Suppression of non-homologous end joining does not rescue DNA repair defects in Fanconi anemia patient cells.
Cell Cycle
; 19(19): 2553-2561, 2020 10.
Article
en En
| MEDLINE
| ID: mdl-32865112
ABSTRACT
Severe cellular sensitivity and aberrant chromosomal rearrangements in response to DNA interstrand crosslink (ICL) inducing agents are hallmarks of Fanconi anemia (FA) deficient cells. These phenotypes have previously been ascribed to inappropriate activity of non-homologous end joining (NHEJ) rather than a direct consequence of DNA ICL repair defects. Here we used chemical inhibitors, RNAi, and Clustered Regularly Interspaced Short Palindromic Repeat (CRISPR)-Cas9 to inactivate various components of NHEJ in cells from FA patients. We show that suppression of DNA-PKcs, DNA Ligase IV, and 53BP1 is not capable of rescuing ICL-induced proliferation defects and only 53BP1 knockout partially suppresses the chromosomal abnormalities of FA patient cells.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Daño del ADN
/
Anemia de Fanconi
/
Reparación del ADN por Unión de Extremidades
/
Fibroblastos
Límite:
Humans
Idioma:
En
Revista:
Cell Cycle
Año:
2020
Tipo del documento:
Article
País de afiliación:
Estados Unidos