Frog embryos (pictured) have helped scientists to discover that just like heart muscle, physical development is also dependent on electrical excitability. A gene called KCNJ2 encodes a protein that regulates electrically-charged (ionic) potassium entering and leaving cells. Potassium ions control the excitability of heart muscle cells, and so if KCNJ2 is faulty, cells don't work properly causing cardiac arrhythmia. The KCNJ2 gene is also known to be important during development ensuring body parts are in the right place. But how a potassium regulator could have this effect wasn't clear. By disrupting bioelectrical signals in developing tadpoles the team found it caused cranio-facial abnormalities (right; normal tadpole left), as did mutating KCNJ2. Drugs that can alter ion flux are already available, so this insight brings the possibility of using them to prevent various physical birth defects including the cranio-facial characteristics associated with foetal alcohol syndrome or congenital disorders such as Andersen-Tawil syndrome.
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