Federico Lazzaro

TL;DR: It is demonstrated that ubiquitination of histone H2B on lysine 123 by the Rad6-Bre1 complex, is necessary for activation of Rad53 kinase and cell cycle arrest and results suggest that histone modifications may have a role in checkpoint function by modulating the interactions of Rad9 with chromatin and active Mec1 kinase.

TL;DR: This work identifies AFG3L2 as a novel cause of dominant neurodegenerative disease and indicates a previously unknown role for this component of the mitochondrial protein quality control machinery in protecting the human cerebellum against neurodegenersation.

TL;DR: It is suggested that both Rad9 and histone H3 methylation allow transmission of the damage signal to checkpoint kinases, and keep resection of damaged DNA under control influencing, both positively and negatively, checkpoint cascades and contributing to a tightly controlled response to DNA damage.

TL;DR: In this paper, Rad9 binding to histone H3-K79 methylated histone methylation has been shown to inhibit resection at DSBs and uncapped telomeres.

TL;DR: It is demonstrated that postreplication repair pathways—MMS2-dependent template switch and Pol ζ-dependent bypass—are crucial for tolerating the presence of rNMPs in the chromosomes, and may be relevant for the pathogenesis of Aicardi-Goutières syndrome.