DNA double-strand breaks (DSBs) and their repair can cause extensive epigenetic changes. As a result, DSBs have been proposed to promote transcriptional and, ultimately, physiological dysfunction via both cell-intrinsic and cell-non-autonomous pathways. Studying the consequences of DSBs in higher organisms has, however, been hindered by a scarcity of tools for controlled DSB induction. Using a mouse model for both tissue-specific and temporally controlled DSB formation, we investigated the transcriptional response to break repair. SOURCE: David Sturgill (davidsturgill@mail.nih.gov) - LRBGE NIH

Pluto Bioinformatics

GSE74855: Transcriptional effects of I-PpoI induced DNA double strand breaks in mouse lymphocytes