International audienceThis study investigates the microplastic contamination of both urban compartments (wastewater and total atmospheric fallout) and surface water in a continental environment (Greater Paris, France). These first investigations on urban environment confirm the presence of microplastics in sewage, freshwater and total atmospheric fallout and provide knowledge on the type and size distribution of microplastics in the [100 µm-5 000 µm] range. For the first time, the presence of microplastics, mostly fibers, is highlighted in total atmospheric fallout (29-280 particles/m2/day). High levels of fibers were found in wastewater (260-320 x103 particles/m3). In treated effluent, the contamination significantly decreases to 14-50 x103 particles/m3. In River Seine, two sampling devices are used to collect both large and small microplastic particles: i) a plankton net (80 µm mesh) and ii) a manta trawl (330 µm mesh). Sampling with the plankton net showed a predominance of fibers with concentrations ranging from 3 to 108 particles/m3. A greater diversity of both microplastic shapes and types was encountered during manta trawl sampling but at much lower concentrations (0.28-0.47 particles/m3). This combined approach could be relevant and implemented in future studies to provide an accurate overview of microplastic distribution in freshwater

Ataxia with oculomotor apraxia 2 (AOA-2) and amyotrophic lateral sclerosis (ALS4) are neurological disorders caused by mutations in the gene encoding for senataxin (SETX), a putative RNA:DNA helicase involved in transcription and in the maintenance of genome integrity. Here, using ChIP followed by high throughput sequencing (ChIP-seq), we report that senataxin is recruited at DNA double-strand breaks (DSBs) when they occur in transcriptionally active loci. Genome-wide mapping unveiled that RNA:DNA hybrids accumulate on DSB-flanking chromatin but display a narrow, DSB-induced, depletion near DNA ends coinciding with senataxin binding. Although neither required for resection nor for timely repair of DSBs, senataxin was found to promote Rad51 recruitment, to minimize illegitimate rejoining of distant DNA ends and to sustain cell viability following DSB production in active genes. Our data suggest that senataxin functions at DSBs in order to limit translocations and ensure cell viability, providing new insights on AOA2/ALS4 neuropathies.

SummaryDouble-strand breaks (DSBs) are extremely detrimental DNA lesions that can lead to cancer-driving mutations and translocations. Non-homologous end joining (NHEJ) and homologous recombination (HR) represent the two main repair pathways operating in the context of chromatin to ensure genome stability. Despite extensive efforts, our knowledge of DSB-induced chromatin still remains fragmented. Here, we describe the distribution of 20 chromatin features at multiple DSBs spread throughout the human genome using ChIP-seq. We provide the most comprehensive picture of the chromatin landscape set up at DSBs and identify NHEJ- and HR-specific chromatin events. This study revealed the existence of a DSB-induced monoubiquitination-to-acetylation switch on histone H2B lysine 120, likely mediated by the SAGA complex, as well as higher-order signaling at HR-repaired DSBs whereby histone H1 is evicted while ubiquitin and 53BP1 accumulate over the entire γH2AX domains.