In neurodegeneration of Gaucher disease, glucosylceramides trigger neuroinflammation via attrition of homeostatic microglia and transition to lipid-laden damage-associated microglia concurrently with infiltration of diverse immune cells including activated NK cells and CCR2⁺ macrophages, ameliorated by substrate reduction therapy.

Linker histone H1 and cytosine DNA methylation in contexts other than CG explain patterns of 24 nucleotide small RNA biogenesis in Arabidopsis thaliana.

Choice history signals bias the interpretation of current sensory input, akin to shifting endogenous attention toward (or away from) the previously selected interpretation.

Attractive and repulsive history biases in visual perception occur simultaneously, yet over dissociable timescales, and are explained by efficient encoding and Bayesian decoding of visual information in a stable environment.

The transcription machinery is required for the disassembly of the promoter-proximal H2A.Z nucleosome, contributing to the constitutive histone turnover at yeast promoters.

Enhancing the management of Gaucher disease patients through multidimensional risk assessment serves as a roadmap towards personalized medicine in the context of a rare disease.

Transposon activation during male gametogenesis is caused by interactions between DNA demethylation and linker histone H1, developmental depletion of which promotes pollen fertility.

Modulation of histone levels in gut enterocytes by rapamycin treatment alters chromatin organisation and induces intestinal autophagy through transcriptional regulation to prevent age-related decline in the intestine and extend lifespan.

By analyzing five purified recombinant histone deacetylase complexes and designer acetylated mononucleosome substrates, the molecular basis of the unusual substrate specificity of the CoREST complex was revealed.

Biochemical approaches reveal that an epigenetic histone deacetylase complex called CoREST is slow to deacetylate histone H3 lysine-14 in nucleosomes, and this inhibits demethylation of histone H3 lysine-4 by the CoREST complex.