By AMY ADAMS

In many ways, the fate of cells mimics the fate of humans. As infants, we all have the potential to become firefighters, teachers, ballerinas or CEOs. But somewhere along the line, life events begin limiting our options. As adults, few of us could backtrack to become art historians after a life spent in computer science classes.

Cells suffer a similar fate. The earliest cells of the human embryo – the so-called stem cells – can go on to form any cell type in the body. But as the cell develops, its DNA accumulates molecular changes that educate the cell about its eventual role. A chunk of adult muscle, no matter how healthy, simply can’t fill in for an ailing liver.

This sealing of fates has long stymied researchers trying to clone new embryos from adult animal cells. Rudolph Jaenisch, MD, biology professor at MIT and faculty member at the Whitehead Institute for Biomedical Research in Cambridge, Mass., has led efforts to understand how the cloning process sporadically lures adult cells to backtrack into their earlier, less-educated state. He discussed this work Feb. 20 before a standing-room-only crowd at Munzer Auditorium.

In animal cloning, researchers take the nucleus from an adult cell and place it into an egg. The egg then begins dividing as if it had been fertilized. As development progresses, all cells of the growing embryo contain the same DNA as the cell that donated the nucleus. This process is rarely successful, in part because DNA from adult cells rarely regresses all the way back to the original, uneducated state.

Jaenisch said that in one set of experiments his lab examined whether embryos cloned from adult tissues made the same proteins as normal embryos. The answer was no. Embryos cloned from stem cells made some proteins inappropriately while those cloned from adult tissues had even more unusual protein production. He said this finding may account for why so many cloned embryos die early and why those that do survive are often abnormal.

“The ones that survive longer are just less abnormal,” Jaenisch said.

The problem isn’t that adult cells lack the genes of embryonic stem cells. Rather, DNA from the adult cell retains its molecular education and passes that education on to all cells in the cloned embryo.

This education determines which genes a cell can or cannot activate – a limitation that can be deadly if required embryonic genes are set to the “off” position.

Now the question is which adult cells have the easiest time reprogramming. These cells would make the best candidates for therapeutic cloning, in which adult cells are used to create new stem cells for treating human disorders such as Alzheimer’s or spinal cord injuries.

“We want to make that process as efficient as possible,” Jaenisch said.