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INO80 and SWR1 are two closely related ATP‐dependent chromatin remodeling complexes that share several subunits. Ino80 was reported to be recruited to the HO endonuclease‐induced double‐strand break (DSB) at the budding yeast mating‐type locus, MAT . We find Swr1 similarly recruited in a manner dependent on the phosphorylation of H2A (γH2AX). This is not unique to cleavage at MAT ; both Swr1 and Ino80 bind near an induced DSB on chromosome XV. Whereas Swr1 incorporates the histone variant H2A.Z into chromatin at promoters, H2A.Z levels do not increase at DSBs. Instead, H2A.Z, γH2AX and core histones are coordinately removed near the break in an INO80‐dependent, but SWR1‐independent, manner. Mutations in INO80‐specific subunits Arp8 or Nhp10 impair the binding of Mre11 nuclease, yKu80 and ATR‐related Mec1 kinase at the DSB, resulting in defective end‐processing and checkpoint activation. In contrast, Mre11 binding, end‐resection and checkpoint activation were normal in the swr1 strain, but yKu80 loading and error‐free end‐joining were impaired. Thus, these two related chromatin remodelers have distinct roles in DSB repair and checkpoint activation.

A genetic screen of a population of Arabidopsis thaliana lines exhibiting enhanced somatic homologous recombination yielded a mutant affected in expression of a gene encoding a caltractin-like protein (centrin). The hyperrecombinogenic phenotype could be reproduced using RNA interference (RNAi) technology. Both the original mutant and the RNAi plants exhibited a moderate UV-C sensitivity as well as a reduced efficiency of in vitro repair of UV-damaged DNA. Transcription profiling of the mutant showed that expression of components of the nucleotide excision repair (NER) pathway and of factors involved in other DNA repair processes were significantly changed. Our data suggest an indirect involvement of centrin in recombinational DNA repair via the modulation of the NER pathway. These findings thus point to a novel interconnection between an early step of NER and homologous recombination, which may play a critical role in plant DNA repair.

Impeded DNA replication or a deficiency of its control may critically threaten the genetic information of cells, possibly resulting in genome alterations, such as gross chromosomal translocations, microsatellite instabilities, or increased rates of homologous recombination (HR). We examined an Arabidopsis thaliana line derived from a forward genetic screen, which exhibits an elevated frequency of somatic HR. These HR events originate from replication stress in endoreduplicating cells caused by reduced expression of the gene coding for the catalytic subunit of the DNA polymerase δ (POLδ1). The analysis of recombination types induced by diverse alleles of polδ1 and by replication inhibitors allows the conclusion that two not mutually exclusive mechanisms lead to the generation of recombinogenic breaks at replication forks. In plants with weak polδ1 alleles, we observe genome instabilities predominantly at sites with inverted repeats, suggesting the formation and processing of aberrant secondary DNA structures as a result of the accumulation of unreplicated DNA. Stalled and collapsed replication forks account for the more drastic enhancement of HR in plants with strong polδ1 mutant alleles. Our data suggest that efficient progression of DNA replication, foremost on the lagging strand, relies on the physiological level of the polymerase δ complex and that even a minor disturbance of the replication process critically threatens genomic integrity of Arabidopsis cells.

Impeded DNA replication or a deficiency of its control may critically threaten the genetic information of cells, possibly resulting in genome alterations, such as gross chromosomal translocations, microsatellite instabilities, or increased rates of homologous recombination (HR). We examined an Arabidopsis thaliana line derived from a forward genetic screen, which exhibits an elevated frequency of somatic HR. These HR events originate from replication stress in endoreduplicating cells caused by reduced expression of the gene coding for the catalytic subunit of the DNA polymerase delta (POLdelta1). The analysis of recombination types induced by diverse alleles of poldelta1 and by replication inhibitors allows the conclusion that two not mutually exclusive mechanisms lead to the generation of recombinogenic breaks at replication forks. In plants with weak poldelta1 alleles, we observe genome instabilities predominantly at sites with inverted repeats, suggesting the formation and processing of aberrant secondary DNA structures as a result of the accumulation of unreplicated DNA. Stalled and collapsed replication forks account for the more drastic enhancement of HR in plants with strong poldelta1 mutant alleles. Our data suggest that efficient progression of DNA replication, foremost on the lagging strand, relies on the physiological level of the polymerase delta complex and that even a minor disturbance of the replication process critically threatens genomic integrity of Arabidopsis cells.

Uracil DNA glycosylases (UDGs) excise uracil from DNA arising from dUMP misincorporation during replication or from cytosine deamination. Besides functioning in canonical uracil repair, UDGs cooperate with DNA base modifying enzymes to effect mutagenesis or DNA demethylation. Mammalian cells express four UDGs, the functional dissection of which represents a challenge. Here, we used Schizosaccharomyces pombe with only two UDGs, Ung1 and Thp1, as a simpler model to study functional interactions in uracil repair. We show that despite a predominance of Ung1 activity in cell extracts, both UDGs act redundantly against genomic uracil accumulation and mutations from cytosine deamination in cells. Notably, Thp1 but not Ung1-dependent repair is cytotoxic under genomic uracil stress induced by 5-fluorouracil exposure or AID expression. Also, Thp1- but not Ung1-mediated base excision is recombinogenic, accounting for more than 60% of spontaneous mitotic recombination events in a recombination assay. Hence, the qualitative outcome of uracil repair depends on the initiating UDG; while Ung1 shows expected features of a bona-fide DNA repair enzyme, Thp1-initiated repair appears slow and rather non-productive, suggesting a function beyond canonical DNA repair. Given the epigenetic role of TDGs, the mammalian orthologs of Thp1, we performed transcriptome analyses and identified a possible function of Thp1 in stabilizing gene expression.Competing Interest StatementThe authors have declared no competing interest.

Neonicotinoids are the most widely used class of insecticides in the world but they have raised numerous concerns regarding their effects on biodiversity. Thus, the objective of this work was to do a critical review of the contamination of the environment (soil, water, air, biota) by neonicotinoids (acetamiprid, clothianidin, imidacloprid, thiacloprid, thiamethoxam) and of their impacts on terrestrial and aquatic biodiversity. Neonicotinoids are very frequently detected in soils and in freshwater, and they are also found in the air. They have only been recently monitored in coastal and marine environments, but some studies already reported the presence of imidacloprid and thiamethoxam in transitional or semi-enclosed ecosystems (lagoons, bays and estuaries). The contamination of the environment leads to the exposure and to the contamination of non-target organisms, and to negative effects on biodiversity. Direct impacts of neonicotinoids are mainly reported on terrestrial invertebrates (e.g., pollinators, natural enemies, earthworms) and vertebrates (e.g., birds), and on aquatic invertebrates (e.g., arthropods). Impacts on aquatic vertebrate populations and communities, as well as on microorganisms, are less documented. In addition to their toxicity to directly exposed organisms, neonicotinoid induce indirect effects via trophic cascades as demonstrated in several species (terrestrial and aquatic invertebrates). However, more data are needed to reach firmer conclusions and to get a clearer picture of such indirect effects. Finally, we identified specific knowledge gaps that need to be filled to better understand the effects of neonicotinoids on terrestrial, freshwater and marine organisms, as well as on ecosystem services associated with these biotas.

Several generations of chamosite, including a red variety, occur in the Ordovician hydrothermalized oolitic ironstone from Saint-Aubin-des-Châteaux (Armorican Massif, France). Their chemical re-examination indicates a low Mg content (0.925 < Fe/(Fe + Mg) < 0.954), but a significant variation in IV Al. Minor vanadium is present at up to 1.1 wt.% oxide. Variations in IV Al, the vanadium content and the colour of chamosite are related to the hydrothermal reworking of the ironstone. Taking into account other published data, the ideal composition of chamosite is (Fe 5– x Al 1+ x )(Si 3– x Al 1+ x )O 10 (OH) 8 , with 0.2 < x < 0.8 (0.2: equilibrium with quartz; 0.8: SiO 2 deficit). The red chamosite (II b polytype) has a mean composition of (Fe 3.87 Mg 0.23 Mn 0.01 □ 0.07 Al 1.74 V 0.07 )(Si 2.33 Al 1.67 )O 10 (OH) 8 . This chamosite is strongly pleochroic, from pale yellow ( E || (001)) to deep orange red ( E ⊥ (001)). Visible–near-infrared absorbance spectra show a specific absorption band centred at ~550 nm for E ⊥ (001), due to a proposed new variety of Fe/V intervalence charge-transfer mechanism in the octahedral sheet, possibly Fe 2+ – V 4+ → Fe 3+ – V 3+ . While the formation of green chamosite varieties is controlled by reducing conditions due to the presence of organic matter as a buffer, that of red chamosite would indicate locally a weak increase of f O 2 related to oxidizing hydrothermal solutions.

Agricultural practices are a major cause of the current loss of biodiversity. Among postwar agricultural intensification practices, the use of plant protection products (PPPs) might be one of the prominent drivers of the loss of wildlife diversity in agroecosystems. A collective scientific assessment was performed upon the request of the French Ministries responsible for the Environment, for Agriculture and for Research to review the impacts of PPPs on biodiversity and ecosystem services based on the scientific literature. While the effects of legacy banned PPPs on ecosystems and the underlying mechanisms are well documented, the impacts of current use pesticides (CUPs) on biodiversity have rarely been reviewed. Here, we provide an overview of the available knowledge related to the impacts of PPPs, including biopesticides, on terrestrial vertebrates (i.e. herptiles, birds including raptors, bats and small and large mammals). We focused essentially on CUPs and on endpoints at the subindividual, individual, population and community levels, which ultimately linked with effects on biodiversity. We address both direct toxic effects and indirect effects related to ecological processes and review the existing knowledge about wildlife exposure to PPPs. The effects of PPPs on ecological functions and ecosystem services are discussed, as are the aggravating or mitigating factors. Finally, a synthesis of knowns and unknowns is provided, and we identify priorities to fill gaps in knowledge and perspectives for research and wildlife conservation.

OBJECTIVES: The etiology of testicular germ cell tumors (TGCT) is suspected to be related to prenatal environmental risk factors. Some solvents have potential endocrine disrupting or carcinogenic properties and may disrupt male genital development in utero. The aim of this study was to examine the association between parental occupational exposure to solvents and TGCT risk among their offspring. METHODS: A French nationwide case–control study, TESTIS included 454 TGCT cases and 670 controls frequency-matched on region and 5-year age strata. Participants were interviewed via telephone and provided information on parental occupations at birth. Job-exposure matrices (JEM) developed in the French Matgéné program were used to assign exposure to five petroleum-based solvents, five solvents or groups of oxygenated solvents, and five chlorinated solvents. Odds ratios (OR) for TGCT and 95% confidence intervals (CI) were estimated using conditional logistic regression, adjusting for TGCT risk factors. RESULTS: Occupational exposure to at least one solvent during the year of their son’s birth was 41% among fathers and 21% among mothers. Paternal exposure to at least one solvent showed OR 0.89 (95% CI 0.68–1.15). Exposure to perchloroethylene (OR 1.41, 95% CI 0.55–3.61), methylene chloride (OR 1.13, 95% CI 0.54–2.34) and diesel/kerosene/fuel oil (OR 1.17, 95% CI 0.80–1.73) disclosed OR >1 but with low precision. Our results suggest a possible modest increase in non-seminoma risk for sons whose fathers were highly exposed to trichloroethylene (OR 1.44, 95% CI 0.79–2.63). Maternal exposure to at least one solvent showed OR 0.90 (95% CI 0.65–1.24). When stratifying by birth year, men born in the 1970s experienced an increased TGCT risk following maternal exposure to fuels and petroleum-based solvents (OR 2.74, 95% CI 1.11–6.76). CONCLUSION: Overall, no solid association was found between parental occupational exposure to solvents and TGCT risk. The association found with maternal occupational exposure to fuels and petroleum solvents among older men needs further investigation.