Valentina Matti

TL;DR: It is proposed that linear genomes are not uniformly reparable and that telomeric DNA tracts, if damaged, are irreparable and trigger persistent DDR and cellular senescence.

TL;DR: It is shown that in human fibroblasts resistant to premature p16INK4a induction, SAHF are preferentially formed following oncogene activation but are not detected during replicative cellular senescence or on exposure to a variety ofsenescence-inducing stimuli.

TL;DR: It is proposed that DDR signalling sites, in addition to sharing a common pool of proteins, individually host a unique set of site-specific RNAs necessary for DDR activation.

TL;DR: It is revealed that damaged induced lncRNAs can form DNA:RNA hybrids at resected DNA-ends, which are involved in recruiting HR-mediated repair machinery which, in turn, controls their level at DSBs.

TL;DR: It is demonstrated that DICER and DROSHA are dispensable for primary recruitment of the DDR sensor NBS1 to DNA damage sites and, together with γH2AX, are essential for enabling the secondary recruitment of DDR factors and fuel the amplification of DDR signaling.