Fei-Long Meng

Abstract Postmitotic neurons have high levels of methylated cytosine and its oxidized intermediates such as 5-hydroxymethylcytosine1. However, the functional relevance of these epigenetic modifications of DNA are poorly understood. Here we show that some cytidine analogues, such as cytarabine, cause DNA double-strand breaks during TET-mediated active 5-methylcytosine demethylation by interrupting TDG-dependent base excision repair.

Keywords class switch recombination somatic hypermutation transcription-coupled repair transcription-coupled damage AID ELOF1 Get full text access Log in, subscribe or purchase for full access. References 1. Alt, F.W. ∙ Zhang, Y. ∙ Meng, F.L. ... Mechanisms of programmed DNA lesions and genomic instability in the immune system Cell. 2013; 152:417-429 2. Honjo, T. ∙ Kinoshita, K. ∙ Muramatsu, M. Molecular mechanism of class switch recombination: linkage with somatic hypermutation Annu. Rev. Immunol.

Abstract Cells undergo tens of thousands of DNA-damaging events each day. Defects in repairing double-stranded breaks (DSBs) can lead to genomic instability, contributing to cancer, genetic disorders, immunological diseases, and developmental defects. Cohesin, a multi-subunit protein complex, plays a crucial role in both chromosome organization and DNA repair by creating architectural loops through chromatin extrusion.