Oocyte mitochondria link maternal environment to offspring phenotype.

During oogenesis and maturation oocytes undergo a recently discovered mitochondrial electron transport chain (ETC) remodeling in flies, frogs, and humans. This conserved oocyte ETC remodeling is regulated by maternal insulin signaling, but its role in biology remains unclear. In the model animal , we previously found that insulin signaling to oocytes regulates offspring's ability to adapt to future osmotic stress by altering offspring metabolism.

A noncanonical polyamine from bacteria antagonizes animal mitochondrial function.

Canonical polyamines such as agmatine, putrescine, and spermidine are evolutionarily conserved metabolites found in nearly all forms of life ranging from bacteria to humans. Recently, interactions between polyamines produced by gut bacteria and human intestinal cells have been proposed to contribute to both Irritable Bowel Syndrome with Diarrhea (IBS-D) and inflammatory bowel diseases. However, the molecular mechanisms that underlie these effects are often unclear due in part to limitations in the methods used to manipulate and study polyamine functions Here, we developed a based screening platform and a modified LC-MS approach for profiling polyamine metabolites.

Oocyte mitochondria link maternal environment to offspring phenotype.

During maturation oocytes undergo a recently discovered mitochondrial proteome remodeling event in flies, frogs, and humans. This oocyte mitochondrial remodeling, which includes substantial changes in electron transport chain (ETC) subunit abundance, is regulated by maternal insulin signaling. Why oocytes undergo mitochondrial remodeling is unknown, with some speculating that it might be an evolutionarily conserved mechanism to protect oocytes from genotoxic damage by reactive oxygen species (ROS).