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Mutation Creates SuperKid
Tzarius writes "It's not exactly regular Slashdot fare, but the NYTimes has a story about a kid in Berlin (now 4 years old) who was born with naturally massive muscles. It's not a new condition, but it apparently hasn't been recorded in humans before. It also looks like the cause is a suppression of the myostatin protein, which could be reproducible." Reader Spazmasta adds "A gene that blocks production of a muscle-limiting protein (called myostatin) has been found in a abnormally muscular German baby. This news comes apparently 7 years after researchers at Johns Hopkins created 'mighty mice' through a related approach, turning off the gene that produces the muscle-limiting protein. I, for one, welcome our new myostatin-free overlords."
Muscle doubling in cattle with the same gene was publishedin 1997, with extraordinary photos of a Belgian Blue bull: HERE
The downside is that your skeletal structure has to be strong enough to support the extra weight, your circulatory system and lungs need to be able to pump enough blood and supply enough oxygen to all that extra tissue and you need to ingest a hell of a lot more food to provide enough energy to grow and sustain your body mass, which in turn requires your digestive system can process the amount of food you'll need to eat.
Think of it as being obese, but with muscle instead of fat. Why would that be an advantage?
Agreed, as a graduate student in the biological sciences, I know that there may be numerous complications from this muscle growth. It depends on the exact function of myostatin, but some problems could be:
enlarged heart - much like someone suffering from chronic ostructive pulmonary disease (COPD). This causes the heart to work more and eventually fail
pseudo neuronal degeneration - failure of the nervous system to keep rewiring itself to accomodate the new muscles. This would lead to all sorts of failure in motor control, and eventual paralysis
These are just two that I can think of off of the top of my head. There may be other, unforeseen consequences. Of course, he could live a "normal" healthy life and get about 20 gold medals in weight lifting.
"Me fail English, that's unpossible." --Ralphie
It is up for free now here.
The method in the article is gene therapy, replacing the natural gene with a gene to block myostatin. The NY Times article talks about a drug antibody to prevent myostatin from reaching muscle satalite cells.
Photo Here.
Life is the leading cause of death in America.
Googling for 'myostatin mutation' finds this, which seems to be an account of another person who has this condition, so you're probably right.
According to the Medical College of Georgia, it weakens ligaments.
From this MSNBC article:
The boy has two copies. He could (absent an extremely unlikely second identical mutation on the other copy of the same gene) only get one from his mother. The other had to come from his father. The mutation is very rare. The mother has four male relatives with one copy of the mutation. The identity of the father has not been disclosed.
Anyone care to connect the dots?
I'm not pointing this out to be cruel or catty; I'm pointing it put because it's a good example of what's called the "founder's effect", a mechanism by which mutations -- by definition unique or nearly unique events -- became part of a general population.
Since this child has two copies of the mutation, not only are phenotypic effects greater -- he's even more muscular than his mother who has a single copy -- but all of his children will have at least a single copy, like his mother.
Were the conditions for founder's effect stronger -- that is, if he were a member of a smaller and more isolated population than modern Germany -- one can easily see how inbreeding could result in the mutation becoming common throughout that population.
When two persons with a single copy of the mutation breed, one-quarter of their offspring (on average) will have, like the child being studied, two copies of the mutated form (or allele) of the gene (and no copies of the gene's normal allele), one-quarter will have two copies of the normal allele, and one-half of the offspring will have, like the mother, one mutated allele and one "normal" allele.
But when a person with two copies breeds with a person with a single copy, one-half the offspring (on average) will have two copies of the mutation, and one-half will have one copy of it.
So if there's any preferential benefit to having the mutation -- if those with the mutation do better and so have more offspring -- and if there's the in-breeding of founder's effect, the mutation should become common in the founder population.
Indeed, it's likely that founder's effect, along with environmental conditions, explains why Germans and other Europeans, despite being descended from Africans 40,000 years ago, are white rather than black: being white is bad under the Africa sun, as, unprotected, it will lead to skin cancer and death by about age twelve. But being black in the weaker sunlight of Europe prevents the metabolization of vitamin D, leading to the weakened bones of rickets. In Africa, mutations that lead to less melanin production and whiteness also lead to death -- but in Europe it allowed a longer, better life.
But how did lessened melanin production and "whiteness" spread in Europe? Likely through founder's effect in small and isolated inbreeding populations -- but certainly not because of any "Aryan" superiority.
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