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  • 1
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    Identification of sister chromatids by DNA template strand sequences (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-12-18
    Description: It is generally assumed that sister chromatids are genetically and functionally identical and that segregation to daughter cells is a random process. However, functional differences between sister chromatids regulate daughter cell fate in yeast and sister chromatid segregation is not random in Escherichia coli. Differentiated sister chromatids, coupled with non-random segregation, have been proposed to regulate cell fate during the development of multicellular organisms. This hypothesis has not been tested because molecular features to reliably distinguish between sister chromatids are not obvious. Here we show that parental 'Watson' and 'Crick' DNA template strands can be identified in sister chromatids of murine metaphase chromosomes using CO-FISH (chromosome orientation fluorescence in situ hybridization) with unidirectional probes specific for centromeric and telomeric repeats. All chromosomes were found to have a uniform orientation with the 5' end of the short arm on the same strand as T-rich major satellite repeats. The invariable orientation of repetitive DNA was used to differentially label sister chromatids and directly study mitotic segregation patterns in different cell types. Whereas sister chromatids appeared to be randomly distributed between daughter cells in cultured lung fibroblasts and embryonic stem cells, significant non-random sister chromatid segregation was observed in a subset of colon crypt epithelial cells, including cells outside positions reported for colon stem cells. Our results establish that DNA template sequences can be used to distinguish sister chromatids and follow their mitotic segregation in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3757939/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3757939/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Falconer, Ester -- Chavez, Elizabeth A -- Henderson, Alexander -- Poon, Steven S S -- McKinney, Steven -- Brown, Lindsay -- Huntsman, David G -- Lansdorp, Peter M -- R01 GM094146/GM/NIGMS NIH HHS/ -- RMF-92093/Canadian Institutes of Health Research/Canada -- England -- Nature. 2010 Jan 7;463(7277):93-7. doi: 10.1038/nature08644. Epub 2009 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Terry Fox Laboratory, B.C. Cancer Agency, Vancouver, British Columbia V5Z 1L3, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016487" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chromatids/*genetics/*metabolism ; Chromosome Segregation/*physiology ; Colon/cytology ; DNA, Satellite/metabolism ; Embryonic Stem Cells/cytology ; Epithelial Cells/cytology ; Fibroblasts/cytology ; Fluorescence ; In Situ Hybridization, Fluorescence/*methods ; Luminescent Measurements ; Lung/cytology ; Mice ; Mice, Inbred C57BL ; Mitosis ; Models, Biological ; Organ Specificity ; Substrate Specificity ; Telomere/metabolism ; Templates, Genetic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    MHC class II transactivator CIITA is a recurrent gene fusion partner in lymphoid cancers (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-03-04
    Description: Chromosomal translocations are critically involved in the molecular pathogenesis of B-cell lymphomas, and highly recurrent and specific rearrangements have defined distinct molecular subtypes linked to unique clinicopathological features. In contrast, several well-characterized lymphoma entities still lack disease-defining translocation events. To identify novel fusion transcripts resulting from translocations, we investigated two Hodgkin lymphoma cell lines by whole-transcriptome paired-end sequencing (RNA-seq). Here we show a highly expressed gene fusion involving the major histocompatibility complex (MHC) class II transactivator CIITA (MHC2TA) in KM-H2 cells. In a subsequent evaluation of 263 B-cell lymphomas, we also demonstrate that genomic CIITA breaks are highly recurrent in primary mediastinal B-cell lymphoma (38%) and classical Hodgkin lymphoma (cHL) (15%). Furthermore, we find that CIITA is a promiscuous partner of various in-frame gene fusions, and we report that CIITA gene alterations impact survival in primary mediastinal B-cell lymphoma (PMBCL). As functional consequences of CIITA gene fusions, we identify downregulation of surface HLA class II expression and overexpression of ligands of the receptor molecule programmed cell death 1 (CD274/PDL1 and CD273/PDL2). These receptor-ligand interactions have been shown to impact anti-tumour immune responses in several cancers, whereas decreased MHC class II expression has been linked to reduced tumour cell immunogenicity. Thus, our findings suggest that recurrent rearrangements of CIITA may represent a novel genetic mechanism underlying tumour-microenvironment interactions across a spectrum of lymphoid cancers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3902849/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3902849/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steidl, Christian -- Shah, Sohrab P -- Woolcock, Bruce W -- Rui, Lixin -- Kawahara, Masahiro -- Farinha, Pedro -- Johnson, Nathalie A -- Zhao, Yongjun -- Telenius, Adele -- Neriah, Susana Ben -- McPherson, Andrew -- Meissner, Barbara -- Okoye, Ujunwa C -- Diepstra, Arjan -- van den Berg, Anke -- Sun, Mark -- Leung, Gillian -- Jones, Steven J -- Connors, Joseph M -- Huntsman, David G -- Savage, Kerry J -- Rimsza, Lisa M -- Horsman, Douglas E -- Staudt, Louis M -- Steidl, Ulrich -- Marra, Marco A -- Gascoyne, Randy D -- 178536/Canadian Institutes of Health Research/Canada -- R00 CA131503/CA/NCI NIH HHS/ -- R00CA131503/CA/NCI NIH HHS/ -- T32 GM007288/GM/NIGMS NIH HHS/ -- England -- Nature. 2011 Mar 17;471(7338):377-81. doi: 10.1038/nature09754. Epub 2011 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics, Vancouver, British Columbia, V5Z4E6, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21368758" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD/genetics/metabolism ; Antigens, CD274 ; Antigens, CD80/genetics/metabolism ; Base Sequence ; Cell Line, Tumor ; Chromosome Breakpoints ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Hodgkin Disease/genetics ; Humans ; In Situ Hybridization, Fluorescence ; Jurkat Cells ; Lymphocyte Activation ; Lymphoma, B-Cell/*genetics ; Molecular Sequence Data ; Nuclear Proteins/*genetics ; Oncogene Proteins, Fusion/*genetics ; Programmed Cell Death 1 Ligand 2 Protein ; RNA, Neoplasm/genetics ; T-Lymphocytes/immunology/metabolism/pathology ; Tissue Array Analysis ; Trans-Activators/*genetics ; Translocation, Genetic/*genetics ; Tumor Microenvironment
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    14-3-3 fusion oncogenes in high-grade endometrial stromal sarcoma (2012)
    National Academy of Sciences
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    Publication Date: 2012-01-05
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    14-3-3 fusion oncogenes in high-grade endometrial stromal sarcoma [Medical Sciences] (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-01-18
    Description: 14-3-3 proteins are ubiquitously expressed regulators of various cellular functions, including proliferation, metabolism, and differentiation, and altered 14-3-3 expression is associated with development and progression of cancer. We report a transforming 14-3-3 oncoprotein, which we identified through conventional cytogenetics and whole-transcriptome sequencing analysis as a highly recurrent genetic mechanism in a clinically aggressive form of uterine sarcoma: high-grade endometrial stromal sarcoma (ESS). The 14-3-3 oncoprotein results from a t(10;17) genomic rearrangement, leading to fusion between 14-3-3ε (YWHAE) and either of two nearly identical FAM22 family members (FAM22A or FAM22B). Expression of YWHAE–FAM22 fusion oncoproteins was demonstrated by immunoblot in t(10;17)-bearing frozen tumor and cell line samples. YWHAE–FAM22 fusion gene knockdowns were performed with shRNAs and siRNAs targeting various FAM22A exons in an t(10;17)-bearing ESS cell line (ESS1): Fusion protein expression was inhibited, with corresponding reduction in cell growth and migration. YWHAE–FAM22 maintains a structurally and functionally intact 14-3-3ε (YWHAE) protein-binding domain, which is directed to the nucleus by a FAM22 nuclear localization sequence. In contrast to classic ESS, harboring JAZF1 genetic fusions, YWHAE–FAM22 ESS display high-grade histologic features, a distinct gene-expression profile, and a more aggressive clinical course. Fluorescence in situ hybridization analysis demonstrated absolute specificity of YWHAE–FAM22A/B genetic rearrangement for high-grade ESS, with no fusions detected in other uterine and nonuterine mesenchymal tumors (55 tumor types, n = 827). These discoveries reveal diagnostically and therapeutically relevant models for characterizing aberrant 14-3-3 oncogenic functions.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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