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.

Genetic loss-of-function approaches and functional calcium imaging reveal cholecystokinin as the primary regulator of follicle-stimulating hormone in zebrafish, redefining our understanding of gonadotropin regulation in vertebrates.

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

An interdisciplinary research platform reveals that the transcriptional identity of metazoan male germ cells is built around a small network of deeply conserved gene interactions with an overarching functional impact.