Dimethylsulfoniopropionate (DMSP) and its catabolite dimethyl sulfide (DMS) are key marine nutrients 1,2 , with roles in global sulfur cycling 2 , atmospheric chemistry 3 , signalling 4,5 and, potentially, climate regulation 6,7. DMSP production was previously thought to be an oxic and photic process, mainly confined to the surface oceans. 2 However, here we show that DMSP concentrations and DMSP/DMS synthesis rates were higher in surface marine sediment from e.g., saltmarsh ponds, estuaries and the deep ocean than in the overlying seawater. A quarter of bacterial strains isolated from saltmarsh sediment produced DMSP (up to 73 mM), and previously unknown DMSPproducers were identified. Most DMSP-producing isolates contained dsyB 8 , but some alphaproteobacteria, gammaproteobacteria and actinobacteria utilised a methionine methylation pathway independent of DsyB, previously only associated with higher plants. These bacteria contained a methionine methyltransferase 'mmtN' gene-a marker for bacterial DMSP synthesis via this pathway. DMSP-producing bacteria and their dsyB and/or mmtN transcripts were present in all tested seawater samples and Tara Oceans bacterioplankton datasets, but were far more abundant in marine surface sediment. Approximately 10 8 bacteria per gram of surface marine sediment are predicted to produce DMSP, and their contribution to this process should be included in future models of global DMSP production. We propose that coastal and marine sediments, which cover a large part of the Earth's surface, are environments with high DMSP and DMS productivity, and that bacteria are important producers within them. Approximately eight billion tonnes of DMSP is produced by phytoplankton in the Earth's surface oceans annually 9. However, surface sediment from saltmarsh ponds, an estuary and the deep ocean (with high pressures and no light) contained DMSP levels (5-128 nmol DMSP g-1) that were up to ~three orders of magnitude higher than the overlying seawater (0.01-0.70 nmol DMSP ml-1) (Fig. 1a-b, Supplementary Tables 1a and 2), a phenomenon also observed in 10,11. DMSP concentration decreased with depth, being much lower in anoxic sediment, but even in deeper sediments the concentration was approximately an order of magnitude higher than in the overlying seawater (Supplementary Table 1a). This study focused on DMSP synthesis in coastal surface sediments, where DMSP concentrations were highest. The

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Bisphenol A (BPA) is a widespread endocrine-disrupting chemical used as the building block for polycarbonate plastics. Epidemiological evidence has correlated BPA exposure with higher risk of heart disease and type 2 diabetes. However, it remains unknown whether there are critical windows of susceptibility to BPA exposure on the development of dysglycemia. This study was an attempt to investigate the critical windows and the long-term consequences of perinatal exposure to BPA on glucose homeostasis. Pregnant mice were given either vehicle or BPA (100 µg/kg/day) at different time of perinatal stage: 1) on days 1–6 of pregnancy (P1–P6, preimplantation exposure); 2) from day 6 of pregnancy until postnatal day (PND) 0 (P6–PND0, fetal exposure); 3) from lactation until weaning (PND0–PND21, neonatal exposure); and 4) from day 6 of gestation until weaning (P6–PND21, fetal and neonatal exposure). At 3, 6 and 8 months of age, offspring in each group were challenged with glucose and insulin tolerance tests. Then islet morphometry and β-cell function were measured. The glucose homeostasis was impaired in P6-PND0 mice from 3 to 6 months of age, and this continued to 8 months in males, but not females. While in PND0-PND21 and P6-PND21 BPA-treated groups, only the 3-month-old male offspring developed glucose intolerance. Moreover, at the age of 3 months, perinatal exposure to BPA resulted in the increase of β-cell mass mainly due to the coordinate changes in cell replication, neogenesis, and apoptosis. The alterations of insulin secretion and insulin sensitivity, rather than β-cell mass, were consistent with the development of glucose intolerance. Our findings suggest that BPA may contribute to metabolic disorders relevant to glucose homeostasis and the effects of BPA were dose, sex, and time-dependent. Fetal development stage may be the critical window of susceptibility to BPA exposure.