Literature DB >> 34283872

Trisomy 21-associated increases in chromosomal instability are unmasked by comparing isogenic trisomic/disomic leukocytes from people with mosaic Down syndrome.

Kelly Rafferty1,2, Kellie J Archer3, Kristi Turner2, Ruth Brown4, Colleen Jackson-Cook1,2.   

Abstract

Down syndrome, which results from a trisomic imbalance for chromosome 21, has been associated with 80+ phenotypic traits. However, the cellular changes that arise in somatic cells due to this aneuploid condition are not fully understood. The primary aim of this study was to determine if germline trisomy 21 is associated with an increase in spontaneous somatic cell chromosomal instability frequencies (SCINF). To achieve this aim, we quantified SCINF in people with mosaic Down syndrome using a cytokinesis-blocked micronucleus assay. By comparing values in their isogenic trisomic/disomic cells, we obtained a measure of differences in SCINF that are directly attributable to a trisomy 21 imbalance, since differential effects attributable to "background" genetic factors and environmental exposures could be eliminated. A cross-sectional assessment of 69 people with mosaic Down syndrome (ages 1 to 44; mean age of 12.84 years) showed a significantly higher frequency of micronuclei in their trisomic (0.37 ± 0.35 [mean ± standard deviation]) compared to disomic cells (0.18 ± 0.11)(P <0.0001). The daughter binucleates also showed significantly higher levels of abnormal patterns in the trisomic (1.68 ± 1.21) compared to disomic (0.35 ± 0.45) cells (P <0.0001). Moreover, a significant Age x Cell Type interaction was noted (P = 0.0113), indicating the relationship between age and SCINF differed between the trisomic and disomic cells. Similarly, a longitudinal assessment (mean time interval of 3.9 years; range of 2 to 6 years) of 18 participants showed a mean 1.63-fold increase in SCINF within individuals over time for their trisomic cells (P = 0.0186), compared to a 1.13-fold change in their disomic cells (P = 0.0464). In summary, these results showed a trisomy 21-associated, age-related increase in SCINF. They also underscore the strength of the isogenic mosaic Down syndrome model system for "unmasking" cellular changes arising from a trisomy 21 imbalance.

Entities:  

Year:  2021        PMID: 34283872     DOI: 10.1371/journal.pone.0254806

Source DB:  PubMed          Journal:  PLoS One        ISSN: 1932-6203            Impact factor:   3.240


  77 in total

1.  Genomic instability in Down syndrome and Fanconi anemia assessed by micronucleus analysis and single-cell gel electrophoresis.

Authors:  S W Maluf; B Erdtmann
Journal:  Cancer Genet Cytogenet       Date:  2001-01-01

2.  Genetic and environmental influences on spontaneous micronuclei frequencies in children and adults: a twin study.

Authors:  Kimberly H Jones; Timothy P York; Jane Juusola; Andrea Ferreira-Gonzalez; Hermine H Maes; Colleen Jackson-Cook
Journal:  Mutagenesis       Date:  2011-07-15       Impact factor: 3.000

3.  Involvement of RAD9-dependent damage checkpoint control in arrest of cell cycle, induction of cell death, and chromosome instability caused by defects in origin recognition complex in Saccharomyces cerevisiae.

Authors:  Keiichi Watanabe; Jun Morishita; Keiko Umezu; Katsuhiko Shirahige; Hisaji Maki
Journal:  Eukaryot Cell       Date:  2002-04

4.  Increased low-level chromosome 21 mosaicism in older individuals with Down syndrome.

Authors:  E C Jenkins; N Schupf; M Genovese; L L Ye; D Kapell; B Canto; M Harris; D Devenny; J H Lee; W T Brown
Journal:  Am J Med Genet       Date:  1997-01-20

Review 5.  Short- and long-term effects of chromosome mis-segregation and aneuploidy.

Authors:  Stefano Santaguida; Angelika Amon
Journal:  Nat Rev Mol Cell Biol       Date:  2015-08       Impact factor: 94.444

6.  The origin of mosaic Down syndrome: four cases with chromosome markers.

Authors:  N Niikawa; T Kajii
Journal:  Am J Hum Genet       Date:  1984-01       Impact factor: 11.025

7.  Buccal micronucleus frequency is associated with age in Down syndrome.

Authors:  F L S Ferreira; D Prá; M G Martino-Roth; G L Garcias
Journal:  Genet Mol Res       Date:  2009-10-13

Review 8.  Superoxide Dismutase 1 in Health and Disease: How a Frontline Antioxidant Becomes Neurotoxic.

Authors:  Benjamin G Trist; James B Hilton; Dominic J Hare; Peter J Crouch; Kay L Double
Journal:  Angew Chem Int Ed Engl       Date:  2020-11-19       Impact factor: 15.336

9.  Trisomy 21 dysregulates T cell lineages toward an autoimmunity-prone state associated with interferon hyperactivity.

Authors:  Paula Araya; Katherine A Waugh; Kelly D Sullivan; Nicolás G Núñez; Emiliano Roselli; Keith P Smith; Ross E Granrath; Angela L Rachubinski; Belinda Enriquez Estrada; Eric T Butcher; Ross Minter; Kathryn D Tuttle; Tullia C Bruno; Mariana Maccioni; Joaquín M Espinosa
Journal:  Proc Natl Acad Sci U S A       Date:  2019-11-07       Impact factor: 11.205

10.  Health comorbidities and cognitive abilities across the lifespan in Down syndrome.

Authors:  Carla M Startin; Hana D'Souza; George Ball; Sarah Hamburg; Rosalyn Hithersay; Kate M O Hughes; Esha Massand; Annette Karmiloff-Smith; Michael S C Thomas; Andre Strydom
Journal:  J Neurodev Disord       Date:  2020-01-23       Impact factor: 4.025

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  2 in total

Review 1.  Future Perspectives in Oxidative Stress in Trisomy 13 and 18 Evaluation.

Authors:  Angelika Buczyńska; Iwona Sidorkiewicz; Ahsan Hameed; Adam Jacek Krętowski; Monika Zbucka-Krętowska
Journal:  J Clin Med       Date:  2022-03-24       Impact factor: 4.241

2.  Drug-Targeted Genomes: Mutability of Ion Channels and GPCRs.

Authors:  Regan Raines; Ian McKnight; Hunter White; Kaitlyn Legg; Chan Lee; Wei Li; Peter H U Lee; Joon W Shim
Journal:  Biomedicines       Date:  2022-03-03
  2 in total

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