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Background  Breast cancer 2, early onset ( BRCA2 ) is a tumor suppressor gene. The protein encoded by this gene plays an important role in homologous recombination (HR)-mediated DNA repair. Deleterious mutations in  BRCA2  and downregulation of its expression have been associated with tumorigenesis in dogs and humans. Thus, regulation of BRCA2 expression level is important for maintaining homeostasis in homologous recombination.    Results  In this study, the mechanisms that regulate the expression of  BRCA2  were proposed. Novel splicing variants were identified in the 5′ untranslated region (UTR) of canine and human  BRCA2  in canine testis, canine ovary, and canine and human cultured cell lines. In cultured cells, the ratio of  BRCA2  splicing variants at the 5′ UTR was altered by serum starvation. These novel splicing variants, excluding one of the canine splicing variants, were found to reduce the translational efficiency. Additionally, the DNA sequence in human  BRCA2  intron 1 harbored novel cis-regulatory elements. Three silencer and two enhancer cis-regulatory elements were identified in human  BRCA2  intron 1.    Conclusions  This study demonstrates that BRCA2 expression level is regulated via 5′ UTR splicing variants and that the  BRCA2  intron 1 region harbors cis-regulatory elements.

bmc molecular and cell biology

Reduced translation efficiency due to novel splicing variants in 5′ untranslated region and identification of novel cis-regulatory elements in canine and human BRCA2