Both the creationist agenda and the "pro-science" eugenics you describe stem from the same root problem. Neither religion nor science is in itself an inherently bad thing--in fact they're both arguably inherently good things. Religion helps people find peace in their lives and science helps us attempt to objectively learn how the world works. The problem occurs when people use these self-contained ideas to justify the imposition of their own agenda on others.
These days as I see how religion is dividing our nation and the world along seemingly arbitrary lines and in some cases denying people what should be standard human rights, it often feels as if the bad aspects of religion might outweigh the good. And as a scientist, I was initially up-in-arms about your comments equating being "pro-science" with promoting eugenics. But it serves as a good reminder that no one is immune, that any idea can be tainted and perverted by people who want to use the power behind that idea to rally people to their own cause. And so at the end of the day, both science and religion must be judged on their own proper merits, and we must learn to draw much sharper distinctions between what being "pro-religion or pro-science" should be (ie.someone supporting the existence of these schools of thought--promoting freedom of religion and funding of scientific research) and crassly using their ideas to achieve his or her own ends.
That's actually a fairly well-studied question. In lower organisms like worms and flies, the nerve map is totally hard-wired. Every neuron is born in a specific location and extends its axons along specific pathways to pre-determined targets. In mammals it's a bit more complicated. There are millions of neurons and billions of precise connections between them. Looked at from a pragmatic point of view, there simply aren't enough genes in the genome to encode all of that specificity directly. So the body generally uses an approach to making its proper connections that you can divide into a few basic phases: getting there, finding your partners, and fighting for survival.
"Getting there" is all about pathfinding. Instead of individual neurons, groups of neurons have molecular identities in that they express cell surface molecules that probe the environment and react to it by either growing towards attractive molecules or away from repulsive molecules. Different groups of neurons can respond in opposite ways (or not respond at all) to the same exact signal, allowing combinatorial groups of signals to be used to guide the groups of neurons in their intricate paths through the brain and body.
The specificity of the "finding your partners" phase varies depending on the system you're looking at. For some groups of neurons it's almost a free-for-all within the group, while other groups of neurons follow very specific patterns. In the visual system, for instance, the neurons in the eye project into the brain in what's called a topographic map. That is, neurons that are near to each other in the eye form connections that are near each other in the brain, allowing the relative orientation of the signals from the eye to be directly mapped onto the correct region of the brain. This is done with 2-dimensional gradients of cues in the targets and of the receptors for those cues in the neurons that allow growing axons to hone in on just the level of the signal that is correct for them and find their correct general area. (See Ephrin and Eph signaling in the eye for more info.)
Once connections have been established, the "fight for survival" begins. Since it's not guaranteed that the connections that the neurons form will be the correct ones, the body has to have some way of keeping only the connections that are correct and eliminating unwanted ones. It often does this by strengthening connections that are properly formed and able to stimulate target neurons at the proper times and weakening those that don't work well by a process called Hebbian competition. This allows the map to be fine-tuned once the general arrangement has been worked out. There is usually a "critical period" during which the map can easily undergo dynamic rearrangement in response to experience. After this time, however, the ability of the brain to rewire in response to experience decreases drastically and the map is fairly fixed. For example, if someone loses function in one eye as a young child, their other eye will take over much more than half of the visual system space in the brain, while this does not happen to anywhere near the same extent if it happens later in life. This is also the reason that children with strabismus (unaligned eyes) have to be treated very early in life in order to ensure that their visual maps from each eye are aligned. If they aren't treated within the critical period, their vision can never be fixed.
Anyway, didn't mean to write such a long post, but there it is in case anyone's interested. I just wanted to add that the article title and summary are fairly misleading. I haven't read the article in full, but even from the abstract it's clear that the scientists did not use any new techniques to "restore walking" in these mice. It's been known for a while that mice have a high incidence and rate of spontaneous recovery after spinal cord injury in the lab. That is, they are often able to regain function of their hindlimbs despite the fact that the injured axons themselves do not grow back
If this was in your textbooks, it was because of their 1998 paper and the subsequent work that has shown that the mechanisms are involved are conserved all the way to mammals. I do know what you mean about the theory that everything started with RNA, which can both act as genetic material and have important enzymatic and structural properties. However, RNAi is very different from the big RNA molecules that act as enzymes (ribosymes) and I'm not really sure what you mean by RNA proteins.
RNAi is a natural mechanism that is used in all cells to regulate gene expression. It turns out that in addition to the mRNAs (messengerRNA) that are translated into protein, the rRNAs (ribosomal RNA) that provide the scaffold for the translation, the tRNAs (transferRNA--the big cross in the article picture) that match the RNA with the amino acid (protein building block) it codes for, and those ribosymes, all of which we've known about for some time, we also have very small RNAs called microRNAs (miRNA). These are transcribed but not turned into protein. Once transcribed, these pieces join up with the proteins that catalyze RNAi in the RISC complex. Normal mRNAs that have sequences that match up with the microRNAs become bound in the complex and may either be prevented from being turned into protein or degraded by the complex. It turns out that most natural microRNAs, due to their small size, can match up with sequences in a large number of mRNAs (on the order of 100-200), and do actually appear to regulate how much protein is made by a large number of different RNAs. It's currently thought that this may be a mechanism by which cells can quickly stop the generation of protein for an entire pathway or process at once by making just one regulatory microRNA.
Although this mechanism has become important for normal regulation in the cell, it appears to have been originally developed to combat foreign RNA that may have been inserted into the cell by viruses. Thus, in addition to the silencing RISC complex, there is also an enzyme called Dicer that chops up any double-stranded RNA it finds lying around into the bite-sized pieces that fit in the RISC complex. mRNAs that match those pieces are then silenced by the mechanism mentioned above, and poof! You have essentially gotten rid of the protein for whatever gene you inserted the double-stranded RNA of.
So this discovery was novel on two levels, both incredibly important. First, uncovered another piece in the puzzle of how our cells are regulated with such incredible speed and specificity. Second, the sudden ability to quickly and specifically get rid of any protein of interest revolutionized molecular and cellular biology. Before, to know what a gene was doing in a particular cell, it took months to years of work to generate an animal or cell line that lacked that gene. Thus, most of our knowledge of the required functions of genes came from either genetic screens in organisms such as yeast, worms, and flies or targeted knock-outs of genes you already thought were pretty important. These are still very important techniques, but now that we have RNAi, we can fairly easily determine the critical functions of almost any gene we want, even in mammalian systems. The technique has been an incredible tool for molecular biologists, and has aided in studying not only cancer (as one poster mentioned), but probably any other molecular/cellular process you can think of as well. I always figured he would win the Nobel prize for it eventually, just not this soon (8 years!). However, given both how much it has changed the field and how many times and ways it has been validated, I can see why they decided to go ahead and give it to them now.
I just found out that Dell is essentially doing this with some of its bundled software. My sister's copy of Nero claims to only work on the computer with which it was originally bundled. I assume it would be pretty easy to work around, but it's still annoying that they do it.
Not a dumb question at all. The images you see of the stringy stuff are actually time-lapse images (ie. still images taken once every few seconds/minutes/hours depending on your application) of the flouresence given off by GFP, or Green Flourescent Protein, attached to Alpha tubulin.
GFP is a natural protein that was originally found in the genome some sort of deep-sea fish (I forget which), but has been used by biologists for myriad purposes since then. Bascially, it's a protein, but because of the specifics of its sequence and configuration, it emits energy (flourescence) when hit with a laser at a particular wavelength. GFP was revolutionary because, while chemists can and have designed many compounds with similar properties, they are all synthetic and have to be physically attached to whatever protein you want to look at. The flourescent properties of GFP, on the other hand, are in the form of a protein, which can be added to any cell by just adding in the DNA that codes for GFP.
In addition, GFP isn't very large, so you can actually make hybrid proteins that have your normal protein you want to look at and the GFP directly in sequence after it all on one piece of contiguous DNA. When it's made into a protein, you get a functional protein (although you have to test this to make sure) that has a little flourescent tag attached. So not only do the cells expressing your protein glow green, but you actually get to follow where that protein is moving in real time in the cell. People have actually taken the GFP sequence and mutated it to make flourescent proteins that are excited at other wavelengths to make YFP, CFP, RFP, etc (Yellow, Cyan, Red, etc). So if you wanted, you could make 2 or 3 proteins labeled with different colors and see what all of them were doing at the same time
The stringy stuff you see is the microtubules that attach the duplicated chromosomes along the midline and pull half of the chromosomes towards what will become one daughter cell, half to the other. The authors have taken one of the proteins that makes up these microtubules, Alpha Tubulin, and attached GFP to it in sequence. They then added that DNA to their cell lines which now express both the normal Alpha Tubulin and the GFP-Alpha Tubulin. This allows them to look at the localization of their tagged Alpha Tubulin with a normal flourescent microscope (most molecular/cell bio labs have them) without killing the cells and see what happens over time.
Slashdot Mirror
Both the creationist agenda and the "pro-science" eugenics you describe stem from the same root problem. Neither religion nor science is in itself an inherently bad thing--in fact they're both arguably inherently good things. Religion helps people find peace in their lives and science helps us attempt to objectively learn how the world works. The problem occurs when people use these self-contained ideas to justify the imposition of their own agenda on others.
These days as I see how religion is dividing our nation and the world along seemingly arbitrary lines and in some cases denying people what should be standard human rights, it often feels as if the bad aspects of religion might outweigh the good. And as a scientist, I was initially up-in-arms about your comments equating being "pro-science" with promoting eugenics. But it serves as a good reminder that no one is immune, that any idea can be tainted and perverted by people who want to use the power behind that idea to rally people to their own cause. And so at the end of the day, both science and religion must be judged on their own proper merits, and we must learn to draw much sharper distinctions between what being "pro-religion or pro-science" should be (ie.someone supporting the existence of these schools of thought--promoting freedom of religion and funding of scientific research) and crassly using their ideas to achieve his or her own ends.
That's actually a fairly well-studied question. In lower organisms like worms and flies, the nerve map is totally hard-wired. Every neuron is born in a specific location and extends its axons along specific pathways to pre-determined targets. In mammals it's a bit more complicated. There are millions of neurons and billions of precise connections between them. Looked at from a pragmatic point of view, there simply aren't enough genes in the genome to encode all of that specificity directly. So the body generally uses an approach to making its proper connections that you can divide into a few basic phases: getting there, finding your partners, and fighting for survival.
"Getting there" is all about pathfinding. Instead of individual neurons, groups of neurons have molecular identities in that they express cell surface molecules that probe the environment and react to it by either growing towards attractive molecules or away from repulsive molecules. Different groups of neurons can respond in opposite ways (or not respond at all) to the same exact signal, allowing combinatorial groups of signals to be used to guide the groups of neurons in their intricate paths through the brain and body.
The specificity of the "finding your partners" phase varies depending on the system you're looking at. For some groups of neurons it's almost a free-for-all within the group, while other groups of neurons follow very specific patterns. In the visual system, for instance, the neurons in the eye project into the brain in what's called a topographic map. That is, neurons that are near to each other in the eye form connections that are near each other in the brain, allowing the relative orientation of the signals from the eye to be directly mapped onto the correct region of the brain. This is done with 2-dimensional gradients of cues in the targets and of the receptors for those cues in the neurons that allow growing axons to hone in on just the level of the signal that is correct for them and find their correct general area. (See Ephrin and Eph signaling in the eye for more info.)
Once connections have been established, the "fight for survival" begins. Since it's not guaranteed that the connections that the neurons form will be the correct ones, the body has to have some way of keeping only the connections that are correct and eliminating unwanted ones. It often does this by strengthening connections that are properly formed and able to stimulate target neurons at the proper times and weakening those that don't work well by a process called Hebbian competition. This allows the map to be fine-tuned once the general arrangement has been worked out. There is usually a "critical period" during which the map can easily undergo dynamic rearrangement in response to experience. After this time, however, the ability of the brain to rewire in response to experience decreases drastically and the map is fairly fixed. For example, if someone loses function in one eye as a young child, their other eye will take over much more than half of the visual system space in the brain, while this does not happen to anywhere near the same extent if it happens later in life. This is also the reason that children with strabismus (unaligned eyes) have to be treated very early in life in order to ensure that their visual maps from each eye are aligned. If they aren't treated within the critical period, their vision can never be fixed.
Anyway, didn't mean to write such a long post, but there it is in case anyone's interested. I just wanted to add that the article title and summary are fairly misleading. I haven't read the article in full, but even from the abstract it's clear that the scientists did not use any new techniques to "restore walking" in these mice. It's been known for a while that mice have a high incidence and rate of spontaneous recovery after spinal cord injury in the lab. That is, they are often able to regain function of their hindlimbs despite the fact that the injured axons themselves do not grow back
RNAi is a natural mechanism that is used in all cells to regulate gene expression. It turns out that in addition to the mRNAs (messengerRNA) that are translated into protein, the rRNAs (ribosomal RNA) that provide the scaffold for the translation, the tRNAs (transferRNA--the big cross in the article picture) that match the RNA with the amino acid (protein building block) it codes for, and those ribosymes, all of which we've known about for some time, we also have very small RNAs called microRNAs (miRNA). These are transcribed but not turned into protein. Once transcribed, these pieces join up with the proteins that catalyze RNAi in the RISC complex. Normal mRNAs that have sequences that match up with the microRNAs become bound in the complex and may either be prevented from being turned into protein or degraded by the complex. It turns out that most natural microRNAs, due to their small size, can match up with sequences in a large number of mRNAs (on the order of 100-200), and do actually appear to regulate how much protein is made by a large number of different RNAs. It's currently thought that this may be a mechanism by which cells can quickly stop the generation of protein for an entire pathway or process at once by making just one regulatory microRNA.
Although this mechanism has become important for normal regulation in the cell, it appears to have been originally developed to combat foreign RNA that may have been inserted into the cell by viruses. Thus, in addition to the silencing RISC complex, there is also an enzyme called Dicer that chops up any double-stranded RNA it finds lying around into the bite-sized pieces that fit in the RISC complex. mRNAs that match those pieces are then silenced by the mechanism mentioned above, and poof! You have essentially gotten rid of the protein for whatever gene you inserted the double-stranded RNA of.
So this discovery was novel on two levels, both incredibly important. First, uncovered another piece in the puzzle of how our cells are regulated with such incredible speed and specificity. Second, the sudden ability to quickly and specifically get rid of any protein of interest revolutionized molecular and cellular biology. Before, to know what a gene was doing in a particular cell, it took months to years of work to generate an animal or cell line that lacked that gene. Thus, most of our knowledge of the required functions of genes came from either genetic screens in organisms such as yeast, worms, and flies or targeted knock-outs of genes you already thought were pretty important. These are still very important techniques, but now that we have RNAi, we can fairly easily determine the critical functions of almost any gene we want, even in mammalian systems. The technique has been an incredible tool for molecular biologists, and has aided in studying not only cancer (as one poster mentioned), but probably any other molecular/cellular process you can think of as well. I always figured he would win the Nobel prize for it eventually, just not this soon (8 years!). However, given both how much it has changed the field and how many times and ways it has been validated, I can see why they decided to go ahead and give it to them now.
I just found out that Dell is essentially doing this with some of its bundled software. My sister's copy of Nero claims to only work on the computer with which it was originally bundled. I assume it would be pretty easy to work around, but it's still annoying that they do it.
Not a dumb question at all. The images you see of the stringy stuff are actually time-lapse images (ie. still images taken once every few seconds/minutes/hours depending on your application) of the flouresence given off by GFP, or Green Flourescent Protein, attached to Alpha tubulin.
GFP is a natural protein that was originally found in the genome some sort of deep-sea fish (I forget which), but has been used by biologists for myriad purposes since then. Bascially, it's a protein, but because of the specifics of its sequence and configuration, it emits energy (flourescence) when hit with a laser at a particular wavelength. GFP was revolutionary because, while chemists can and have designed many compounds with similar properties, they are all synthetic and have to be physically attached to whatever protein you want to look at. The flourescent properties of GFP, on the other hand, are in the form of a protein, which can be added to any cell by just adding in the DNA that codes for GFP.
In addition, GFP isn't very large, so you can actually make hybrid proteins that have your normal protein you want to look at and the GFP directly in sequence after it all on one piece of contiguous DNA. When it's made into a protein, you get a functional protein (although you have to test this to make sure) that has a little flourescent tag attached. So not only do the cells expressing your protein glow green, but you actually get to follow where that protein is moving in real time in the cell. People have actually taken the GFP sequence and mutated it to make flourescent proteins that are excited at other wavelengths to make YFP, CFP, RFP, etc (Yellow, Cyan, Red, etc). So if you wanted, you could make 2 or 3 proteins labeled with different colors and see what all of them were doing at the same time
The stringy stuff you see is the microtubules that attach the duplicated chromosomes along the midline and pull half of the chromosomes towards what will become one daughter cell, half to the other. The authors have taken one of the proteins that makes up these microtubules, Alpha Tubulin, and attached GFP to it in sequence. They then added that DNA to their cell lines which now express both the normal Alpha Tubulin and the GFP-Alpha Tubulin. This allows them to look at the localization of their tagged Alpha Tubulin with a normal flourescent microscope (most molecular/cell bio labs have them) without killing the cells and see what happens over time.