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Microbial community composition varies across stream habitats. However, there is little understanding of how varying hydraulic and geomorphic factors influence microbial distribution along a succession of pools. This study examines how substrate, geomorphological and hydraulic habitat variables may drive bacterial community composition within different stream pool habitats of a temperate headwater stream. Microbial community structures from rock biofilm and sediment samples within each of the 10 selected stream pools of White Clay Creek, PA, were determined by high‐throughput sequencing of 16S rRNA genes. The grain size distribution, organic matter content, streamflow velocity, temperature regime and morphology of each pool were quantified to characterize the pool habitats' variability. Multivariate statistical analysis revealed significant differences in the microbial community composition linked to the substrate's stability within the pool units. Indeed, soft and more mobile sediments were dominated by heterotrophic bacteria, while photosynthetic microorganisms (e.g., microalgae and cyanobacteria) were mainly found on rock biofilm. The difference in the distribution of bacterial communities can be explained by variations in the local hydraulic (i.e., depth and velocity) and the thermal conditions (daily fluctuation, min and max). These results highlight the geomorphological and hydrologic drivers for small‐scale diversity in bacterial communities and provide a better understanding of how maintaining and promoting variability in streambed physical properties may enhance microbial diversity. Better integration of these drivers into stream restoration practices will allow the inclusion of microorganisms, the trophic levels that are usually overlooked but still play critical roles in stream ecology. [ABSTRACT FROM AUTHOR]

Background: Children exposed to gestational diabetes mellitus (GDM) are at a higher risk of developing obesity and type 2 diabetes. This susceptibility might involve brown adipose tissue (BAT), which is suspected to protect against obesity. The objective of this study is to assess whether fetal exposure to maternal hyperglycemia is associated with DNA methylation variations in genes involved in BAT genesis and activation. Methods: DNA methylation levels at the PRDM16, BMP7, CTBP2, and PPARGC1α gene loci were measured in placenta samples using bisulfite pyrosequencing in E-21 (n = 133; 33 cases of GDM) and the HumanMethylation450 array in Gen3G (n = 172, all from non-diabetic women) birth cohorts. Glucose tolerance was assessed in all women using an oral glucose tolerance test at the second trimester of pregnancy. Participating women were extensively phenotyped throughout pregnancy, and placenta and cord blood samples were collected at birth. Results: We report that maternal glycemia at the second and third trimester of pregnancy are correlated with variations in DNA methylation levels at PRDM16, BMP7, and PPARGC1α and with cord blood leptin levels. Variations in PRDM16 and PPARGC1α DNA methylation levels were also correlated with cord blood leptin levels. Mediation analyses support that DNA methylation variations at the PPARGC1α gene locus explain 0.8 % of the cord blood leptin levels variance independently of maternal fasting glucose levels (p = 0.05). Conclusions: These results suggest that maternal glucose in pregnancy could produce variations in DNA methylation in BAT-related genes and that some of these DNA methylation marks seem to mediate the impact of maternal glycemia on cord blood leptin levels, an adipokine regulating body weight. Electronic supplementary material The online version of this article (doi:10.1186/s13148-016-0239-9) contains supplementary material, which is available to authorized users.