Ok so prove its not a meteor. Haven't seen very good science done here =/
The rock was found on Earth, where there are many Earth rocks and few rocks of recent space origin. Given this context, the rock in question is mostly likely an Earth rock. This is not an exceptional claim. The exceptional claim is that the rock is a meteor, a claim for which the researcher has shown no evidence
Just a bunch of curmudgeony professorial types demanding that Chandra Wickramasinghe is a heretic. Just because Mr Wickramasinghe's theory postulates its evidence for fossilized life in a meteor doesn't mean it must be tossed out. Add it to your body of "things to investigate more fully".
His theory isn't being tossed out because it is 'heretical'. It is being tossed out because he has shown absolutely no evidence for it. I'd wager that eventually, some real evidence will be found which supports the panspermia idea... but even then it wouldn't support his claims.
Why would you assume that life is unlikely on the time- and size-scales of planets, just because we haven't yet seen it in very small lab experiments over very short periods of time? The longest running experiment to examine abiogenesis has been going for 151 years in about a liter of liquid. The lessons learned from this do not apply to whole planets over billions of years.
Why would you assume that life only happened once here on Earth? Once there was an existing bio-system, any newly formed nascent life would be less well adapted than previously formed life... and would have quickly been consumed.
Why are all Y-chromosomes derived from one Y-chromosome in the past? Just because everything else died out doesn't mean that there was only one Y-chromosome around.
Arguing that life didn't start here, but instead started somewhere else... simply avoids the issue of how life started. Panspermia advocates have routinely claimed that "DNA from space" gave key adaptations to earth life forms. Instead of the hypothetical new enzyme to digest an odd sugar, they claim such key adaptations as wings and eyes. This is nonsense.
There are plenty of ways in which life could spread from other places/stars. Even at incredibly low odds of surviving the transit from another star system, one origination of life in an otherwise sterile galaxy would quickly result in that life system being found everywhere it could survive... but there is plenty of evidence in our biology that the life system here was formed here. There is plenty of evidence suggesting that the origination of life is, while not trivial, likely to be commonplace in our galaxy. The life that is floating around in space (under the Panspermia model) very likely would get eaten by whatever native life it encounters, because that native life is in better shape for not being mostly dead due to the the long travels. If you sterilized a world with a directed Gamma-Ray-Burst, then that space life might possibly, maybe, have a chance... except that native life will have survived deep under ground and would reclaim the surface in large numbers before the rare space microbe came by.
I bet they did mean security from people. Plenty of anti-GMO folks out there who would have stolen (or just killed) the animal if they were given the chance. No, Dolly was not an example of GMO. Yes, people are that stupid.
The normal shape of a skull can be worked out easily from looking at lots of other people... the scanning of the patient allow the replacement piece to fit precisely with what remains of the original skull.
I hope that by "battery of mechanical and chemical tests", they meant "showed it to a geologist for five minutes". There are a number of minerals which can mimic calcite to the untrained eye, but they're easy for the specialist to distinguish.
That is one of the things they're testing. They see an initial growth defect upon adding the new amino acid. Basically, every place the altered codon is found the resulting protein acts somewhat weird. Biology is flexible and the cells keep going anyway. After a short while, the cells get over the issue one way or another and there is no remaining growth defect apparent.
[A different experimental group...] If you have an ongoing culture and take isolates at incremental time points, the isolates show interesting behavior when compared. Each isolate will outcompete the isolate just prior when in a common culture, as expected. If you compare each isolate to the second back, most (but not all) will win. If you compare each culture to earlier isolates, it is essentially random which one will win. The expectation was that each isolate would outcompete all prior isolates...
The modified cells will lose to normal ones after the initial change... but once they have had time to get over the shock, it then becomes anyone's guess which way any particular competition experiment will go.
I think the group modifying amino acids is looking to convert them all to types not found in nature... resulting in E. coli with no natural amino acids. At that point, things start to get real interesting. Lots of aspects of our biology are tuned in some way to deal with the existing distribution of amino acids, so these highly modified cells will have lots of changes to lots of systems. Evolution is a really powerful thing. Once you start feeding the culture with less and less of the new amino acids, the cells will figure out how to synthesize them and do so efficiently. Some metabolic circuits will be tweaked, others will be scrapped and scrambled whole-sale.
They've only found a position until the preliminary exam process, sometime in year #2. They have to pass the exams in order to have the remaining time they seem to be thinking they have.
As my handle suggests, I am a research biologist. Mostly, that just means I like to think about this sort of topic. Don't take it as me attempting to shut you or others down.
Your logic is more or less on the ball... DNA isn't made of amino acids. There are plenty of other nitrogenous bases which could have been used in DNA without any other complications. The paired bases do have to match up in a consistent way. Various forms of synthetic DNA has been made with alternate bases and it seems to behave like DNA in a physical sense.
I too prefer to think that the bases our DNA use has do do with which ones were most readily available, or which were most available in the little puddle where the biosystem started. Those basic organisms which started later or used things 'almost as good' got eaten in the endgame.
Similar logic comes in to play with the amino acids which we use to make proteins. There are many alternatives, several of which have been experimentally introduced into living biosystems. (There are E.coli which now use amino acids not found in any natural biological system; labs at University of Texas-Austin study this topic.) With amino acids, there is even more room for random chance in the initial choise of basic modules. Once that first living system started, it probably ate every other nascent living system. There is good reason to believe that amino acids will be used to form proteins and that a certain diversity of amino acids is needed, covering several basic chemistries, but that the specific amino acids isn't so important. (The E.coli types with chemically novel amino acids grow just fine.)
Though there are some that think we should never disturb the pristine natural environment of other planets... I think the primary concern is that if we're looking for living things on other planets, then it would be better not to contaminate the sites we're studying with random biocrap we brought with us.
90% ethanol leads to bacterial spores precipitating out of solution, which is why clinical labs use 70% ethanol to sterilize surfaces. The lower dosage leads to faster overall kill rates because the spores stay in solution where the ethanol can disrupt their processes.
If we could examine its DNA with any of our advanced tools, we will know it came from earth before we get around to doing any sequencing.
Though there are good reasons that DNA might be used in other biogenesis events, there is no particular reason that the bases our DNA uses would also be used.
The treaty and such refer to states, but since in our current reality, state power is what secures private property rights... the two are somewhat linked.
Proponents of ID try to use it to explain where current life came from, while ignoring the initiation of life. Since they don't believe in evolution, it makes sense to them to focus on all the myriad ways life is now... instead of the simple one way life started.
Evolution explains where current life came from, but does not explain where/how the first biological replicator formed.
Which is to say, the "so-called failing" of ID to which you refer is not the reason that anyone takes issue with ID.
People use sheep to train sheepdogs, since the sheep know how to be sheep already. Why not use dogs to train cows, as the dogs are relatively easy to potty train already.
Folks have been working to produce inbred lines of pigmy marmoset for use as an improved model for drug testing. It has a 2-3 year life cycle, making it much more useful than typical primate (rhesus monkey, chimpanzee, etc) studies for early stage work like mice are used for. Unfortunately, there's still a lot of work before people will be using them instead of mice.
You have the right to change the contract, they have to then approve it. The original statement was the claim that only HQ had the right to change it. These are different scenarios.
You justify an assumption with assumption. The core promoter sequences are so degenerate that they can be found pretty much anywhere. This has lead to misannotation of long genes as multiple single genes. There are a number other causes of annotation errors.
Annotation Error in Public Databases: Misannotation of Molecular Function in Enzyme Superfamilies
Alexandra M. Schnoes, Shoshana D. Brown, Igor Dodevski, Patricia C. Babbitt
Misannotations of rRNA can now generate 90% false positive protein matches in metatranscriptomic studies.
Tripp HJ, Hewson I, Boyarsky S, Stuart JM, Zehr JP.
There are also numerous examples of manually curated entries that are wrong because people studied non-existent proteins as a result of cloning artifacts or ignoring nonsense mediated decay. Here is one example where a transcripts containing unspliced introns that are eliminated by NMD have been studied and ascribed a function Zhu J, Chen X. MCG10, a novel p53 target gene that encodes a KH domain RNA-binding protein, is capable of inducing apoptosis and cell cycle arrest in G(2)-M. Mol Cell Biol. 2000 Aug;20(15):5602-18. (accessions AF257770, AF257771)
Those long single genes which are sometimes miss-annotated as a series of smaller genes... are sometimes transcribed as a long single gene and sometimes as a series of smaller genes. You've primarily pointed out that biology is hard and that most published papers are full of crap.
Your pretty good idea is applicable to about 60% of the long reading frames and even less applicable to short ORFs: Ingolia NT, Lareau LF, Weissman JS. Ribosome profiling of mouse embryonic stem cells reveals the complexity and dynamics of mammalian proteomes. Cell. 2011 Nov 11;147(4):789-802.. Mind you this does not include processes like RNA editing, that can further complicate how we predict protein sequence based on gene sequence.
This counter-argument doesn't counter my argument.
I wasn't commenting on ploidity. I had in mind things like trans-splicing, where you assemble mature RNA from transcripts that belong to different genes sometimes located on different chromosomes, or the way protozoan genomes are rearranged prior to expression in the macronucleus.
I wasn't commenting on ploidy either. Protozoans do things in all sorts of ways, most of which we have no idea about... and don't care about for the most part. The knowledge we have about the systems we have applies best to the systems we have studied.
See the MCG10 example above. Even for well studied proteins like p53 (there are over 65,000 publication out there on p53) we keep finding new functions (p53 controlling energy metabolism for example).
You're referring to the network of downstream effects which are influenced by p53. That is a whole order or few of magnitude of difficulty beyond identifying protein function.
Yet, sequence homology is in the base of all algorithms for predicting protein function. I know it is the best tool we have (I use it on daily basis), but still this limits its applicability to generating a testable hypothesis. Which bring is back to my point that we have to experimentally validate all these computational predictions.
...which isn't a point I ever disagreed with. We can most easily predict functions which are the result of sequences we have seen before... but we don't assume that similar sequences will result in similar functions.
Again, you are supporting one assumption with another. Here are couple of examples that fly in the face of it: VPS39/Vam6/TLP is involved in lysosome fusion, but it also regulates TGF-beta signaling. Disruption of any of these functions is lethal for the organism. So which one is the primary?; FAM48A in the nucleus is a part of chromatin remodeling complex that controls transcription. In the cytopla
The ribosome is a complex of protein and ribosomal RNA (rRNA). The catalytic subunit of the ribosome, which adds new amino acids to the nascent protein, is the rRNA. A single protein can be folded an infinite number of ways, but only a small subset of that possibility is stable. Proteins which have failed to fold 'properly' will be bound by 'heat shock proteins' (HSPs) which assist the new protein in folding. These complexes provide some buffering against the problems of incorrectly manufactured or mutant proteins. If the protein can't fold 'correctly' even with this help, it will be degraded by a complex called a 'proteaseome'.
Parkinson's disease is characterized by the death of seratonin-producing neurons in the brain, which can be caused by the buildup of toxic protein precipitates that the proteasomes cannot degrade (but can be also be caused by alternate mechanisms). Creutzfeldt-Jacob's disease occurs when prion proteins refold into a super-stable configuration. This super-stable configuration induces other prion proteins to also fold into the super-stable configuration, resulting in large amounts of the protein folding 'correctly' as far as the proteasome is concerned, but 'incorrectly' as far as neurobiology is concerned. These proteins also form into large protein precipitates which interfere with cell function. The presence of large protein precipitates is a characteristic of many neurodegenerative diseases, though the proteins which form the precipitates differ in each case.
It is definitely helpful to understand the folding, as it provides lots of information which can be useful in making predictions about what a protein will do. It is not needed, however, to understand protein folding completely in order to make useful predictions about proteins from sequence. We've known for a while how to robustly predict small structural motifs called alpha-helices and beta-pleated-sheets. We can recognize certain patterns of helices and sheets as similar to the structures of proteins we've already solved. We can also infer that a protein functions within a membrane if it has enough helices of a certain length with a high density of hydrophobic amino acids along its length. The more we learn about how proteins fold, the better our predictions will become.
There are many proteins which include a 'random coil' domain, which is generally thought to be an unfolded/unstructured sequence... it turns out these sequences are often critical to the protein in its recognition of diverse binding partners, using subtle features of electrostatic binding and thermodynamics to 'correctly' recognize other proteins for interactions. This category of functions is currently being studied mostly by one lab (to my knowledge), in large part because they're hard to study and researchers tend to be drawn to things they know how to approach.
Slashdot Mirror
Ok so prove its not a meteor. Haven't seen very good science done here =/
The rock was found on Earth, where there are many Earth rocks and few rocks of recent space origin. Given this context, the rock in question is mostly likely an Earth rock. This is not an exceptional claim. The exceptional claim is that the rock is a meteor, a claim for which the researcher has shown no evidence
Just a bunch of curmudgeony professorial types demanding that Chandra Wickramasinghe is a heretic. Just because Mr Wickramasinghe's theory postulates its evidence for fossilized life in a meteor doesn't mean it must be tossed out. Add it to your body of "things to investigate more fully".
His theory isn't being tossed out because it is 'heretical'. It is being tossed out because he has shown absolutely no evidence for it. I'd wager that eventually, some real evidence will be found which supports the panspermia idea... but even then it wouldn't support his claims.
Why would you assume that life is unlikely on the time- and size-scales of planets, just because we haven't yet seen it in very small lab experiments over very short periods of time? The longest running experiment to examine abiogenesis has been going for 151 years in about a liter of liquid. The lessons learned from this do not apply to whole planets over billions of years.
Why would you assume that life only happened once here on Earth? Once there was an existing bio-system, any newly formed nascent life would be less well adapted than previously formed life... and would have quickly been consumed.
Why are all Y-chromosomes derived from one Y-chromosome in the past? Just because everything else died out doesn't mean that there was only one Y-chromosome around.
Not exactly.
Arguing that life didn't start here, but instead started somewhere else... simply avoids the issue of how life started. Panspermia advocates have routinely claimed that "DNA from space" gave key adaptations to earth life forms. Instead of the hypothetical new enzyme to digest an odd sugar, they claim such key adaptations as wings and eyes. This is nonsense.
There are plenty of ways in which life could spread from other places/stars. Even at incredibly low odds of surviving the transit from another star system, one origination of life in an otherwise sterile galaxy would quickly result in that life system being found everywhere it could survive... but there is plenty of evidence in our biology that the life system here was formed here. There is plenty of evidence suggesting that the origination of life is, while not trivial, likely to be commonplace in our galaxy. The life that is floating around in space (under the Panspermia model) very likely would get eaten by whatever native life it encounters, because that native life is in better shape for not being mostly dead due to the the long travels. If you sterilized a world with a directed Gamma-Ray-Burst, then that space life might possibly, maybe, have a chance... except that native life will have survived deep under ground and would reclaim the surface in large numbers before the rare space microbe came by.
I bet they did mean security from people. Plenty of anti-GMO folks out there who would have stolen (or just killed) the animal if they were given the chance. No, Dolly was not an example of GMO. Yes, people are that stupid.
That is the only picture which is getting passed around... but that replacement part is nowhere near 75% of the skull.
Yes they can. It has already been done. http://www.geek.com/articles/geek-cetera/elderly-woman-has-lower-jaw-replaced-with-3d-printed-titanium-implant-2012026/
The normal shape of a skull can be worked out easily from looking at lots of other people... the scanning of the patient allow the replacement piece to fit precisely with what remains of the original skull.
And you've now come to the fundamental understanding of biology which evolutionary theory gives us. ;-)
I hope that by "battery of mechanical and chemical tests", they meant "showed it to a geologist for five minutes". There are a number of minerals which can mimic calcite to the untrained eye, but they're easy for the specialist to distinguish.
That is one of the things they're testing. They see an initial growth defect upon adding the new amino acid. Basically, every place the altered codon is found the resulting protein acts somewhat weird. Biology is flexible and the cells keep going anyway. After a short while, the cells get over the issue one way or another and there is no remaining growth defect apparent.
[A different experimental group...] If you have an ongoing culture and take isolates at incremental time points, the isolates show interesting behavior when compared. Each isolate will outcompete the isolate just prior when in a common culture, as expected. If you compare each isolate to the second back, most (but not all) will win. If you compare each culture to earlier isolates, it is essentially random which one will win. The expectation was that each isolate would outcompete all prior isolates...
The modified cells will lose to normal ones after the initial change... but once they have had time to get over the shock, it then becomes anyone's guess which way any particular competition experiment will go.
I think the group modifying amino acids is looking to convert them all to types not found in nature... resulting in E. coli with no natural amino acids. At that point, things start to get real interesting. Lots of aspects of our biology are tuned in some way to deal with the existing distribution of amino acids, so these highly modified cells will have lots of changes to lots of systems. Evolution is a really powerful thing. Once you start feeding the culture with less and less of the new amino acids, the cells will figure out how to synthesize them and do so efficiently. Some metabolic circuits will be tweaked, others will be scrapped and scrambled whole-sale.
They've only found a position until the preliminary exam process, sometime in year #2. They have to pass the exams in order to have the remaining time they seem to be thinking they have.
perhaps not strangely, it is much the same in biology programs.
As my handle suggests, I am a research biologist. Mostly, that just means I like to think about this sort of topic. Don't take it as me attempting to shut you or others down.
Your logic is more or less on the ball... DNA isn't made of amino acids. There are plenty of other nitrogenous bases which could have been used in DNA without any other complications. The paired bases do have to match up in a consistent way. Various forms of synthetic DNA has been made with alternate bases and it seems to behave like DNA in a physical sense.
I too prefer to think that the bases our DNA use has do do with which ones were most readily available, or which were most available in the little puddle where the biosystem started. Those basic organisms which started later or used things 'almost as good' got eaten in the endgame.
Similar logic comes in to play with the amino acids which we use to make proteins. There are many alternatives, several of which have been experimentally introduced into living biosystems. (There are E.coli which now use amino acids not found in any natural biological system; labs at University of Texas-Austin study this topic.) With amino acids, there is even more room for random chance in the initial choise of basic modules. Once that first living system started, it probably ate every other nascent living system. There is good reason to believe that amino acids will be used to form proteins and that a certain diversity of amino acids is needed, covering several basic chemistries, but that the specific amino acids isn't so important. (The E.coli types with chemically novel amino acids grow just fine.)
Though there are some that think we should never disturb the pristine natural environment of other planets... I think the primary concern is that if we're looking for living things on other planets, then it would be better not to contaminate the sites we're studying with random biocrap we brought with us.
90% ethanol leads to bacterial spores precipitating out of solution, which is why clinical labs use 70% ethanol to sterilize surfaces. The lower dosage leads to faster overall kill rates because the spores stay in solution where the ethanol can disrupt their processes.
If we could examine its DNA with any of our advanced tools, we will know it came from earth before we get around to doing any sequencing.
Though there are good reasons that DNA might be used in other biogenesis events, there is no particular reason that the bases our DNA uses would also be used.
The treaty and such refer to states, but since in our current reality, state power is what secures private property rights... the two are somewhat linked.
Proponents of ID try to use it to explain where current life came from, while ignoring the initiation of life. Since they don't believe in evolution, it makes sense to them to focus on all the myriad ways life is now... instead of the simple one way life started.
Evolution explains where current life came from, but does not explain where/how the first biological replicator formed.
Which is to say, the "so-called failing" of ID to which you refer is not the reason that anyone takes issue with ID.
People use sheep to train sheepdogs, since the sheep know how to be sheep already. Why not use dogs to train cows, as the dogs are relatively easy to potty train already.
Folks have been working to produce inbred lines of pigmy marmoset for use as an improved model for drug testing. It has a 2-3 year life cycle, making it much more useful than typical primate (rhesus monkey, chimpanzee, etc) studies for early stage work like mice are used for. Unfortunately, there's still a lot of work before people will be using them instead of mice.
You have the right to change the contract, they have to then approve it. The original statement was the claim that only HQ had the right to change it. These are different scenarios.
You justify an assumption with assumption. The core promoter sequences are so degenerate that they can be found pretty much anywhere. This has lead to misannotation of long genes as multiple single genes. There are a number other causes of annotation errors.
There are also numerous examples of manually curated entries that are wrong because people studied non-existent proteins as a result of cloning artifacts or ignoring nonsense mediated decay. Here is one example where a transcripts containing unspliced introns that are eliminated by NMD have been studied and ascribed a function Zhu J, Chen X. MCG10, a novel p53 target gene that encodes a KH domain RNA-binding protein, is capable of inducing apoptosis and cell cycle arrest in G(2)-M. Mol Cell Biol. 2000 Aug;20(15):5602-18. (accessions AF257770, AF257771)
Those long single genes which are sometimes miss-annotated as a series of smaller genes... are sometimes transcribed as a long single gene and sometimes as a series of smaller genes. You've primarily pointed out that biology is hard and that most published papers are full of crap.
Your pretty good idea is applicable to about 60% of the long reading frames and even less applicable to short ORFs: Ingolia NT, Lareau LF, Weissman JS. Ribosome profiling of mouse embryonic stem cells reveals the complexity and dynamics of mammalian proteomes. Cell. 2011 Nov 11;147(4):789-802.. Mind you this does not include processes like RNA editing, that can further complicate how we predict protein sequence based on gene sequence.
This counter-argument doesn't counter my argument.
I wasn't commenting on ploidity. I had in mind things like trans-splicing, where you assemble mature RNA from transcripts that belong to different genes sometimes located on different chromosomes, or the way protozoan genomes are rearranged prior to expression in the macronucleus.
I wasn't commenting on ploidy either. Protozoans do things in all sorts of ways, most of which we have no idea about... and don't care about for the most part. The knowledge we have about the systems we have applies best to the systems we have studied.
See the MCG10 example above. Even for well studied proteins like p53 (there are over 65,000 publication out there on p53) we keep finding new functions (p53 controlling energy metabolism for example).
You're referring to the network of downstream effects which are influenced by p53. That is a whole order or few of magnitude of difficulty beyond identifying protein function.
Yet, sequence homology is in the base of all algorithms for predicting protein function. I know it is the best tool we have (I use it on daily basis), but still this limits its applicability to generating a testable hypothesis. Which bring is back to my point that we have to experimentally validate all these computational predictions.
...which isn't a point I ever disagreed with. We can most easily predict functions which are the result of sequences we have seen before... but we don't assume that similar sequences will result in similar functions.
Again, you are supporting one assumption with another. Here are couple of examples that fly in the face of it: VPS39/Vam6/TLP is involved in lysosome fusion, but it also regulates TGF-beta signaling. Disruption of any of these functions is lethal for the organism. So which one is the primary?; FAM48A in the nucleus is a part of chromatin remodeling complex that controls transcription. In the cytopla
The ribosome is a complex of protein and ribosomal RNA (rRNA). The catalytic subunit of the ribosome, which adds new amino acids to the nascent protein, is the rRNA. A single protein can be folded an infinite number of ways, but only a small subset of that possibility is stable. Proteins which have failed to fold 'properly' will be bound by 'heat shock proteins' (HSPs) which assist the new protein in folding. These complexes provide some buffering against the problems of incorrectly manufactured or mutant proteins. If the protein can't fold 'correctly' even with this help, it will be degraded by a complex called a 'proteaseome'.
Parkinson's disease is characterized by the death of seratonin-producing neurons in the brain, which can be caused by the buildup of toxic protein precipitates that the proteasomes cannot degrade (but can be also be caused by alternate mechanisms). Creutzfeldt-Jacob's disease occurs when prion proteins refold into a super-stable configuration. This super-stable configuration induces other prion proteins to also fold into the super-stable configuration, resulting in large amounts of the protein folding 'correctly' as far as the proteasome is concerned, but 'incorrectly' as far as neurobiology is concerned. These proteins also form into large protein precipitates which interfere with cell function. The presence of large protein precipitates is a characteristic of many neurodegenerative diseases, though the proteins which form the precipitates differ in each case.
It is definitely helpful to understand the folding, as it provides lots of information which can be useful in making predictions about what a protein will do. It is not needed, however, to understand protein folding completely in order to make useful predictions about proteins from sequence. We've known for a while how to robustly predict small structural motifs called alpha-helices and beta-pleated-sheets. We can recognize certain patterns of helices and sheets as similar to the structures of proteins we've already solved. We can also infer that a protein functions within a membrane if it has enough helices of a certain length with a high density of hydrophobic amino acids along its length. The more we learn about how proteins fold, the better our predictions will become.
There are many proteins which include a 'random coil' domain, which is generally thought to be an unfolded/unstructured sequence... it turns out these sequences are often critical to the protein in its recognition of diverse binding partners, using subtle features of electrostatic binding and thermodynamics to 'correctly' recognize other proteins for interactions. This category of functions is currently being studied mostly by one lab (to my knowledge), in large part because they're hard to study and researchers tend to be drawn to things they know how to approach.
If a contract is not legally able to take away your rights, then it can't take away your rights even if it claims to do so.
HQ can claim whatever they want. It has little relevance to your legal rights.