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DNA damage response (DDR) is activated in cardiomyocytes of the failing heart, but the type of DNA damage leading to DDR is unclear. Higo et al. show that in mice heart failure is caused in part by unrepaired DNA single-strand breaks in cardiomyocytes, which activate persistent DDR and trigger an NF-κB-dependent cardiac inflammation.
The expansion of trinucleotide repeats has been linked to several neurodegenerative disorders. Here, the authors show that the CRISPR-Cas9 nuclease induces both expansions and contractions of the repeat region, whereas the nickase leads predominantly to contractions.
It is recognized that cellular senescence is triggered by DNA damage as a protective mechanism against tumorigenesis. Here the authors show that DNA single-strand breaks of oxidative origin can induce a transient senescent state followed by the emergence of clonal transformed cells.
In the absence of RNase H2, ribonucleotides incorporated during DNA replication can be processed by Top1. This activity is directed to the nascent leading strand, because gaps in the lagging strand would limit torsional tension.
Many mobile genetic elements, such as transposons, plasmids and viruses, must
cleave their own DNA to effect transposition, replication or conjugation. Here, Chandler
and colleagues describe the HUH endonucleases, which use a unique mechanism to cleave
and rejoin single-stranded DNA in order to mobilize and disseminate such