ScienceDaily (Mar. 16, 2010) — A quest that began over a decade ago with a chance observation has reached a milestone: the identification of a gene that may regulate regeneration in mammals. The absence of this single gene, called p21, confers a healing potential in mice long thought to have been lost through evolution and reserved for creatures like flatworms, sponges, and some species of salamander.
Are scientists playing ‘God’ with this amazing discovery? One might ask, though, why was mammalian regeneration of limbs was ‘lost’ over evolutionary time? Wouldn’t that ability have been a life-sustaining evolutionary development? After all, mammals without an important limb such as a leg or arm are essentially less likely to be able to survive.
Or perhaps God ‘forgot’ to turn off the P21 gene when Adam was being formatted.
Why would gene p21 be active when it inhibits such regeneration? When it is deactivated, the cells of those mice behaved more like embryonic stem cells than adult mammalian cells and thus the re-growth of the lost limb. It was known to science that p21 acts like a brake to block cell cycle progression in the event of DNA damage, preventing the cells from dividing and potentially becoming cancerous. Yet surprisingly, these laboratory mice in the study showed no signs of cancerous aggression.
Odd stuff. I wonder how a theologian might tackle this question. Did God NOT want mammals to be able to regrow limbs? Did God NOT KNOW that gene p21 inhibits regeneration? Or was it because Eve at the apple and we mammals are being PUNISHED for her ‘sin’?
Although p21 is involved with blocking viral infection of HIV-1, that benefit is far out weighed by this new discovery. The recent regenerative qualities of p21 suppression opens up a totally new world of hope to the millions of humans who have lost one or more limbs. Surely the many U.S. Military amputees lying in VA hospitals or learning to use prosthetics may see some flicker of hope that one day they may be able to regrow that lost limb. We surely hope so.