Portal de Periódicos da CAPES

Non-homologous end joining mediated DNA repair is impaired in the NUP98-HOXD13 mouse model for myelodysplastic syndrome

2012; Elsevier BV; Volume: 37; Issue: 1 Linguagem: Inglês

10.1016/j.leukres.2012.10.012

1873-5835

Abdul Gafoor Puthiyaveetil, Christopher M. Reilly, Timothy S. Pardee, David L. Caudell,

Genomics and Chromatin Dynamics

Chromosomal translocations typically impair cell differentiation and often require secondary mutations for malignant transformation. However, the role of a primary translocation in the development of collaborating mutations is debatable. To delineate the role of leukemic translocation NUP98-HOXD13 (NHD13) in secondary mutagenesis, DNA break and repair mechanisms in stimulated mouse B lymphocytes expressing NHD13 were analyzed. Our results showed significantly reduced expression of non-homologous end joining (NHEJ)-mediated DNA repair genes, DNA Pkcs, DNA ligase4, and Xrcc4 leading to cell cycle arrest at G2/M phase. Our results showed that expression of NHD13 fusion gene resulted in impaired NHEJ-mediated DNA break repair.