Scientists have successfully used the African frog Xenopus as a tool to identify important clues about the effects of maternal consumption of alcohol in early pregnancy.
As the Xenopus embryos are large, easy to work with and very responsive to environmental cues, they make for ideal instruments to understand early vertebrate development.
Fetal alcohol spectrum disorder (FASD) and Fetal alcohol syndrome (FAS) cause malformations in babies, including facial defects, short stature, and mental and behavioural abnormalities.
Alcohol consumption prevents normal development by inhibiting the production of retinoic acid.
Normally, the levels of retinoic acid made in different areas of the embryo provide cells with necessary information about their proper location and fate.
In the new research, it has been shown that alcohol steals away the molecules that make retinoic acid and use them for its own process of detoxification, resulting in cellular disorientation during a critical period of development.
The study, provides evidence that the characteristics associated with FASD and FAS come from competition of alcohol for key molecules in a pathway that produce retinoic acid from vitamin A.
Retinoic acid is needed for correct positioning of cells in developing embryos and by preventing its normal production.
Alcohol keeps cells from migrating to their correct positions and maturing properly.
Researchers at the Hebrew University in Israel have found that shutting down a molecule needed to produce retinoic acid, known as retinaldehyde dehydrogenase (RALDH2), increases sensitivity of developing embryos to low doses of alcohol.
On the other hand, more of the molecule RALDH2 protected embryos from the negative effects of alcohol.
The research provides evidence that alcohol 'hijacks' RALDH2 molecules for its own breakdown process, and steals it away from its important role in synthesizing positional and maturation cues during development.
The study has been published in Disease Models and Mechanisms (DMM).