When I saw the title of the column at the top of the main page this morning, I got all excited. You see, we had a discussion about this very subject in my genetics course last year, and so I wanted to see if Unca Cece came up with the same info as we did.
Well, the first thing I noticed was that this column was written in 1978 - nearly 20 years before we had ever sequenced any genome, let alone began sequencing our own. Cecil says, “Graying seems to be genetically determined, but again, the connection is not all that clear,” and that they can see what happens, but they don’t exactly know why. I think it’s time for an update…
Nowadays, we know all about telomeres, which are chunks of protein and nucleic acids on the ends of chromosomes. Every time we replicate our DNA, we lose a little bit of these telomeres, and our chromosomes get shorter. The human genome hasn’t been completely sequenced yet, but it’s my understanding that the genes that control hair pigmentation are near the ends of the chromosomes. After all of the telomeres have been lost, replication causes some of the actual genetic information to be left behind. Thus, the melanocytes no longer have the directions for producing pigment, and hair appears gray (which is due to the empty, airy space in the hair shaft).
Somewhat relevant cite: Shortened Chromosomes Impact Aging and Cancer
Although most of what I just spouted off came from that genetics course, so additions/corrections are very much welcomed.
Just thought that if we’re going to continue this fight against ignorance, perhaps we should stay a little more updated
Meanwhile, while the 1978 Cecil and the modern 2003 “telemere” enlightened students sit around pedantically examining the molecular mechanisms of the process, the people who think beyond their navels now realize that greying in homo sapiens is a most important visual signal that enhances the ready recognition of the wisest members of human breeding groups.
What? Did you think that 600 pound silverback male gorillas are merely cute?
Wow, lovelyluka! I was sure progress had been made since the article was originally written, came over to this board and BAM! There’s your post! Good stuff, thanks!!
“Air bubbles, which may mysteriously work their way into the hair shaft, also contribute to graying by blocking the passage of the melanin.”
This implies hair is hollow and has some sort of flow of melanin running up it. But if that was so, hair would bleed melanin when you cut it. What is he on about here?
Unfortunately, the picture is probably a little more complicated:
Canities (the medical term for graying of the hair), appears to be timed and genetically regulated in aging. It does not appear to be from a loss of genetic information. The genes involved in hair coloration are the same genes involved in other melanin biosynthetic pathways (hence people with hypomorphic melanin pathways have pale skin and light hair, albinos have white hair). The deletion of these genes would presumably lead to a loss of melanin biosynthesis everywhere. We don’t see this – in fact, in places like liver spots melanin is overproduced. Furthermore, I haven’t seen literature about these genes being concentrated in telomeres, which is just the kind of evolutionary oddity to which I normally find myself drawn.
I’m not ruling out the possibilities that telomeres alone can explain it. Telomere loss is certainly part of aging, but it doesn’t appear to explain it entirely. Lots of things go wrong in aging. The progeroid (premature aging) syndromes are so far uniformly mutations in DNA damage response genes and not telomerase mutations. A recent paper in Nature created a progeroid syndrome in mice by mutating a telomerase gene as well as a gene which usually leads to a cancer prone syndrome in humans called ataxia-telengectasia.
DNA loss by diminishing telomerase activity certainly is a contributor. But much of it is left to the stresses of life and metabolism, namely oxidative damage, ionizing radiation, exposure history, naturally occuring mutations, and replication errors.
