Slashdot Mirror
Researchers Create "Mighty Mouse" With Gene Tweak
cylonlover writes "He can't fly just yet, but a team of scientists have made a big step towards creating a real-life Mighty Mouse. By tweaking a gene that normally inhibits muscle growth the researchers created a batch of super-strong mice and worms. The scientists acted on a genome regulator — known as NCOR1 — and were able to change the activity of certain genes. In simpler English, the scientists shut off the thyroid hormone that keeps most mammals from turning into the Incredible Hulk. The result was a strain of mice with muscles that were twice as strong as normal."
I have this sneaking suspicion that if genome 'brakes' are present in most animals, they're probably there for a reason.
I wonder what sort of long term side effects you'd be looking at with vastly increased muscle growth.
Seems to me that a whole lot of biological processes follow the "use it or lose it" paradigm. From muscle growth, to brain function and even living itself (get fat and lazy, you die sooner).
So what I'd like to see is research to counter-act that. Instead of a new gene-therapy replacement for steroids, how about something prevents muscle loss even for people who are sedentary? Something to counter-act the "maintenance" requirement to staying fit. That would be really nice.
When information is power, privacy is freedom.
I reject the notion that mice were "designed" or that a mouses body is the way it is due to any reasoning.
You give these mice that growth of musculature, something's going to take a beating
Yeah, any unaltered mice are going to take a beating for sure.
One meaning of the word reason is "explanation". We can explain why many genetic traits have been beneficial and helped a species to survive and propagate. He didn't say anything about "due to reason", he said "there must be a reason".
which is totally what she said
"reason" wasn't the problematic term, "designed" was, as in "... the body's designed to ...".
It is not designed to do anything, because it isn't designed in the first place.
However, even the reason part is crap. "There must be a reason, a LONG TERM REASON" is just plain wrong.
Evolution makes no claims of optimal outcomes in the first place.
Maybe said mutation just never happened in the wild? Maybe the disadvantages it also produced are no longer disadvantages due to environmental changes or other genome changes? Maybe it doesn't actually give an advantage to survival or reproduction? Maybe is requires more energy input which is bad in the short term? Maybe there's one of a million other short term disadvantages that don't apply in a lab setting.
Assuming it must be bad is the antithesis of evolution - a theory in which the core concept is that such a change might be beneficial.
Natural selection results in 'good enough' genetics. There isn't any reason why people couldn't have eyesight as good as predatory birds (though some diet changes would be needed), or hearing as good as bats, or olfactory senses as good as canines, etc. but the conditions under which we evolved did not include pressures that selected for senses beyond our current state. Our sense were not maximized, simply good enough for most to survive, and that is natural selection's ultimate standard.
Speciation is not about some 'ultimate lifeform' so much as it is about lifeforms that are best adapted to their niche and environment. Predatory birds need top eyesight to catch quick small prey on the ground. We don't need it because our prey was usually bigger, or stationary (being omnivores). By the same token mice might just not have needed more strength to survive. Furthermore, and more importantly, if environmental pressures were such that only stronger mice were surviving, you could damn near bet money that these sorts of genetic changes would occur naturally. In a model of punctuated equilibrium, you'll find that changes usually occur when they have to, not simply because they are 'objectively better' in some abstract sense that doesn't significantly impact survival rate in a given environmental condition.
I support the Slashcott and will not be reading or commenting from 2/10/14 to 2/17/14. Beta is steaming pile of dog shit
Yep, though it's easy to let words like design and creature slip into this kind of thing even if you're not religious. What you're saying is repeated so often that I just would assume he already knows it, thougn I may be wrong of course. It's okay to point out common mistakes, but it's just as bad if you repeat the "truth" without thinking. It's groupthink ast its worst.
Reason was a valid word in context, taken to mean "explanation". Not an explanation by some anthropomorphic incarnation of evolution, but by logical being examining environment, behavior, genome, etc. Replace "maybe" with "because" in your second paragraph and you have a whole load of reasons. The reason for the mutation is an imperfect copying process, and the reason the mutation sticks or not goes along the lines of what you were saying.
which is totally what she said
The same thing we do every night: Use your super-strength and my wits to take over the world!
How did this get an insightful mod? Clearly flame bait. The commenter didn't put any emphasis on the word designed.
They were just pointing out, regardless of whether you believe in evolution or creationism, that there is likely some purpose served by the presence of a limiting hormone. Thus, by eliminating that trait, you can expect there might potentially be side effects. Of course it might be some evolutionary artifact that is no longer necessary in today's environment, but I wouldn't place bets on that.
It's like some layman who doesn't understand the purpose of a firewall going and disabling it and saying "Hey look how much faster our internet is now that this stupid firewall isn't having to inspect packets".
This is a gift horse we absolutely need to look in the mouth.
IANAB, but...
NCoR1 (nuclear receptor corepressor number 1) is coregulatory protein which (according to this paper) apparently inhibits MEF2 (myocite enhancer factor number 2) and PPAR (peroxisome proliferator-activated receptor) and ERRs (estrogen related receptors). MCoR1 is encoded by the NCOR1 gene. Since it is a co-regulator, blocking the expression of this gene will allow for more MEF2, PPAR, and ERRs activity causing more muscle generation and more mitochondrial activity (according to this paper anyhow). There are four MEF2 variants in humans which all seem to do slightly different things. Not sure how all these things work with NCoR1. PPAR and ERRs on the other hand deals with mitochondrial activity. Increase mitochondrial efficiency might mean more efficient conversion of sugar into energy..
On the other hand, Myostatin is a growth factor (TGF8) that generally inhibits muscle development. Myostain is encoded by the MSTN gene (in humans). Blocking this growth factor seems to increase muscle development by increasing muscle fiber size. There seems to be some indication that myostatin somehow just keeps muscle stem cells from differentiating into muscle cells (by promoting the formation of MyoD) and that if you knock Myostatin out, then those muscle stem cells just become muscle cells. Other indications are that myostatin inhibition also inhibits MEF2C (one of the 4 human MEF2 variants). Also, in some studies, inhibiting Myostatin increases the number of fast glycolytic (type IIB or so called fast-twitch) fiber which develop. However, myostatin seems to do the opposite for tendons, so where you are stronger, your tendons might get more brittle.
Not sure how the former is different from the latter, but if it can promote more type I or type IIA muscle rather than type IIB and if there is an increase in mitochondrial genesis (allowing more energy/power), that would be a difference.
There are tradeoffs involved here. There's only so much surface area in an eyeball to hold photosensors, and only so many nerve paths between the eye and the brain. Human vision is a compromise: we've got strong color vision, moderate low-resolution peripheral vision, moderate high-resolution central vision, and a balance between day (cone) and night (rod) photosensors. Birds of prey tend to devote almost all their vision to high-resolution central vision, at the cost of peripheral vision (it's easier to sneak up on them), color vision (they can't tell a ripe apple from an unripe one), vision during their "off" lighting conditions (a day hunter is almost blind at night, and vice-versa), or all of the above. Similar tradeoffs exist with smell, sound, and any other sensory system: there's no "best" option, just the one that gives a creature the tools it needs to survive.
"They redundantly repeated themselves over and over again incessantly without end ad infinitum" -- ibid.