Highlights d Rad51 and Rad52 interact with MCM in a nuclease-insoluble nucleoprotein scaffold d MCM/Rad51/Rad52 accumulation is regulated by cell cycle and replicative DNA damage d Cdc7 prevents Rad51/Rad52 release from the scaffold under replicative DNA damage d MCM/Rad51 promotes MMS-induced gap filling and fork progression by non-HR processes

Purpose of review To review the evidence about video game-based therapeutic intervention for people diagnosed with depressive disorders. Recent findings Psychotherapy has been proved to reduce depressive symptoms and is a key element in the treatment of depressive disorders. However, geographical, economical and stigmatized concerns are barriers to access to psychotherapy. New technologies and videos games can overcome some of these barriers by providing teleconferencing evidence-based therapy as time as they may offer an interactive entertainment. Summary Overall, video game-based interventions were useful and effective in reducing symptoms of depressive disorders. Seven of the studies were published in the last 5 years, which reflects the increased research interest in video game-based interventions for depression. Overall, when adherence was reported, rates of acceptability and feasibility were high.

Cdc7 and its regulator Dbf4 (Dbf4‐dependent kinase; DDK) form an essential complex due to its function in replication initiation, which is carried out by phosphorylating different residues at the helicase MCM during the G1/S transition. In response to replication stress, late origins are inhibited to prevent cell cycle progression until the problems are resolved. In yeast, this inhibition is partially achieved by attenuating DDK activity. In addition, evidence from yeast to human shows that Cdc7 is required for a successful DNA damage response by coordinating multiple processes dealing with replication stress (replication checkpoint, DNA damage tolerance and break‐induced replication) through mechanisms that go beyond its role in origin activation. These studies reveal the importance of getting a better understanding of the spatiotemporal regulation of DDK. Here, we will discuss how DDK operates in these processes and its putative role in controlling the activity of replication and repair factors at specific nuclease‐resistant nucleoprotein scaffolds.

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The advance and stability of replication forks rely on a tight co-regulation of the processes of DNA synthesis and nucleosome assembly. We have addressed the relevance of parental histone recycling in the mechanisms of DNA damage tolerance (DDT) – homologous recombination (HR) and translesion synthesis (TLS) – that assist replication forks under conditions that block their advance. We show that mutants affected in the deposition of parental histones are impaired in the recombinational repair of the single-strand DNA gaps generated during DDT, with the defects being more severe in mutants impaired in the lagging strand-specific deposition pathway. These recombinational defects are not due to a deficit of parental histones at the nascent strands but to an excess of parental nucleosomes at the invaded strand that destabilizes the sister chromatid junction formed after strand invasion. In conclusion, parental histone distribution at stressed forks regulates HR and provides a potential mechanism for the choice between HR and TLS that would depend on whether DNA synthesis is blocked at the lagging or the leading strand.

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