Some of the best moments in a scientist’s life come when things don’t go as planned. Or rather, when the world tells you something you never suspected and weren’t even looking for. Ah, those lucky folks at the University of Warwick:
The researchers were exploring whether release of ATP (an important signaling and energy carrying molecule) influenced the development of locomotion in frogs. Their experiment introduced molecules called ectoenzymes (normally found on the outside surface of cells) into frog embryos at one of the earliest stages when the frogs-to-be were just 8 cells in size. Three ectoenzymes were used: E-NTPDase1, E-NTPDase2 and E-NTPDase3. These ectoenzymes degrade ATP following its release from cells, however each version of the ectoenzyme has slightly different effects on this degradation.
The Warwick research team’s interest in locomotion was quickly eclipsed when they were amazed to find that the introduction of just one of the ectoenzemes (E-NTPDase2) had a dramatic affect on eye development in the tadpoles grown from these embryos. When introduced in cells that would form the head area of the tadpole multiple eyes appeared to be created. That was not the only surprise. When it was introduced in some cells that formed body parts outside the head area it could still produce an additional “ectopic” eye leading to tadpoles with an additional eye in their side, abdomen or even along their tail. (ScienceDaily)
So instead of locomotion, now they are looking at eye development. As a result of their chance observation, the Warwick group posits that the signal for an eye to develop is the production of a short burst of ATP, the energy storage unit of the cell. Warwick’s Nick Dale has developed a new technique to locate and measure these ATP bursts, although we still don’t know what produces them. In any event, the package of ATP is converted to ADP by E-NTPDase2, producing the signal to activate expression of a well-known set of genes called the Eye Field Transcription Factors” (EFTFs). Apparently what they’ve stumbled upon is a switch that sets the EFTF in motion. This is work on frogs, but there is also an E-NTPDase2 gene on the human 9th chromosome and it is known that when this is mutated it results in severe congenital defects of the head and eyes.
Even though we don’t know what initiates flipping the switch to the “on” position, we now know where and what the switch is, opening new ways to manipulate the EFTF system. One never knows what the result will be, but there are good reasons to think this is a big deal. The paper appeared in the October 25 issue of Nature (subscription).
Science goes like this sometimes. If you’re lucky.