Bed-Sharing in Couples Is Associated With Increased and Stabilized REM Sleep and Sleep-Stage Synchronization

Methods Young healthy heterosexual couples underwent sleep-lab-based polysomnography of two sleeping arrangements: individual sleep and co-sleep. Individual and dyadic sleep parameters (i.e., synchronization of sleep stages) were collected. The latter were assessed using cross-recurrence quantification analysis. Additionally, subjective sleep quality, relationship characteristics, and chronotype were monitored. Data were analyzed comparing co-sleep vs. individual sleep. Interaction effects of the sleeping arrangement with gender, chronotype, or relationship characteristics were moreover tested. Results As compared to sleeping individually, co-sleeping was associated with about 10% more REM sleep, less fragmented REM sleep (p = 0.008), longer undisturbed REM fragments (p = 0.0006), and more limb movements (p = 0.007). None of the other sleep stages was significantly altered. Social support interacted with sleeping arrangement in a way that individuals with suboptimal social support showed the biggest impact of the sleeping arrangement on REM sleep. Sleep architectures were more synchronized between partners during co-sleep (p = 0.005) even if wake phases were excluded (p = 0.022). Moreover, sleep architectures are significantly coupled across a lag of ± 5min. Depth of relationship represented an additional significant main effect regarding synchronization, reflecting a positive association between the two. Neither REM sleep nor synchronization was influenced by gender, chronotype, or other relationship characteristics. Conclusion Depending on the sleeping arrangement, couple's sleep architecture and synchronization show alterations that are modified by relationship characteristics. We discuss that these alterations could be part of a self-enhancing feedback loop of REM sleep and sociality and a mechanism through which sociality prevents mental illness

PTBP1 enforces ATR-CHK1 signalling determining the potency of CDC7 inhibitors

Background:CDC7 kinase is crucial for the initiation of DNA replication and is important for replication stress responses. Several ATP-competitive CDC7 inhibitors (CDC7is) are being developed as possible cancer therapeutics. CDC7 inhibition causes a dose-dependent delay in S-phase progression and mild activation of the S-phase checkpoint pathway, which further limits origin firing through ATR activation.Methodology:To identify genes that modulate the cellular responses to CDC7is, we established a CRISPR/Cas9 genome-wide loss-of-function screen. The following data represent the closer investigation of one of these genes, PTBP1, using RNA sequencing, flow cytometry, immunofluorescence analysis and additional techniques as described in the manuscript 'PTBP1 enforces ATR-CHK1 signalling determining the potency of CDC7 inhibitors'.Data:Data represent source data for main figures and supplemental items in support of the manuscript 'PTBP1 enforces ATR-CHK1 signalling determining the potency of CDC7 inhibitors', Göder et al. Data collection, interpretation and findings are addressed in the manuscript

CDC7 kinase promotes MRE11 fork processing, modulating fork speed and chromosomal breakage

The CDC7 kinase is essential for the activation of DNA replication origins and has been implicated in the replication stress response. Using a highly specific chemical inhibitor and a chemical genetic approach, we now show that CDC7 activity is required to coordinate multiple MRE11-dependent processes occurring at replication forks, independently from its role in origin firing. CDC7 localizes at replication forks and, similarly to MRE11, mediates active slowing of fork progression upon mild topoisomerase inhibition. Both proteins are also retained on stalled forks, where they promote fork processing and restart. Moreover, MRE11 phosphorylation and localization at replication factories are progressively lost upon CDC7 inhibition. Finally, CDC7 activity at reversed forks is required for their pathological MRE11-dependent degradation in BRCA2-deficient cells. Thus, upon replication interference CDC7 is a key regulator of fork progression, processing and integrity. These results highlight a dual role for CDC7 in replication, modulating both initiation and elongation steps of DNA synthesis, and identify a key intervention point for anticancer therapies exploiting replication interference

Correction: The economic burden of inpatient care of depression in Poznan (Poland) and Kiel (Germany) in 2016.

[This corrects the article DOI: 10.1371/journal.pone.0198890.]