Atlantic salmon aquaculture is undergoing an expansion of land-based recirculating aquaculture systems (RAS), especially for freshwater (FW) stages of production. Juvenile salmon undergo parr-smolt transformation, also known as smoltification and become pre-adapted to tolerate seawater (SW). One aspect requiring study is the development of microbial communities during this time, especially in RAS systems. Here we analyzed temporal changes in microbiome associated with the intestine in Atlantic salmon during smolt production in a commercial RAS production facility and followed the same cohort of fish post-seawater transfer (SWT), using 16S rRNA gene sequencing. Microbial diversity and richness showed an increase over time across FW production, but declined sharply and significantly 1-week post-SWT before re-establishing itself with a completely different community structure after 4 weeks. Core microbial taxa could be assigned to three distinct categories; (1) omnipresent, (2) salinity specific, or (3) transient. By including diet and water samples in the analyses, we classified true core taxa associated with the host, those associated with the diet, and transient cores associated with microbial communities in tank water. The rising trend observed in microbial richness in the water may be a consequence of a temporal increase in organic load while dominance of Vibrionaceae may be attributed to the higher temperatures maintained during RAS production and above average natural water temperatures post-SWT. Functional analysis suggests modulation of metabolic pathways post-SWT, but downstream impacts on fish growth and health in a commercial setting remain to be elucidated. A deeper understanding of the interplay between microbial composition and functionality can play a role in optimizing fish performance in tightly regulated RAS production.

Genomic imprinting is important for normal brain development and aberrant imprinting has been associated with impaired cognition. We studied the imprinting status in selected imprints (H19, IGF2, SNRPN, PEG3, MEST1, NESPAS, KvDMR, IG-DMR and ZAC1) by pyrosequencing in blood samples from longitudinal cohorts born in 1936 (n = 485) and 1921 (n = 223), and anterior hippocampus, posterior hippocampus, periventricular white matter, and thalamus from brains donated to the Aberdeen Brain Bank (n = 4). MEST1 imprint methylation was related to childhood cognitive ability score (-0.416 95% CI -0.792,-0.041; p = 0.030), with the strongest effect evident in males (-0.929 95% CI -1.531,-0.326; p = 0.003). SNRPN imprint methylation was also related to childhood cognitive ability (+0.335 95%CI 0.008,0.663; p = 0.045). A significant association was also observed for SNRPN methylation and adult crystallised cognitive ability (+0.262 95%CI 0.007,0.517; p = 0.044). Further testing of significant findings in a second cohort from the same region, but born in 1921, resulted in similar effect sizes and greater significance when the cohorts were combined (MEST1; -0.371 95% CI -0.677,-0.065; p = 0.017; SNRPN; +0.361 95% CI 0.079,0.643; p = 0.012). For SNRPN and MEST1 and four other imprints the methylation levels in blood and in the five brain regions were similar. Methylation of the paternally expressed, maternally methylated genes SNRPN and MEST1 in adult blood was associated with cognitive ability in childhood. This is consistent with the known importance of the SNRPN containing 15q11-q13 and the MEST1 containing 7q31-34 regions in cognitive function. These findings, and their sex specific nature in MEST1, point to new mechanisms through which complex phenotypes such as cognitive ability may be inherited. These mechanisms are potentially relevant to both the heritable and non-heritable components of cognitive ability. The process of epigenetic imprinting—within SNRPN and MEST1 in particular—and the factors that influence it, are worthy of further study in relation to the determinants of cognitive ability.

Epigenetic imprinting is important for neurogenesis and brain function. Hippocampal volumes and brain hyperintensities in late life have been associated with early life circumstances. Epigenetic imprinting may underpin these associations. Methylation was measured at 982 sites in 13 imprinted locations in blood samples from a longitudinal cohort by bisulphite amplicon sequencing. Hippocampal volumes and hyperintensities were determined at age 64y and 72y using MRI. Hyperintensities were determined in white matter, grey matter and infratentorial regions. Permutation methods were used to adjust for multiple testing. At 64y, H19/IGF2 and NESPAS methylation predicted hippocampal volumes. PEG3 predicted hyperintensities in hippocampal grey matter, and white matter. GNASXL predicted grey matter hyperintensities. Changes with age were predicted for hippocampal volume (MEST1, KvDMR, L3MBTL, GNASXL), white matter (MEST1, PEG3) and hippocampal grey matter hyperintensities (MCTS2, GNASXL, NESPAS, L3MBTL, MCTS2, SNRPN, MEST1). Including childhood cognitive ability, years in education, or socioeconomic status as additional explanatory variables in regression analyses did not change the overall findings. Imprinting methylation in multiple genes predicts brain structures, and their change over time. These findings are potentially relevant to the development of novel tests of brain structure and function across the life-course, strategies to improve cognitive outcomes, and our understanding of early influences on brain development and function.

No abstract

No abstract