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A genetic switch that gives tadpoles three eyes could allow stem-cell scientists to eventually grow human eyeballs or at least create replacement parts needed for repair jobs.

If scientists could grow eyeballs from stem cells in the lab, the process would be a boon to individuals with damage to cells within the eye, including retinal disorders.

"If you knew all the genes, and how to turn them on, that you needed to make an eye, you could start with very early embryonic cells and turn on all the right genes and grow an eye in a dish," said co-leader of the study Nicholas Dale, a neuroscientist at the University of Warwick in England.

"What I think is the more realistic possibility is to make precursor cells for different bits of the eye, which could then be transplanted and differentiate in-situ to replace damage to the retina or the lens or iris," Dale told LiveScience.

Scientists already had established the amphibian genes that initiate and direct eye development, which they refer to as Eye Field Transcription Factors (EFTFs). How these genes get activated in the right location at a certain time during development had been cloaked in mystery.

The new study, detailed in the Oct. 25 issue of the journal Nature, suggests a nitrogen-bearing molecule sets off a series of steps that result in eye formation in frogs. The mechanism probably also applies to humans and other animals with eyes, the researchers say.

Dale and University of Warwick developmental biologist Elizabeth Jones, along with colleagues, discovered the eye-switch while investigating how "ectoenzyme" molecules located on the external surface of cells contributed to the development of locomotion in the African clawed frog (Xenopus laevis). The biologists injected the molecules into frog embryos that comprised just eight cells.

One of the ectoenzymes triggered wonky eye development. When added to cells that would eventually form the head, the resulting tadpole sported three eyes instead of two. An even stranger sight resulted when they injected the ectoenzyme into other developing body cells. The molecule caused an additional "ectopic" eye, leading to tadpoles with a spare peeper growing out of the side, abdomen or even along the tail.

On a molecular level, the scientists say the enzyme converts a burst of the energy-carrying molecule ATP into ADP, which ultimately turns on the embryo's eye-making machinery.

The researchers think the same mechanism for triggering eye development applies across a wide range of species, including us. Mutations to the human equivalent of this enzyme lead to severe head and eye defects in humans.

And we all know that once they make the initial breakthrough on how to do it, then it just becomes an engineering problem on how to improve it.
Seeing things like this make me glad. Im -8 in my eyes, with my right eye even a little worse than my left. They havn't gotten worse in awhile thankfully, the degeneration stopped around when i was in my early 20s. Still, to be able to actually get my peepers fixed one day, without the laser surgery(ive read it's a bit iffy for those of us who have really bad eyes, and that sometimes it's not forever and they can degenerate again) is something i look forward to.
bah, why go vatgrown when one could get eyes that can see heat, or under very low light. gimme cybereyes already!
Rotbart van Dainig
Because the available technological sensors are still inferior to natural ones.
Anybody see contact info for this team? I'm wondering if these vatgrown eyes could replace my natural ones and fix retinopathy of prematurity. (Search it on wiki if you're curious.)
And more news on the spare body parts front:

QUOTE (Text of Article)
LONDON (Reuters) - Scientists have found a key protein that helps newts regrow severed limbs and which may guide future research into human regenerative medicine.

Biologists have long been intrigued by the ability of newts and salamanders to renew damaged body parts. But how they do it has been unclear.

Now new research by a British team published on Thursday shows that a protein called nAG, secreted by nerve and skin cells, plays a central role in producing a clump of immature cells, known as a blastema, which regrows the missing part.

The importance of nAG was demonstrated by the fact that even when a nerve was severed below the stump tip, which would normally prevent regrowth, the scientists were able to coax regeneration by artificially making cells produce the protein.

Anoop Kumar and colleagues from University College London (UCL), writing in the journal Science, said the finding "may hold promise for future efforts to promote limb regeneration in mammals."

David Stocum of Indiana University-Purdue University Indianapolis said it could help explain why mammals have limited regrowth abilities and thus help direct the field of regenerative medicine.


A clear understanding of the molecular signals involved in blastema formation and limb regeneration could eventually allow medics to program similar patterns into cells of non-regenerating body parts.

"How soon this might be possible, particularly in humans, is anyone's guess but the addition of nAG to the repertoire of necessary factors is an important step forward," Stocum said.

In effect, newts are able to manipulate their bodies by turning cells into undifferentiated stem cells and then back into mature tissue again.

It is a clever trick -- but understanding how they do it does not mean humans will necessarily be able to copy them and regrow lost arms or legs, according to Jeremy Brockes of UCL.

"It would be very desirable for regenerative medicine to understand the specification of the blastema and to try to recreate that in a mammalian context. But we are a long way away from being able to do that," he said in an interview.

Regenerative medicine is a growing area of research, with much of it centered on stem cells, the master cells that act as a source for various cells and tissues in the body.
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