The study focused on two modern Hox genes:
-- The Hoxa1 gene, which helps control how an embryo's brain stem develops and is compartmentalized into seven sections called rhombomeres. When Hoxa1 is disabled or "knocked out" in an embryonic mouse, the embryo dies shortly after birth because the brain stem is malformed, including the part necessary for breathing. (About 20 people with the same defect have been found among Apache and Navajo Indians in Arizona and in families in Turkey and Saudi Arabia. Their brain stem defects result in problems with breathing, hearing, balance and con-trol of the eyeballs.)
-- The Hoxb1 gene, which orders the formation of particular nerve cells in rhombomere 4 ?nerves that ultimately control facial expressions in animals. When a mouse is born with a disabled Hoxb1 gene, it suffers facial paralysis, and is unable to blink its eyes, wiggle its whiskers or pull back its ears.
Tvrdik and Capecchi say that by combining critical portions of Hoxa1 and Hoxb1, they effectively recreated a gene with the function that the original Hox1 performed more than 530 million years ago.
The result: A mouse with a disabled Hoxb1 gene still was able to move eyelids, whiskers and ears because the reconstructed gene made up for the loss of Hoxb1.
How the Study was Conducted
Evolution proceeds as cells divide and each gene within them duplicates. Having two identical genes allows one to keep doing its normal job and the other can change, or mutate. Most mutations are for the worse and disappear. Others persist because they perform a new job that holds some advantage for allowing an
Source:University of Utah Health Sciences Center