Highlights d Loss of ATRX in neurons has sexually dimorphic effects on long-term spatial memory d Targeted deletion of neuronal ATRX in mice causes ultrastructural synaptic defects d ATRX null neurons show sex-specific changes in miR-137 and target synaptic transcripts d ATRX directly binds and suppresses miR-137 in males via enrichment of H3K27me3

Effective aquaculture management strategies are paramount to global food security. Growing demands stimulate the intensification of production and create the need for practices that are both economically viable and environmentally sustainable. Importantly, pathogenic microbes continue to be detrimental to fish growth and survival. In terms of host health, the intestinal mucosa and its associated consortium of microbes have a critical role in modulating fitness and present an attractive opportunity to promote health at this interface. In light of this, the administration of probiotic microorganisms is being considered as a means to restore and sustain health in fish. Current evidence suggests that certain probiotic strains might be able to augment immunity, enhance growth rate, and protect against infection in salmonids, the most economically important family of farmed finfish. This review affirms the relevance of host-microbe interactions in salmonids in light of emerging evidence, with an emphasis on intestinal health. In addition, the current understanding of the mode of action of probiotics in salmonid fish is discussed, along with delivery systems that can effectively carry the living microbes.

statement: Ablation of the ATRX chromatin remodeler specifically in forebrain excitatory neurons of mice causes male-specific deficits in long-term spatial memory associated with miR-137 overexpression, transcriptional changes and structural alterations corresponding to pre-and post-synaptic abnormalities. AbstractMutations in the ATRX chromatin remodeler are associated with syndromic and non-syndromic intellectual disability. Emerging evidence points to key roles for ATRX in preserving neuroprogenitor cell genomic stability, whereas ATRX function in differentiated neurons and memory processes are still unresolved. Here, we show that Atrx deletion in mouse forebrain glutamatergic neurons causes distinct hippocampal structural defects identified by magnetic resonance imaging. Ultrastructural analysis revealed fewer presynaptic vesicles and an enlarged postsynaptic area at CA1 apical dendrite-axon junctions. These synaptic defects are associated with impaired long-term contextual memory in male, but not female mice. Mechanistically, we identify ATRXdependent and sex-specific alterations in synaptic gene expression linked to Mir137 levels, a known regulator of presynaptic processes and spatial memory. We conclude that ablation of Atrx in excitatory forebrain neurons leads to sexually dimorphic outcomes on miR-137 and on spatial memory, identifying a promising therapeutic target for neurological disorders caused by ATRX dysfunction.