Epigenomic and transcriptomic analysis reveals that paternal obesity influences sperm histone H3 lysine 4 tri-methylation enrichment and placenta gene expression, which in turn negatively impact its development and function in a manner that may contribute to metabolic disease in offspring.

Aphid and mildew read counts leftover from the sequencing of greenhouse plants correlated with the environment of origin of the plants, and allowed the mapping of pathogen resistance genes.

Maternal obesity mouse model reveal that melatonin deficiency causes the genomic hyper-methylation of oocytes via increasing the expression of DNA methyltransferases.

Ageing is broadly accepted as a by-product of evolution, as thus, models allowing to conceive ageing as an adaptive force of evolution could show significant importance at a time of biogerontology mostly aiming at curing ageing.

Large extracellular vesicle extrusion that eliminates neuronal protein aggregates and organelles is potentiated by uterine filling, linking reproductive status to maternal nervous system health, and demonstrating mechanobiology components in exophergenesis.

A foundation for analyzing epigenetic changes within the context of regulatory architectures that enable heredity.

Although developing oocytes and sperm of mice both harbor the glucocorticoid receptor, fetal oocytes are resistant to differing levels of gluocorcorticoid stress hormones, while spermatogonia alter RNA splicing.

Exposure of embryonic stem cells to physiological concentrations of Δ9-THC remodels cellular metabolism across differentiation.