
Chromosome 11 ©Chromosome Disorder Outreach Inc. (CDO) Technical genetic content provided by Dr. Iosif Lurie, M.D. Ph.D Medical Geneticist and CDO Medical Consultant/Advisor. Ideogram courtesy of the University of Washington Department of Pathology: ©1994 David Adler.hum_11.gif Introduction The genetic size of chromosome 11 is ~134 Mb (almost the same as the size of chromosome 10). It is ~4–4.5% of the total human genome. The length of its short arm is ~50 Mb; the length of its long arm in ~84 Mb. Chromosome 11 is a very gene–rich area. It contains ~1,500 genes. Mutations of ~200 of these genes are known to cause birth defects or some functional abnormalities. The short arm of chromosome 11 contains a region which is known to be imprinted. As a result duplications of this region will have different manifestations depending on the sex of the parent responsible for this defect. Phenotypes of persons with duplications of the maternal origin will be different from the phenotypes of the persons with a paternal duplication of the same area. There are ~1,400 patients with different structural abnormalities of chromosome 11 as the only abnormality or in association with abnormalities for other chromosomes. At least 800 of these patients had different deletions of chromosome 11. Deletions of the short arm have been reported in ~250 patients (including those with an additional imbalance); deletions of the long arm have been described in ~550 patients. There are two syndromes caused by deletions of the short arm (both of these syndromes have been known for several years) and one well–known syndrome caused by distal deletions of the long arm (Jacobsen syndrome). -
Whole Exome Sequencing in Families at High Risk for Hodgkin Lymphoma: Identification of a Predisposing Mutation in the KDR Gene
Hodgkin Lymphoma SUPPLEMENTARY APPENDIX Whole exome sequencing in families at high risk for Hodgkin lymphoma: identification of a predisposing mutation in the KDR gene Melissa Rotunno, 1 Mary L. McMaster, 1 Joseph Boland, 2 Sara Bass, 2 Xijun Zhang, 2 Laurie Burdett, 2 Belynda Hicks, 2 Sarangan Ravichandran, 3 Brian T. Luke, 3 Meredith Yeager, 2 Laura Fontaine, 4 Paula L. Hyland, 1 Alisa M. Goldstein, 1 NCI DCEG Cancer Sequencing Working Group, NCI DCEG Cancer Genomics Research Laboratory, Stephen J. Chanock, 5 Neil E. Caporaso, 1 Margaret A. Tucker, 6 and Lynn R. Goldin 1 1Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 2Cancer Genomics Research Laboratory, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 3Ad - vanced Biomedical Computing Center, Leidos Biomedical Research Inc.; Frederick National Laboratory for Cancer Research, Frederick, MD; 4Westat, Inc., Rockville MD; 5Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; and 6Human Genetics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA ©2016 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol.2015.135475 Received: August 19, 2015. Accepted: January 7, 2016. Pre-published: June 13, 2016. Correspondence: [email protected] Supplemental Author Information: NCI DCEG Cancer Sequencing Working Group: Mark H. Greene, Allan Hildesheim, Nan Hu, Maria Theresa Landi, Jennifer Loud, Phuong Mai, Lisa Mirabello, Lindsay Morton, Dilys Parry, Anand Pathak, Douglas R. Stewart, Philip R. Taylor, Geoffrey S. Tobias, Xiaohong R. Yang, Guoqin Yu NCI DCEG Cancer Genomics Research Laboratory: Salma Chowdhury, Michael Cullen, Casey Dagnall, Herbert Higson, Amy A. -
The KMT1A-GATA3-STAT3 Circuit Is a Novel Self-Renewal Signaling of Human Bladder Cancer Stem Cells Zhao Yang1, Luyun He2,3, Kais
The KMT1A-GATA3-STAT3 circuit is a novel self-renewal signaling of human bladder cancer stem cells Zhao Yang1, Luyun He2,3, Kaisu Lin4, Yun Zhang1, Aihua Deng1, Yong Liang1, Chong Li2, 5, & Tingyi Wen1, 6, 1CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China 2Core Facility for Protein Research, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China 3CAS Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China 4Department of Oncology, the Second Affiliated Hospital of Soochow University, Suzhou 215000, China 5Beijing Jianlan Institute of Medicine, Beijing 100190, China 6Savaid Medical School, University of Chinese Academy of Sciences, Beijing 100049, China Correspondence author: Tingyi Wen, e-mail: [email protected] Chong Li, e-mail: [email protected] Supplementary Figure S1. Isolation of human bladder cancer stem cells. BCMab1 and CD44 were used to isolate bladder cancer stem cells (BCSCs: BCMab1+CD44+) and bladder cancer non-stem cells (BCNSCs: BCMab1-CD44-) from EJ, samples #1 and #2 by flow cytometry. Supplementary Figure S2. Gene ontology analysis of downregulated genes of human BCSCs. (A) Pathway enrichment of 103 downregulated genes in BCSCs. (B) The seven downregulated genes in BCSCs participating in centromeric heterochromatin, mRNA-3’-UTR binding and translation regulator activity signaling pathways were validated by qRT-PCR. Data are presented as mean ± SD. P < 0.05; P < 0.01. Supplementary Figure S3. The expression of KMT1A is higher in human BC than that in peri-tumor tissues. (A) The expression of KMT1A was higher in BC samples than that in peri-tumors as assessed by immunohistochemistry, Scale bar = 50 m. -
Usbiological Datasheet
MLLT10, CT (AF10) (Protein AF-10, AF10, ALL1-fused Gene From Chromosome 10 Protein) (Biotin) Catalog number A0923-60C-Biotin Supplier United States Biological Translocations affecting chromosome 11q23 involve many partner chromosome regions and occur in various leukemias. The 11q23 gene involved in the translocations is MLL. MLLT10 is the partner gene to MLL1 involved in t(10;11)(p12;q23) translocations. In an analysis of two leukemia patients, the in t(10;11)(p12;q23) translocation fuses MLL1, a SET domain containg histone methyltransferase, to the MLLT10 gene. The MLLT10 gene encodes a predicted 1,027aa protein containing an N-terminal zinc finger and a C-terminal leucine zipper domain. The MLLT10 gene is one of the few MLL partner genes to be independently rearranged with a third gene in leukemia, the CALM gene in the t(10;11)(p12;q14) translocation. Chimeric fusion proteins MLL/AF10 and CALM/AF10 consistently retain the leucine zipper motif of MLLT10. The leucine zipper interacts with GAS41, a protein previously identified as the product of an amplified gene in a glioblastoma. GAS41 interacts with integrase interactor-1 (INI1), a component of the SWI/SNF complex, which acts to remodel chromatin and to modulate transcription. Retention of the leucine zipper in the MLL and CALM fusions suggested that a key feature of these chimeric proteins may be their ability to interfere in normal gene regulation through interaction with the adenosine triphosphate-dependent chromatin remodeling complexes. Applications Suitable for use in ELISA, Western Blot, and Immunohistochemistry. Other applications not tested. Recommended Dilution ELISA: 1:1,000 Western Blot: 1:100-1:500 Immunohistochemistry: 1:10-1:50 Optimal dilutions to be determined by the researcher. -
Evidence for Linkage of Regions on Chromosomes 6 and 11 to Plasma Glucose Concentrations in Mexican Americans Michael P
Downloaded from genome.cshlp.org on September 26, 2021 - Published by Cold Spring Harbor Laboratory Press RESEARCH Evidence for Linkage of Regions on Chromosomes 6 and 11 to Plasma Glucose Concentrations in Mexican Americans Michael P. Stern, 1'4 Ravindranath Duggirala, 1 Braxton D. Mitchell, 2 Laurie J. Reinhart, ~ Sailaja Shivakumar, ~ Patricia A. Shipman, 3 Olga C. Uresandi, 3 Edgardo Benavides, 3 John Blangero, 2 and Peter O'Connell 3 1Division of Clinical Epidemiology, Department of Medicine, and 3Department of Pathology, University of Texas Health Science Center, San Antonio, Texas 78284; 2Department of Genetics, Southwest Foundation for Biomedical Research, San Antonio, Texas 78245 The genetic factors involved in type I1 diabetes are still unknown. To address this problem, we are creating a I0 to 15; cM genetic map on 444 individuals from 32 Mexican American families ascertained on a type !I diabetic proband. Using highly polymorphic microsatellite markers and a multipoint variance components method, we found evidence for linkage of plasma glucose concentration 2 hr after oral glucose administration to two regions on chromosome I1: Ig-hemoglobin (HBB} and markers DllS899/DIISI324 near the sulfonylurea receptor (SUR) gene. lod scores at these two loci were 2.77 and 3.37, respectively. The SUR gene region accounted for 4-4.7% of the phenotypic variance. Evidence for linkage to fasting glucose concentration was also observed for two loci on chromosome 6, one of which is identical to a proposed susceptibility locus for type I diabetes {D6S290). When diabetics were excluded from the analyses, all lod scores became zero, suggesting that the observed linkages were with the trait diabetes rather than with normal variation in glucose levels. -
Recurrent Involvement of Ring-Type Zinc Finger Genes in Complex
Leukemia (2013) 27, 1745–1791 & 2013 Macmillan Publishers Limited All rights reserved 0887-6924/13 www.nature.com/leu LETTERS TO THE EDITOR Recurrent involvement of ring-type zinc finger genes in complex molecular rearrangements in childhood acute myelogeneous leukemia with translocation t(10;11)(p12;q23) Leukemia (2013) 27, 1745–1791; doi:10.1038/leu.2013.1 the MLL/MLLT10 fusion gene had been detected by conventional FISH and RT-PCR (Table S1). A specimen of the initial and remission sample was obtained in six children; in three of them a Complex rearrangements involving the MLL gene on chromosome relapse sample was available and additionally analyzed after 11q23 and MLLT10 on 10p have been reported in 15% of pediatric informed consent. By analyzing paired-end reads, we were able to patients with MLL rearranged acute myelogeneous leukemia describe these alterations in depth, revealing the precise pattern (AML). Owing to the opposite direction of MLL and MLLT10 of molecular rearrangement and finding other involved chromo- rearrangements (inversion and subsequent translocation or somes. For paired-end sequencing, DNA was isolated from insertion) with three or more breaks are required to result in a peripheral blood lymphocytes, and fragment libraries with a fusion gene.1,2 There are several additional reported median insert size of 450 bp were prepared. Samples of patients recombination partners of the MLL gene, in which a simple 1–3 were sequenced on a GAIIx platform; samples of patients 4–6 reciprocal translocation is insufficient due to incompatible on a HiSeq 2000 (Illumina Inc., San Diego, CA, USA). -
Application of Microarray-Based Comparative Genomic Hybridization in Prenatal and Postnatal Settings: Three Case Reports
SAGE-Hindawi Access to Research Genetics Research International Volume 2011, Article ID 976398, 9 pages doi:10.4061/2011/976398 Case Report Application of Microarray-Based Comparative Genomic Hybridization in Prenatal and Postnatal Settings: Three Case Reports Jing Liu, Francois Bernier, Julie Lauzon, R. Brian Lowry, and Judy Chernos Department of Medical Genetics, University of Calgary, 2888 Shaganappi Trail NW, Calgary, AB, Canada T3B 6A8 Correspondence should be addressed to Judy Chernos, [email protected] Received 16 February 2011; Revised 20 April 2011; Accepted 20 May 2011 Academic Editor: Reha Toydemir Copyright © 2011 Jing Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Microarray-based comparative genomic hybridization (array CGH) is a newly emerged molecular cytogenetic technique for rapid evaluation of the entire genome with sub-megabase resolution. It allows for the comprehensive investigation of thousands and millions of genomic loci at once and therefore enables the efficient detection of DNA copy number variations (a.k.a, cryptic genomic imbalances). The development and the clinical application of array CGH have revolutionized the diagnostic process in patients and has provided a clue to many unidentified or unexplained diseases which are suspected to have a genetic cause. In this paper, we present three clinical cases in both prenatal and postnatal settings. Among all, array CGH played a major discovery role to reveal the cryptic and/or complex nature of chromosome arrangements. By identifying the genetic causes responsible for the clinical observation in patients, array CGH has provided accurate diagnosis and appropriate clinical management in a timely and efficient manner.