A Physical Map of Chromosome 7 of Candida Albicans
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Diversity in the Organization of Centromeric Chromatin
Available online at www.sciencedirect.com ScienceDirect Diversity in the organization of centromeric chromatin 1 Florian A Steiner and Steven Henikoff Centromeric chromatin is distinguished primarily by lacking. In most species, cenH3 nucleosomes assemble nucleosomes containing the histone variant cenH3, which on particular families of tandemly repetitive satellite organizes the kinetochore that links the chromosome to the DNA, and the intractability of long satellite repeat arrays spindle apparatus. Whereas budding yeast have simple ‘point’ has greatly hindered the analysis of centromeric chroma- centromeres with single cenH3 nucleosomes, and fission yeast tin. Recent studies have begun to shed light on these have ‘regional’ centromeres without obvious sequence enigmatic regions of chromosomes, in part through specificity, the centromeres of most organisms are embedded improvements in sequencing technologies and in part in highly repetitive ‘satellite’ DNA. Recent studies have revealed through analysis of model systems that circumvent the a remarkable diversity in centromere chromatin organization challenges presented by the repeat-richness of most among different lineages, including some that have lost cenH3 higher eukaryotic centromeres. The emerging picture altogether. We review recent progress in understanding point, shows that cenH3 is incorporated into well-positioned regional and satellite centromeres, as well as less well-studied nucleosomes at centromeres that are distinct from canon- centromere types, such as holocentromeres. -
5885.Full.Pdf
Research Article 5885 Assembly of additional heterochromatin distinct from centromere-kinetochore chromatin is required for de novo formation of human artificial chromosome Hiroshi Nakashima1,2,3, Megumi Nakano1,*, Ryoko Ohnishi1, Yasushi Hiraoka4, Yasufumi Kaneda2, Akio Sugino1,3 and Hiroshi Masumoto1,*,‡ 1Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa-ku, Nagoya 464-8602, Japan 2Division of Gene Therapy Science, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan 3Laboratories for Biomolecular Networks, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871, Japan 4Kansai Advanced Research Center, National Institute of Information and Communications Technology, 588-2 Iwaoka, Iwaoka-cho, Nishi-ku, Kobe 651-2492, Japan *Present address: Laboratory of Biosystems and Cancer, National Cancer Institute, National Institutes of Health, Bldg. 37, Rm 5040, 9000 Rockville Pike, Bethesda, MD 20892, USA ‡Author for correspondence (e-mail: [email protected]) Accepted 20 September 2005 Journal of Cell Science 118, 5885-5898 Published by The Company of Biologists 2005 doi:10.1242/jcs.02702 Summary Alpha-satellite (alphoid) DNA is necessary for de novo arms. However, on the stable HAC, chromatin formation of human artificial chromosomes (HACs) in immunoprecipitation analysis showed that HP1␣ and human cultured cells. To investigate the relationship trimethyl histone H3-K9 were enriched at the non- among centromeric, transcriptionally -
20P Deletions FTNW
20p deletions rarechromo.org Deletions from chromosome 20p A chromosome 20p deletion is a rare genetic condition caused by the loss of material from one of the body’s 46 chromosomes. The material has been lost from the short arm (the top part in the diagram on the next page) of chromosome 20. Chromosomes are the structures in the nucleus of the body’s cells that carry the genetic information that controls development and function. In total every human individual normally has 46 chromosomes. Of these, two are a pair of sex chromosomes, XX (a pair of X chromosomes) in females and XY (one X chromosome and one Y chromosome) in males. The remaining 44 chromosomes are grouped in pairs. One chromosome from each pair is inherited from the mother while the other one is inherited from the father. Each chromosome has a short arm (called p) and a long arm (called q). Chromosome 20 is one of the smallest chromosomes in man. At present it is known to contain 737 genes out of the total of 20,000 to 25,000 genes in the human genome. You can’t see chromosomes with the naked eye, but if you stain them and magnify their image enough - about 850 times - you can see that each one has a distinctive pattern of light and dark bands. The diagram on the next page shows the bands of chromosome 20. These bands are numbered outwards starting from the point where the short and long arms meet (the centromere ). A low number, as in p11 in the short arm, is close to the centromere. -
Aneuploidy and Aneusomy of Chromosome 7 Detected by Fluorescence in Situ Hybridization Are Markers of Poor Prognosis in Prostate Cancer'
[CANCERRESEARCH54,3998-4002,August1, 19941 Advances in Brief Aneuploidy and Aneusomy of Chromosome 7 Detected by Fluorescence in Situ Hybridization Are Markers of Poor Prognosis in Prostate Cancer' Antonio Alcaraz, Satoru Takahashi, James A. Brown, John F. Herath, Erik J- Bergstralh, Jeffrey J. Larson-Keller, Michael M Lieber, and Robert B. Jenkins2 Depart,nent of Urology [A. A., S. T., J. A. B., M. M. U, Laboratory Medicine and Pathology (J. F. H., R. B. fl, and Section of Biostatistics (E. J. B., J. J. L-JCJ, Mayo Clinic and Foundation@ Rochester, Minnesota 55905 Abstract studies on prostate carcinoma samples. Interphase cytogenetic analy sis using FISH to enumerate chromosomes has the potential to over Fluorescence in situ hybridization is a new methodologj@which can be come many of the difficulties associated with traditional cytogenetic used to detect cytogenetic anomalies within interphase tumor cells. We studies. Previous studies from this institution have demonstrated that used this technique to identify nonrandom numeric chromosomal alter ations in tumor specimens from the poorest prognosis patients with path FISH analysis with chromosome enumeration probes is more sensitive ological stages T2N@M,Jand T3NOMOprostate carcinomas. Among 1368 than FCM for detecting aneuploid prostate cancers (4, 5, 7). patients treated by radical prostatectomy, 25 study patients were ascer We designed a case-control study to test the hypothesis that spe tamed who died most quickly from progressive prostate carcinoma within cific, nonrandom cytogenetic changes are present in tumors removed 3 years of diagnosis and surgery. Tumors from 25 control patients who from patients with prostate carcinomas with poorest prognoses . -
Centromere Chromatin: a Loose Grip on the Nucleosome?
CORRESPONDENCE Stanford, California, USA. 7. Black, B.E. et al. Nature 430, 578–582 (2004). Natl. Acad. Sci. USA 104, 15974–15981 (2007). e-mail: [email protected] 8. Walkiewicz, M.P., Dimitriadis, E.K. & Dalal, Y. Nat. 16. Godde, J.S. & Wolffe, A.P.J. Biol. Chem. 270, 27399– Struct. Mol. Biol. 21, 2–3 (2014). 27402 (1995). 1. Dalal, Y., Wang, H., Lindsay, S. & Henikoff, S. PLoS 9. Codomo, C.A., Furuyama, T. & Henikoff, S. Nat. Struct. 17. de Frutos, M., Raspaud, E., Leforestier, A. & Livolant, F. Biol. 5, e218 (2007). Mol. Biol. 21, 4–5 (2014). Biophys. J. 81, 1127–1132 (2001). 2. Dimitriadis, E.K., Weber, C., Gill, R.K., Diekmann, S. 10. Yoda, K. et al. Proc. Natl. Acad. Sci. USA 97, 7266– 18. Gansen, A. et al. Proc. Natl. Acad. Sci. USA 106, & Dalal, Y. Proc. Natl. Acad. Sci. USA 107, 20317– 7271 (2000). 15308–15313 (2009). 20322 (2010). 11. Tomschik, M., Karymov, M.A., Zlatanova, J. & Leuba, S.H. 19. Zhang, W., Colmenares, S.U. & Karpen, G.H. Mol. Cell 3. Bui, M. et al. Cell 150, 317–326 (2012). Structure 9, 1201–1211 (2001). 45, 263–269 (2012). 4. Furuyama, T., Codomo, C.A. & Henikoff, S. Nucleic 12. Bui, M., Walkiewicz, M.P., Dimitriadis, E.K. & Dalal, Y. 20. Tachiwana, H. et al. Nature 476, 232–235 (2011). Acids Res. 41, 5769–5783 (2013). Nucleus 4, 37–42 (2013). 21. Hasson, D. et al. Nat. Struct. Mol. Biol. 20, 687–695 5. Dunleavy, E.M., Zhang, W. & Karpen, G.H. -
7Q Deletions Proximal Interstitial FTNP
Support and Information Rare Chromosome Disorder Support Group, G1, The Stables, Station Road West, Oxted, Surrey RH8 9EE, United Kingdom Tel/Fax: +44(0)1883 723356 [email protected] III www.rarechromo.org Join Unique for family links, information and support. 7q deletions Unique is a charity without government funding, existing entirely on donations and grants. If you can, please make a donation via our website at www.rarechromo.org Please help us to help you! proximal interstitial Facebook group for 7q deletions and duplications: www.facebook.com/groups/493223084038489 Unique lists external message boards and websites in order to be helpful to families looking for information and support. This does not imply that we endorse their content or have any responsibility for it. This information guide is not a substitute for personal medical advice. Families should consult a medically qualified clinician in all matters relating to genetic diagnosis, management and health. Information on genetic changes is a very fast-moving field and while the information in this guide is believed to be the best available at the time of publication, some facts may later change. Unique does its best to keep abreast of changing information and to review its published guides as needed. The guide was compiled by Unique and reviewed by Dr Steve Scherer, Centre for Applied Genomics, Hospital for Sick Children, Toronto, Canada and by Professor Maj Hultén, BSc, PhD, MD, FRCPath, Professor of Medical Genetics, University of Warwick, 2009. Copyright © Unique 2009 Rare Chromosome Disorder Support Group Charity Number 1110661 Registered in England and Wales Company Number 5460413 rrraraaarrrreeeecccchhhhrrrroooommmmoooo....oooorrrrgggg 24 A 7q deletion the development of an embryo. -
Ongoing Human Chromosome End Extension Revealed by Analysis of Bionano and Nanopore Data Received: 4 May 2018 Haojing Shao , Chenxi Zhou , Minh Duc Cao & Lachlan J
www.nature.com/scientificreports OPEN Ongoing human chromosome end extension revealed by analysis of BioNano and nanopore data Received: 4 May 2018 Haojing Shao , Chenxi Zhou , Minh Duc Cao & Lachlan J. M. Coin Accepted: 22 October 2018 The majority of human chromosome ends remain incompletely assembled due to their highly repetitive Published: xx xx xxxx structure. In this study, we use BioNano data to anchor and extend chromosome ends from two European trios as well as two unrelated Asian genomes. At least 11 BioNano assembled chromosome ends are structurally divergent from the reference genome, including both missing sequence and extensions. These extensions are heritable and in some cases divergent between Asian and European samples. Six out of nine predicted extension sequences from NA12878 can be confrmed and flled by nanopore data. We identify two multi-kilobase sequence families both enriched more than 100- fold in extension sequence (p-values < 1e-5) whose origins can be traced to interstitial sequence on ancestral primate chromosome 7. Extensive sub-telomeric duplication of these families has occurred in the human lineage subsequent to divergence from chimpanzees. Te genome sequence of chromosome ends in the reference human genome remains incompletely assembled. In the latest draf of the human genome1 21 out of 48 chromosome ends were incomplete; amongst which fve chromosome ends (13p, 14p, 15p, 21p, 22p) are completely unknown and the remaining chromosome ends are capped with 10–110 kb of unknown sequence. Tere are many interesting observations in the chromosome end regions which remain unexplained, such as the observed increase in genetic divergence between Chimpanzee and Humans towards the chromosome ends2. -
Familial Bone Marrow Monosomy 7 Evidence That the Predisposing Locus Is Not on the Long Arm of Chromosome 7 Kevin M
Familial Bone Marrow Monosomy 7 Evidence That the Predisposing Locus Is Not on the Long Arm of Chromosome 7 Kevin M. Shannon,* All G. Turhan,*$ Sharon S. Y. Chang,"1 Anne M. Bowcock,' Paul C. J. Rogers,** William L. Carroll,# Morton J. Cowan,* Bertil E. Glader,* Connie J. Eaves, *1111 Allen C. Eaves,t1111 and Yuet Wai Kan1ltl Departments of*Pediatrics and "'Medicine and 1lHoward Hughes Medical Institute, University of California, San Francisco, San Francisco, California 94143; Departments of Pathology, **Pediatrics, and 111IMedicine, University ofBritish Columbia, and the §Terry Fox Laboratory, British Columbia Cancer Centre, Vancouver, British Columbia, Canada; Departments of'Genetics and "Pediatrics, Stanford University Medical School, Stanford, California 94303; and t*Department ofPediatrics, Washington University School of Medicine, St. Louis, Missouri 63110 Abstract cinogen exposure (3, 6). The age distribution of these de novo cases shows peaks in the first and fifth decades (6). Overall, Loss of expression of a tumor-suppressing gene is an attractive monosomy 7 or 7q- is identified in - 5% of de novo and in model to explain the cytogenetic and epidemiologic features of 40% of secondary cases of AML (1, 3-5). Although childhood cases of myelodysplasia and acute myelogenous leukemia bone marrow monosomy 7 is an uncommon disorder, it has (AML) associated with bone marrow monosomy 7 or partial been observed in two or more siblings at least seven times deletion of the long arm (7q-). We used probes from within the (7-10, Lange, B. J., personal communication, and our unpub- breakpoint region on 7q- chromosomes (7q22-34) that detect lished data). -
CENP-B ANTIGEN AROTEC CENP-B Product Info.Pdf Version/Date: A/08.04.09 ATC02-02 CENP-B Antigen 0.20 Mg ATC02-10 CENP-B Antigen 1.0 Mg ______
CENP-B ANTIGEN AROTEC_CENP-B_Product_Info.pdf Version/Date: A/08.04.09 ATC02-02 CENP-B antigen 0.20 mg ATC02-10 CENP-B antigen 1.0 mg _________________________________________________________________________________ Description of the Product 2. Coat ELISA plates with 100 µl of diluted antigen per well. Cover and incubate 24 hours at +4oC. Purified recombinant full-length human sequence protein. After 3. Empty the plates and remove excess liquid by tapping on a coating onto ELISA plates the product will bind autoantibodies to paper towel. CENP-B. 4. Block excess protein binding sites by adding 200 µl PBS containing 1% BSA per well. Cover and incubate at +4oC Purity: The CENP-B autoantigen (80 kDa) is more than 90% overnight. pure, as assessed by SDS-polyacrylamide gel electrophoresis. 5. Empty plates and apply 100 µl of serum samples diluted 1:100 in PBS / 1% BSA / 1% casein / 0.1% Tween 20. Incubate at room temperature for 1 hour. Storage: Store at -65oC or below (long term). Avoid repeated 6. Empty plates and add 200 µl PBS / 0.1% Tween 20 per freezing and thawing. Mix thoroughly before use. well. Incubate 5 minutes then empty plates. Repeat this step twice. Clinical and Biochemical Data 7. Apply 100 µl anti-human IgG-enzyme conjugate (horseradish peroxidase or alkaline phosphatase) diluted in Autoantibodies to centromeric proteins in the sera of patients PBS / 1% BSA / 1% casein / 0.1% Tween 20 per well and with scleroderma were first described in 19801. Subsequent incubate for 1 hour. studies confirmed that anti-centromere antibodies (ACA) were 8. -
RNA Interference, Heterochromatin, and Centromere Function
46_Symp69_Allshire_p.389_396 4/21/05 10:34 AM Page 389 RNA Interference, Heterochromatin, and Centromere Function R.C. ALLSHIRE Wellcome Trust Centre for Cell Biology, University of Edinburgh, The King’s Buildings, Edinburgh EH9 3JR, Scotland, United Kingdom The centromere regions of most eukaryotic metaphase poacetylated state is important for centromere integrity chromosomes are distinctive. The narrower, more com- and function (Ekwall et al. 1997). pact appearance of these regions reflects two important The formation of a functional centromere and kineto- related features: centromeric cohesion and extensive chore assembly requires at least one outer repeat and a blocks of heterochromatin. First, sister centromeres re- central core region (Takahashi et al. 1992; Marschall and main associated because the cohesin complex remains in- Clarke 1995; Ngan and Clarke 1997). The central core tact at centromeres until anaphase. Second, the chromatin alone is unable to be packaged in unusual chromatin coating these regions is very different since they remain when replicated on an extrachromosomal plasmid or condensed throughout the cell cycle and are clearly visi- other sites in the genome or when replicated in Saccha- ble as the most concentrated foci of DNA in interphase romyces cerevisiae (Polizzi and Clarke 1991; Takahashi cells; this has been termed heterochromatin (Bernard and et al. 1992). Thus, this “unusual” CENP-A chromatin is Allshire 2002). not specified by the underlying DNA sequence within It has been known for many years that marker genes this region alone, but it must be induced by the context in placed close to or within such centromeric heterochro- which these sequences are placed. -
The Genomic Landscape of Centromeres in Cancers Anjan K
www.nature.com/scientificreports OPEN The Genomic Landscape of Centromeres in Cancers Anjan K. Saha 1,2,3, Mohamad Mourad3, Mark H. Kaplan3, Ilana Chefetz4, Sami N. Malek3, Ronald Buckanovich5, David M. Markovitz2,3,6,7 & Rafael Contreras-Galindo3,4 Received: 8 March 2019 Centromere genomics remain poorly characterized in cancer, due to technologic limitations in Accepted: 23 July 2019 sequencing and bioinformatics methodologies that make high-resolution delineation of centromeric Published: xx xx xxxx loci difcult to achieve. We here leverage a highly specifc and targeted rapid PCR methodology to quantitatively assess the genomic landscape of centromeres in cancer cell lines and primary tissue. PCR- based profling of centromeres revealed widespread heterogeneity of centromeric and pericentromeric sequences in cancer cells and tissues as compared to healthy counterparts. Quantitative reductions in centromeric core and pericentromeric markers (α-satellite units and HERV-K copies) were observed in neoplastic samples as compared to healthy counterparts. Subsequent phylogenetic analysis of a pericentromeric endogenous retrovirus amplifed by PCR revealed possible gene conversion events occurring at numerous pericentromeric loci in the setting of malignancy. Our fndings collectively represent a more comprehensive evaluation of centromere genetics in the setting of malignancy, providing valuable insight into the evolution and reshufing of centromeric sequences in cancer development and progression. Te centromere is essential to eukaryotic biology due to its critical role in genome inheritance1,2. Te nucleic acid sequences that dominate the human centromeric landscape are α-satellites, arrays of ~171 base-pair monomeric units arranged into higher-order arrays throughout the centromere of each chromosome3–103 1–3. -
Telomere Erosion and Chromosomal Instability in Cells Expressing the HPV Oncogene 16E6
Oncogene (2004) 23, 3561–3571 & 2004 Nature Publishing Group All rights reserved 0950-9232/04 $25.00 www.nature.com/onc Telomere erosion and chromosomal instability in cells expressing the HPV oncogene 16E6 Annemieke W Plug-DeMaggio*,1, Terri Sundsvold1, Michelle A Wurscher1, Jennifer I Koop1, Aloysius J Klingelhutz1,3 and James K McDougall1,2,4 1Cancer Biology Program, Fred Hutchinson Cancer Research Center, Seattle, WA 98109-1024, USA; 2Departmentof Pathology, University of Washington, Seattle, WA 98195, USA Progression to advanced-stage cervical carcinomas is Introduction characterized by a recurrent pattern of chromosomal rearrangements. Structural chromosome rearrangements Human cancers are subject to ongoing chromosomal are generated through the fusion of broken chromosome changes as a result of defects in the checkpoints that ends. These chromosome breaks may be induced by normally ensure stability of the genome. Two types of mutagenic agents such as ionizing radiation, or chromo- chromosomal instability are recognized: (1) aneuploidy, some ends may be exposed through extensive telomere or change in chromosome copy number and (2) shortening. The human papilloma virus oncogene 16E6 structural aberrations of chromosomes. Chromosomal induces telomerase activity in human keratinocytes, a instability is an early event in the development of human model system for cervical tumor formation. The present (Heselmeyer et al., 1996, 1997; Kirchhoff et al., 1999; study explores the relationship between 16E6 expression, Matthews et al., 2000) papillomavirus (HPV) associated telomerase activity, and chromosomal instability. We anogenital carcinoma. Epidemiological studies have show that the frequency of anaphase bridges is dependent determined that high-risk type HPVs are the main on the level of telomerase activity in 16E6/E7-expressing etiological factors for cervical cancer (Zur Hausen, clones, and is the result of telomere shortening.