Posted on 11/22/2002 9:09:10 PM PST by forsnax5
NSF awards grants to discover the relationships of 1.75 million species
One of the most profound ideas to emerge in modern science is Charles Darwin's concept that all of life, from the smallest microorganism to the largest vertebrate, is connected through genetic relatedness in a vast genealogy. This "Tree of Life" summarizes all we know about biological diversity and underpins much of modern biology, yet many of its branches remain poorly known and unresolved.
To help scientists discover what Darwin described as the tree's "everbranching and beautiful ramifications," the National Science Foundation (NSF) has awarded $17 million in "Assembling the Tree of Life" grants to researchers at more than 25 institutions. Their studies range from investigations of entire pieces of DNA to assemble the bacterial branches; to the study of the origins of land plants from algae; to understanding the most diverse group of terrestrial predators, the spiders; to the diversity of fungi and parasitic roundworms; to the relationships of birds and dinosaurs.
"Despite the enormity of the task," said Quentin Wheeler, director of NSF's division of environmental biology, which funded the awards, "now is the time to reconstruct the tree of life. The conceptual, computational and technological tools are available to rapidly resolve most, if not all, major branches of the tree of life. At the same time, progress in many research areas from genomics to evolution and development is currently encumbered by the lack of a rigorous historical framework to guide research."
Scientists estimate that the 1.75 million known species are only 10 percent of the total species on earth, and that many of those species will disappear in the decades ahead. Learning about these species and their evolutionary history is epic in its scope, spanning all the life forms of an entire planet over its several billion year history, said Wheeler.
Why is assembling the tree of life so important? The tree is a picture of historical relationships that explains all similarities and differences among plants, animals and microorganisms. Because it explains biological diversity, the Tree of Life has proven useful in many fields, such as choosing experimental systems for biological research, determining which genes are common to many kinds of organisms and which are unique, tracking the origin and spread of emerging diseases and their vectors, bio-prospecting for pharmaceutical and agrochemical products, developing data bases for genetic information, and evaluating risk factors for species conservation and ecosystem restoration.
The Assembling the Tree of Life grants provide support for large multi-investigator, multi-institutional, international teams of scientists who can combine expertise and data sources, from paleontology to morphology, developmental biology, and molecular biology, says Wheeler. The awards will also involve developing software for improved visualization and analysis of extremely large data sets, and outreach and education programs in comparative phylogenetic biology and paleontology, emphasizing new training activities, informal science education, and Internet resources and dissemination.
-NSF-
For a list of the Assembling the Tree of Life grants, see: http://www.nsf.gov/bio/pubs/awards/atol_02.htm
Not sure I understand this statement. Does it require the assumption that the speed of light has always remained a constant? There is some debate in the scientific community relative to the speed of light over time.
Yes, but the reason you don't simply compare the whole string is because not all substrings are equally important. In this case, as per the description, they chose a substring that is known to be important in the formation of functional membranes. Since, evolutionary theory suggests that critical functions are more likely to be conserved than non-critical functions, mutations are less likely to accumulate there, and so you look for correspondences in the important bits of the gene, rather than just throwing the whole thing up and pretending that all the parts are interchangeable.
As an aside, if the rate of correspondences in the important parts do not exceed the rate of correspondences in the less important parts, or if the correspondences in the important parts do not exceed what you would expect from random chance, that would be an excellent way of falsifying the hypothesis that these two share a common ancestor. Or, if they are known by other means to be related, but the correspondences don't fit that pattern, then you'll have blown a big hole in the molecular evidence for evolution itself. Just one more way that evolutionary theory is put to the test every day. But I imagine you already know this... ;)
Yes science would reject a hypothesis when it is proven wrong. However, evolutionists have stuck with their theory in spite of being proven wrong numerous times. As shown in post #807 evolutionists prefer 'hopeful monsters' than what science tells them. In fact this has been true since Darwin who constantly claimed that the future would prove him correct. Well it has not. That's why your friend admits in 1052 that "I don't actually know anyone who argues that point mutations and genetic drift are responsible for everything any more. " after having admitted that "What a shame you put it to use refuting a strict sort of Darwinism that nobody really believes any more anyway. " in post# 852. In addition to which he (and the rest of the evolutionists) while demanding that others give their theory with all i's dotted and all the t's crossed completely decline to say exactly what the theory of evolution is. They treat it like a guessing game and every time someone shows something wrong with it they say that that is not evolution. Now that's not science. Scientists do not decline to give their hypothesis, they are proud to state it. So no, evolution is not science.
So 11 amino acids in a range of 50 or so out of a total of about 250 define the "functions" of MOTA?
No. 11 out of 55 is the number of correspondences between ALL of the following: ExbB (V. cholerae), ExbB (D. radiodurans), MTH1022 (M. thermoautotrophicum), motA (A. aeolicus), motA (D. vulgaris). 23 out of the 55 are correspondences between motA in A. aeolicus and MTH1022. 22 of the 55 are correspondences between motA in D. vulgaris and MTH1022.
This sequence of 55 residues is not the sum total of motA, but it is a substring known to be important to the functioning of motA. Or, to put it another way:
Pro and Asp residues important for function and conserved in both systems are shown....The arrow indicates a Pro residue that is conserved in both systems and known to be important for function of MotA.
And those are the critical "functions" as you described. Otherwise you must count all of the things. In fact you have reduced the "functionality" of MOTA to 2 aa. This is with respect to what to count.
Not 11, because the idea was to compare MTH1022 to motA as you did. If you compare strictly those two things, there are 23 (or 22) correspondences in this substring known to contain parts critical to functionality. There are 11 correspondences only when you compare motA, MTH1022, and ExbB. There are 18 correspondences if you compare motA (D. vulgaris) directly to ExbB (V. cholerae), for example.
Yes, but it was the total protein not a part. What is trying to be established is the gradualist, stochastic change from MTH1022(or a predecessor) to MOTA. That involves the complete protein. It would be like attempting to establish the change of a 'Tale of two cities" into 'Tale of Mudville' by taking the first book and showing the erasures, additions and other changes that made the one book into the other. This would be differentiated from the plagiarizing of relevant passages. IOW there are other mechanisms capable of explaining the similarity between MOTA and MTH1022. Among these are the mentioned horizontal transfer and a common "toolkit" for solving problems.
Almost. They weren't really looking at MTH1022 - they were actually looking at the correspondences between ExdB and motA to establish a connection between those two.
IOW there are other mechanisms capable of explaining the similarity between MOTA and MTH1022. Among these are the mentioned horizontal transfer and a common "toolkit" for solving problems.
Again keeping in mind that they're looking at ExdB versus motA, and not really MTH1022, they're not hanging their hats entirely on the correspondences in making a case for common ancestry.
Other features also point to a connection between the Mot and Exb systems. MotA functions in a complex with MotB, which as noted contains the critical residue Asp32 near the cytoplasmic end of its single membrane segment. ExbB functions in a complex with ExbD, which likewise has a single membrane segment with a critical Asp residue near its cytoplasmic end (Asp25 in ExbD of E. coli; ref 59). Although ExbB has only three membrane segments in contrast to the four in MotA, the membrane segments that show sequence similarity have the same topology. The protein TonB is also present in the complex with ExbB and ExbD (59, 60) and would provide an additional membrane segment to round out the topological correspondence (Figure 9). ExbB contains a well-conserved Pro residue (Pro141 in E. coli ExbB) that is the counterpart of Pro173 of MotA. Although MotB and ExbD do not share close sequence similarity apart from the critical Asp residue, in certain positions in the membrane segment the residues most common in MotB proteins are also common in ExbD proteins. Finally, like the MotA/MotB complex the ExbB/ExbD complex contains multiple copies of each protein (61). Together, these facts make a reasonable case for an evolutionary connection between the Mot proteins of the flagellar motor and the Exb proteins of outer-membrane transport (and by extension the TolQ/TolR proteins, which are related to ExbB/ExbD but whose functions are less understood).
The question was discussed on this Free Republic thread back in 1999. You might find the comments interesting, in particular Physicist's at #58.
Also back in 1999, some Australian scientists found evidence that the Fine Structure Constant might be changing. As I recall, that was the top physics story of the year.
But these would have little to do with my approximations which use the rule that each time the universe doubled in size, the perception in time was cut in half. In cosmology, the rate of expansion reflects this exponentiation.
But seriously, if functionally equivalent bits can be so different, the genome clearly doesn't need anywhere near as much fine-tuning as is assumed/asserted in certain quarters. In fact it seems quite plastic.
Now a query. Given the differences, what is the basis for equating the two MotAs?
Good question. I am guessing - in the hopes that Nebullis will correct me if I'm wrong ;) - that you call it that way based on the functional equivalence of the product. The underlined (sort of underlined, anyway) bits apparently correspond to the third and fourth (of four) membrane segments in motA, and to the second and third (of three) membrane segments in ExbB. So the products of those two motA segments are known to be functionally/structurally equivalent, and the ExbB segment is analogous to the motA in structure and function.
And it may be the case that only the Pro/Asp sections are really critical to the functioning here, and everything else is somewhat more flexible in terms of substitution. Indeed, in the article, they authors note that mutations of the Asp and Pro complexes in motA strongly and negatively affected motility:
Correlation of Conformational Changes with Dominance of Asp32 Mutations. We reported previously that Asp32-mutations in MotB are very dominant, meaning that the mutant proteins impair motility strongly when expressed in wild-type cells (42). We also noted strong dominance in mutations of the conserved residues Pro173 and Pro222 in MotA, and proposed that such mutations might put the stator in an aberrant conformation that impedes rotation driven by functional (wild-type) complexes present in a motor. Since the initial experiments showed that mutations of Asp32 do cause conformational changes, we asked whether these conformational changes are correlated with the dominance of the mutations. To allow better quantification of dominant-negative effects, a set of motB mutations (D32N, D32A, D32E, and D32R) was transferred onto a plasmid that allows variable, IPTG-regulated expression of MotB. The mutant plasmids were introduced into wild-type cells, and rates of swarming were measured in soft-agar plates containing various concentrations of IPTG. Results are shown in Figure 4 (bottom). The magnitude of dominant-negative effects varied with the mutation, following the sequence D32A ≈ D32N > D32E > D32R. Thus, the most strongly dominant mutations are the same as the ones that produced the largest effects on conformation in limited-proteolysis experiments (compare top and bottom panels of Figure 4).
.....
Effects of Mutating Key Residues of MotA. Residue Pro173 of MotA is conserved across species and is important for motor rotation. It is probably an important determinant of conformation, and on the basis of mutant phenotypes, we proposed that it might control conformational changes in the stator that couple proton movement to rotor movement (41). To probe the effects of Pro173 replacements on conformation, we examined patterns of proteolysis of MotA with 5 different mutations in this position (P173G, P173A, P173F, P173R, or P173T), in complexes with either wild-type MotB or D32N-mutant MotB.The MotA mutations P173F and P173R are nonfunctional and strongly dominant (41). These mutations caused a substantial change in the proteolysis pattern that was different from the effects of MotB Asp32 mutations (Figure 7). The 8-kDa fragment was produced in somewhat higher yield than in the wild-type, and a number of larger fragments were produced in much lower yield. Further, the P173F and P173R mutations prevented the conformational change ordinarily induced by the D32N mutation (Figure 7). A co-isolation assay using His-tagged MotB showed that MotA and MotB remained associated with each other in the P173F/D32N double mutant (data not shown). These results show that the P173F and P173R replacements produce an altered and possibly locked conformation in the MotA/MotB complexes.
The P173G and P173A mutations of MotA are also nonfunctional, but unlike the P173F and P173R mutations, they are recessive (41). These mutations did not affect MotA conformation as judged by patterns of limited proteolysis and also did not hinder the conformational change induced by the D32N mutation in MotB. The mutation P173T is partially functional and recessive. Like the P173G and P173A mutations, it did not alter the MotA-proteolysis pattern and did not prevent the conformational change induced by the D32N mutation (Figure 7).
The idea is, I think, to compare the functionally similar portions of of the string, rather than trying to compare the whole thing, as AC is doing. If you wanted to know if the spell-checker of my mail program shared a common ancestry with the spell-checker of your word-processor, you wouldn't compare the whole programs to each other - any similarities in the spell-checker routines would get lost in the noise of all the other differences. Instead, you'd compare the functionally equivalent parts, and compare my spell-checker routine to your spell-checker routine to find out the relationship of the two.
Asp(D) is probably the most critical part of MOTB, although Glu(E) looks like a suitable chemical substitute(the structure might be a problem since the extra carbon in the side chain significantly alters the position of the carboxyl group). I suppose it is akin to the magnets in an electric motor.
You would compare the spell-checker routines and not the text compare subroutines alone. I haven't suggested that the entire genomes of the bugs be compared when trying to establish the connection between two proteins. Compare the complete proteins.
Are you familiar with Halton Arp? His biography and struggle also makes a great read.
Another of the (lesser known) strugglers is Ray Tomes who extends quantization to a cosmic scale Harmonics Theory. Here's more from Tomes:
Confirmation of Harmonic Theory Redshift Predictions (conversation with Tifft)
As I have said before, I suspect there is a primordial algorithm that will be manifest by harmonics. Therefore, I suspect Tome is in the right ballpark, though I'm not comfortable with all of his conclusions.
I can't recall anyone actually attacking Christianity, but there have certainly been objections to literal interpretations of the Bible.
All atheists use that method of attacking Christianity. As pointed out they know that a direct attack is less effective than a flank attack.
I think you are using the term "atheist" in the sense of "anti-theist." Christianity is not surrounded by enemies seeking to destroy it (with the notable exception of Islam, but that's another subject).
Phrases that include absolutes (i.e. "all atheists...") are rhetoric, in the sense that they are pretentious -- they assume facts that you cannot know. That is not a personal attack, by the way, but a characterization of your statement.
Well, there's this thing about beginnings. You want life to be created by existing life, so you're kind of fudging the "first life" thing. Or maybe God is not alive? And the fact that "evolution" doesn't include "abiogenesis" is just simply that evolution describes change, not beginnings.
Hard to discern your intended meaning. However, on this very thread the evolutionists are all defending abiogenesis tooth and nail. The opponents of evolution are all against it. I don't believe in such great coincidence. More importantly, the evolutionists claim that their beliefs are based on science. Abiogenesis as has been shown already has been totally discredited by science. Therefore evolutionist's insistence on abiogenesis shows that their guiding principle is not science.
My intended meaning is that life had to start somewhere -- even Dembski admits to a first time. He defines it as:
"Nonbiogenic emergence. Organisms emerge without the direct causal agency of other organisms. In place of life begetting life, here we have nonlife begetting life."
Then he goes on to say:
"Nonbiogenic emergence had to happen at least once, namely, at the origin of life."
The above quotes are from his paper dated October 25, 2002, which can be found here.
And you state that abiogenesis has been discredited by science. I've seen you refer to Pasteur's debunking of spontaneous generation in this context, but that's not abiogensis, so what else do you have?
This is a really odd proposal. I can see you arguing for ALL species being created, or for all "kinds" being created, but what would ONE species do for you? As to the question itself (why not one?), because that would make no sense to either side of the discussion.
You are answering my question with a question. Thus your answer is an evasion. If evolution were adhered to as science, then evolutionists should have no problem making such a concession. But man is the ultimate goal of evolution because it is the goal of evolution to 'refute' Christianity. In fact they have brought themselves much grief on this account alone. Why get into a fight against all if the goal is a scientific one instead of a teleological one?
The first part of my statement was a question, no doubt about it. Accusing me of evasion is rather disingenuous, however, since I answered your question in the very next sentence. You reiterate here that designating ONE creature as designed is a reasonable concession. Such a concession makes no sense, not to an evolutionist, not to a creationist, and not to a proponent of Intelligent Design.
And Man is not the ultimate goal of evolution, because evolution has no observable goals, no designated plan, no particular destination.
Intelligent Design is engaging in teleology, not science.
If an Intelligent Designer designed anything at all, then everything could have been designed. If everything was designed, then nothing is related. If nothing is related, then all of our biological inferences are imaginary. ID simply creates more problems than it solves. Stick with God.
The above shows that evolution is an ideology, an ideology whose purpose is to completely eradicate God's hand from nature. Just what I am asserting. It also shows again that in spite of overwhelming evidence for the ID position, the evolutionists reject it out of hand in favor of 'hopeful monsters'. Showing again that evolution is not about science, but about atheism.
Evolution doesn't eradicate God's hand from nature, it simply doesn't observe it.
And I can't find the "hopeful monster" quote in my paragraph, nor the "overwhelming evidence for the ID position" that you credit me with.
More of the same rant.
Not quite and your only 'refutation' is a personal attack. Science is not ideological but evolutionists are, that is why they cannot give an inch. They cannot allow God into anything because their purpose is the promotion of atheism. Let me note that Darwin himself asserted that a single example that could not be explained by evolution would completely destroy the theory. This does not seem to be the mentality or type of thinking of a scientist, but the mindset of an ideologue which has an axe to grind. This axe is the attack on Christianity which his atheism required.
You seem to think that the word "rant" is a personal attack. It's not, it's a description of a rhetorical style, one which you engage in frequently. It's a very popular style in internet discussion groups, and many people, myself included, enjoy a good rant. VadeRetro tosses off good rants on occasion, for example.
Good rants don't involve repetitive shouting, however. Placing EVOLUTION = ATHEISM between every paragraph does not help your arguments.
The balance of the above paragraph seems to be a summary of your position on the whole matter. So be it.
I'd have to say that this is about as blatant an example of argument from incredulity as one could get. (i.e. I don't know how it could happen, therefore it cannot). His argument here is even more specious than his c-decay arguments, if that is possible.
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