Altered chromatin structure associated with a partial trisomy of chromosome 7 in the mouse

1987 ◽  
Vol 25 (9-10) ◽  
pp. 671-686 ◽  
Author(s):  
A. V. Rake ◽  
R. H. Edwards
Keyword(s):  
Chromatin Structure ◽  
Partial Trisomy ◽  
Chromosome 7

Partial trisomy for the long arm of chromosome 7. Case report and review

1982 ◽  
Vol 62 (4) ◽  
pp. 378-381 ◽  
Author(s):  
M. A. Novales ◽  
C. Fernandez-Novoa ◽  
A. Hevia ◽  
V. San Martin ◽  
H. Galera
Keyword(s):  
Case Report ◽  
Partial Trisomy ◽  
Chromosome 7

Partial trisomy for the long arm of chromosome 7 due to familial balanced translocation

1979 ◽  
Vol 49 (3) ◽  
pp. 283-289 ◽  
Author(s):  
M. Schmid ◽  
J. Wolf ◽  
H. Nestler ◽  
W. Krone
Keyword(s):  
Partial Trisomy ◽  
Chromosome 7 ◽  
Balanced Translocation

scholarly journals Epigenetic rewriting at centromeric DNA repeats leads to increased chromatin accessibility and chromosomal instability

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Sheldon Decombe ◽  
François Loll ◽  
Laura Caccianini ◽  
Kévin Affannoukoué ◽  
Ignacio Izeddin ◽  
...  
Keyword(s):  
Chromatin Structure ◽  
Genome Stability ◽  
Chromatin Accessibility ◽  
Chromosome 7 ◽  
Epigenetic Mark ◽  
Dna Repeats ◽  
Direct Role ◽  
Artificial Chromosomes ◽  
Natural Context

Abstract Background Centromeric regions of human chromosomes contain large numbers of tandemly repeated α-satellite sequences. These sequences are covered with constitutive heterochromatin which is enriched in trimethylation of histone H3 on lysine 9 (H3K9me3). Although well studied using artificial chromosomes and global perturbations, the contribution of this epigenetic mark to chromatin structure and genome stability remains poorly known in a more natural context. Results Using transcriptional activator-like effectors (TALEs) fused to a histone lysine demethylase (KDM4B), we were able to reduce the level of H3K9me3 on the α-satellites repeats of human chromosome 7. We show that the removal of H3K9me3 affects chromatin structure by increasing the accessibility of DNA repeats to the TALE protein. Tethering TALE-demethylase to centromeric repeats impairs the recruitment of HP1α and proteins of Chromosomal Passenger Complex (CPC) on this specific centromere without affecting CENP-A loading. Finally, the epigenetic re-writing by the TALE-KDM4B affects specifically the stability of chromosome 7 upon mitosis, highlighting the importance of H3K9me3 in centromere integrity and chromosome stability, mediated by the recruitment of HP1α and the CPC. Conclusion Our cellular model allows to demonstrate the direct role of pericentromeric H3K9me3 epigenetic mark on centromere integrity and function in a natural context and opens interesting possibilities for further studies regarding the role of the H3K9me3 mark.

scholarly journals Epigenetic rewriting at centromeric DNA repeats leads to increased chromatin accessibility and chromosomal instability

2021 ◽  
Author(s):  
Sheldon Decombe ◽  
François Loll ◽  
Laura Caccianini ◽  
Kévin Affannoukoué ◽  
Ignacio Izeddin ◽  
...  
Keyword(s):  
Chromatin Structure ◽  
Genome Stability ◽  
Chromatin Accessibility ◽  
Chromosome 7 ◽  
Epigenetic Mark ◽  
Dna Repeats ◽  
Artificial Chromosomes ◽  
Chromosomal Passenger ◽  
The Stability ◽  
Lysine Demethylase

AbstractCentromeric regions of human chromosomes contain large numbers of tandemly repeated α-satellite sequences. These sequences are covered with constitutive heterochromatin which is enriched in trimethylation of histone H3 on lysine 9 (H3K9me3). Although well studied using artificial chromosomes and global perturbations, the contribution of this epigenetic mark to chromatin structure and genome stability remains poorly known in a more natural context. Using transcriptional activator-like effectors (TALEs) fused to a histone lysine demethylase (JMJD2B), we were able to reduce the level of H3K9me3 on the α-satellites repeats of human chromosome 7. We show that the removal of H3K9me3 affects chromatin structure by increasing the accessibility of DNA repeats to the TALE protein. Tethering TALE-demethylase to centromeric repeats impairs the recruitment of HP1α and proteins of Chromosomal Passenger Complex (CPC) on this specific centromere. Finally, the epigenetic re-writing by the TALE-JMJD2B affects specifically the stability of chromosome 7 upon mitosis, highlighting the importance of H3K9me3 in centromere integrity and chromosome stability, mediated by the recruitment of HP1α and the CPC.

Partial trisomy of the short arm of chromosome 7 due to a familial translocation rcp(7;14) (p11;p11)

2008 ◽  
Vol 14 (4) ◽  
pp. 202-206 ◽  
Author(s):  
Alessandra Carnevale ◽  
Sara Frías ◽  
Victoria del Castillo
Keyword(s):  
Partial Trisomy ◽  
Chromosome 7 ◽  
Familial Translocation

Characterization of a de novo Supernumerary Neocentric Ring Chromosome Derived from Chromosome 7

2015 ◽  
Vol 147 (2-3) ◽  
pp. 111-117 ◽  
Author(s):  
Camille Louvrier ◽  
Grégory Egea ◽  
Audrey Labalme ◽  
Vincent Des Portes ◽  
Sophie Gazzo ◽  
...  
Keyword(s):  
Array Cgh ◽  
De Novo ◽  
Ring Chromosome ◽  
Partial Trisomy ◽  
Complete Characterization ◽  
Chromosome 7 ◽  
Oligonucleotide Array ◽  
Facial Dysmorphism ◽  
Bioinformatic Tools

Supernumerary ring chromosomes (SRC) are usually derived from regions adjacent to the centromere. Their identification may be challenging, particularly in case of low mosaicism. Here, we report on a patient who was referred for major in utero growth retardation, severe developmental delay, facial dysmorphism, cleft palate, and hypospadias. The karyotype showed a small SRC in mosaic. The combination of FISH, M-FISH and array-CGH was necessary for a complete characterization of this SRC. M-FISH revealed that the SRC originated from chromosome 7. Array-CGH performed with a 400K oligonucleotide array showed a gain in region 7q22.1q31.1 present in low mosaic. This result was confirmed by FISH using BAC probes specific for chromosome 7. The SRC was a neocentric ring derived from 7q22.1q31.1 and was found in only 8% of the cells. This is the first patient carrying a mosaic neocentric SRC derived from the long arm of chromosome 7. Our study emphasizes the need to combine different techniques and to use adapted bioinformatic tools for low-mosaicism marker identification. It also contributes to the delineation of the partial trisomy 7q phenotype.

scholarly journals Divergent leukaemia subclones as cellular models for testing vulnerabilities associated with gains in chromosomes 7, 8 or 18

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Michael Maher ◽  
Jeannine Diesch ◽  
Marguerite-Marie Le Pannérer ◽  
Marta Cabezón ◽  
Mar Mallo ◽  
...  
Keyword(s):  
Cell Lines ◽  
Synthetic Lethality ◽  
Partial Trisomy ◽  
In Vitro Models ◽  
Chromosome 8 ◽  
Chromosome 7 ◽  
Specific Response ◽  
Cellular Models ◽  
Mutational Pattern

AbstractHaematopoietic malignancies are frequently characterized by karyotypic abnormalities. The development of targeted drugs has been pioneered with compounds against gene products of fusion genes caused by chromosomal translocations. While polysomies are equally frequent as translocations, for many of them we are lacking therapeutic approaches aimed at synthetic lethality. Here, we report two new cell lines, named MBU-7 and MBU-8, that differ in complete trisomy of chromosome18, a partial trisomy of chromosome 7 and a tetrasomy of the p-arm of chromosome 8, but otherwise share the same mutational pattern and complex karyotype. Both cell lines are divergent clones of U-937 cells and have the morphology and immunoprofile of monocytic cells. The distinct karyotypic differences between MBU-7 and MBU-8 are associated with a difference in the specific response to nucleoside analogues. Taken together, we propose the MBU-7 and MBU-8 cell lines described here as suitable in vitro models for screening and testing vulnerabilities that are associated with the disease-relevant polysomies of chromosome 7, 8 and 18.

scholarly journals Three cases of partial trisomy 7q owing to rare structural rearrangements of chromosome 7.

1990 ◽  
Vol 27 (2) ◽  
pp. 109-113 ◽  
Author(s):  
D R Romain ◽  
H Cairney ◽  
D Stewart ◽  
L M Columbano-Green ◽  
M Garry ◽  
...  
Keyword(s):  
Partial Trisomy ◽  
Chromosome 7 ◽  
Structural Rearrangements
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