The first genetic link that can explain how the heart evolved from being a three-chambered to four-chambered organ has been discovered by scientists.
The discovery has shed light on how cold-blooded birds and mammals became warm-blooded.
Frogs have a three-chambered heart consisting of two atria and one ventricle, which sends a concoction of blood that is not fully oxygenated to the rest of the frog's body.
However, birds and mammals have a fully septated ventricle-a bona fide four-chambered heart, which ensures the separation of low-pressure circulation to the lungs, and high-pressure pumping into the rest of the body.
As warm-blooded animals, we use a lot of energy and therefore need a great supply of oxygen for our activities. The four-chambered heart gives us an evolutionary advantage, we're able to roam, hunt and hide even in the cold of night, or the chill of winter.
But many humans suffer from congenital heart disease, a very common birth defect, which is usually caused by VSD, or ventricular septum defects-a condition that is frequently correctable with surgery.
Benoit Bruneau of the Gladstone Institute of Cardiovascular Disease, who studies the transcription factor, Tbx5, in early stages of embryological development, has called it "a master regulator of the heart."
He teamed up with scientists at Michigan State University to examine a wide evolutionary spectrum of animals and found that in the cold-blooded, Tbx5 is expressed uniformly throughout the forming heart's wall.
On the other hand, warm-blooded embryos showed the protein very clearly restricted to the left side of the ventricle, which allowed for the separation between right and left ventricle.
Interestingly, in the turtle, the molecular signature was found to be transitional as well.
A higher concentration of Tbx5 is found on the left side of the heart, gradually dissipating towards the right.
"The great thing about looking backwards like we've done with reptilian evolution is that it gives us a really good handle on how we can now look forward and try to understand how a protein like Tbx5 is involved in forming the heart and how in the case of congenital heart disease its function is impaired," concluded Bruneau.