Jump to content


Photo

Evolution-tested And Falsified


  • This topic is locked This topic is locked
118 replies to this topic

#21 jason777

jason777

    Moderator

  • Moderator Team
  • PipPipPipPip
  • 2,670 posts
  • Gender:Male
  • Interests:Machining, Engine Building, Geology, Paleontology, Fishing
  • Age: 40
  • Christian
  • Young Earth Creationist
  • Springdale,AR.

Posted 28 March 2010 - 02:04 PM

Lol, what data? If you can produce any data gathered by creation science ill be amazed.


:rolleyes: The data you keep ignoring on purpose because it does'nt support the predictions of evolution.

You havent read what ive written. Antibiotics are naturally occurring compounds, produced by many organisms (bacteria included). By design or coincidence, modern antibiotic(s) shared structural similarity with the resistance patterns found in gut-microbes, or closely related species (or indeed simply species using the same antibiotic via convergent evolution - quite a common occurrence). Has "PhD" considered these options?


We've all read it and noticed that you are reject the scientists research in the Naure article referenced. Why? If synthetic antibiotics were a natural occurance don't you think they would know? <_<

In September 2007, we examined domestic cattle (n = 48; 31 cows,
4 haifers, and 13 calves) , wild rodents (n = 45; Rattus rattus 33,
Arvicola ansorgei 4, Myomys daltoni 3, Mastomys erythroleucos 2,
Tatera guinea 2, Mus musculus 1) and chiropterans (n = 24;
Epomorphorus gambianus 19, Micropteropus pusilus 3,
Hiposideros gigas 2) sympatric to humans, from two locations in
southeastern Senegal for the presence of antibiotic-resistant
Enterobacteriaceae. Wild rodents and chiropterans were caught
using live traps and mist nets, respectively, in places inhabited by
humans. Rectal swabs obtained from all the sampled animals were
stored in Amies transport medium before laboratory testing.
Individual rectal swabs were placed overnight in Buffered
Peptone Water (BPW) (Oxoid, UK) at 37°C, and then cultured for E.
coli on Chromogenic medium for E. coli and coliform bacteria
(Oxoid). One suspect colony of each plate was identified using
API10S test kit (bioMérieux, France) and tested for susceptibility to
antimicrobial agents in accordance with CLSI (The Clinical and
Laboratory Standards Institute). Antibiotic susceptibility was tested
by disk diffusion method on Mueller-Hinton agar (Oxoid) using the following antimicrobials and concentrations: amoxicillin-clavulanic
acid (30 μg), ampicillin (10 μg), cephalothin (30 μg), ceftazidime (30
μg), chloramphenicol (30 μg), ciprofloxacin (5 μg), gentamicin (10
μg), nalidixic acid (30 μg), streptomycin (10 μg), sulphamethoxazole-
trimethoprim (25 μg), sulphonamides (300 μg), and
tetracycline (30 μg) (Oxoid).In E. coli isolates found to be resistant
to one or more of the antibiotics listed above, polymerase chain
reaction (PCR) was used to detect specific antibiotic-resistance
genes, integrase genes int1 and int2, and gene cassettes within
class 1 and 2 integrons (Dolejska et al. 2007, for the list of primers
see Literak et al., in press).


http://www.academicj...P...k et al.pdf

The article references modern antibiotics that do not occur in nature.


Enterobacteria: Antibiotic resistance found in wild rodents

Moira A. Gilliver1, Malcolm Bennett1, Michael Begon1, Sarah M. Hazel1 & C. Anthony Hart1
Top of page
Abstract

Resistance to antibiotics is an increasingly common problem in both veterinary and human medicine, and its management is the subject of urgent debate1, 2, 3, 4. Efforts to reduce this resistance are based on the assumption that it is maintained in bacterial populations as a result of exposure to antibiotics, and that restricting the use of antibiotics should therefore restrain the spread of resistance. But we have found that antibiotic resistance is prevalent in populations of wild rodents that have not been exposed to antibiotics, indicating that approaches to control it based on this assumption may be overoptimistic.


http://www.nature.com › Journal home › Table of Contents

#22 Guest_McStone_*

Guest_McStone_*
  • Guests

Posted 29 March 2010 - 02:50 PM

The data you keep ignoring on purpose because it does'nt support the predictions of evolution.


....No, you havent actually presented any data, and neither has "PhD". Look:

12,43,22,22,45,90,87,65,43,23,45

Thats data. Something that can be statistically analysed. Compare with this data set:

7,9,9,6,5,10,15,30,2,5,8,9,9,

Is there a significant difference between the two, beyond what we would expect from random chance? (P<0.05?; P<0.001?). (Yes there is).

Creationism does not produce data; it reviews the conclusions of data. Not the data itself. Not the technique, not the hypothesis; the conclusion.

A scientific journal of creationism (if one could be made) would contain review after review after review. Just ideas (and ideas with striking similarity with a book. What was its name? Oh yes, the bible) There would be no testing and no substance. How does one experiment, exactly, with creation science?

Compare a model of no-god with a model of god?

What would a model of no-god even look like? Evolution?

We've all read it and noticed that you are reject the scientists research in the Naure article referenced. Why? If synthetic antibiotics were a natural occurance don't you think they would know


Yes... Lets have a closer look at the Nature article shall we?

Ive actually had lectures and discussions with mike begon, who has done excellent work on rodent disease cycles. He marked my work. He actually studies bubonic plague. He gave a lecture, once, about speciation, evolution, just a background to.. well... ecology really. You should read his book: begon, harper and townsend: Ecology.

If only you read more than just the abstract (perhaps you havent a subscription, which is fair enough, but you should get one: it is NATURE).

First sentences:

The source of antibiotic-resistance genes is not always known. They can evolve within the treated host species or, frequently, like the genes encoding the antibiotics themselves, as a result of natural inter- and intraspecific bacterial competition.


(after Gilliver et al. 1999)

There are four cited peer reviewed references for that claim:

Medeiros, A. A. Clin. Infect. Diseases 24 (suppl. 1), 19–45 (1997).
Davies, J. E. Ciba Found. Symp. 207, 15–27 (1997).
Waters, B. & Davies, J. Antimicrob. Agents Chemother. 41, 2766–2769 (1997).
Wiener, P. , Egan, S. & Wellington, E. M. H. Mol. Ecol. 7, 1205–1216 (1998).

Instances of natural resistance to antibiotics, as a consequence of competition, are documented in these. Please read them.

The authors go on:

The expression of antibiotic resistance in bacteria may also involve a fitness cost that is disadvantageous compared with susceptible bacteria unless antibiotics are present in the environment, and resistance would gradually be lost from untreated populations. This idea is supported by some laboratory experiments and by a low prevalence (but, importantly, not absence) of resistance in human and animal populations not exposed to antibiotics.

If this is the case then improving the management of antibiotics should reduce the prevalence of resistance. However, compensatory mechanisms can evolve to overcome any small disadvantage of resistance in the absence of antibiotic selection, and resistance can be maintained in populations in the apparent absence of specific antibiotic selection for several years.

To test whether the development of antibiotic resistance is less prevalent in the absence of exposure to antibiotics, we surveyed resistance in commensal, enteric Enterobacteriaceae isolated from two wild populations of small rodents. Faeces from 38 bank voles (Clethrionomys glareolus) and 70 wood mice (Apodemus sylvaticus) were collected from two woodland sites on the Wirral peninsula in northwest England. The first wood is surrounded by more woodland, gardens and an ornamental lake; the second wood is surrounded by woods and by meadows in which heifers (but not dairy cows) are occasionally kept. Pheasant feed containing the antibiotic tylosin was sometimes distributed in the second site, but otherwise the rodents had minimal contact with antibiotics or with domestic animals routinely treated with them.

The most abundant enterobacterial isolate from each sample was screened for resistance using minimum inhibitory concentrations (MICs) of seven representative antibiotics, and the prevalence of resistance was calculated for 'breakpoint' MICs to reflect its clinical significance (at least for humans)(Table 1); only those species isolated six or more times are included, although the patterns were the same for less frequently isolated bacteria.

Overall, 90% of coliforms were resistant to amoxycillin, amoxycillin/clavulanic acid and cefuroxime. Depending on the bacterial species, 14–76% of coliforms were tetracycline resistant and 0–67% were trimethoprim resistant, but all of them were sensitive to chloramphenicol. Controlled disc diffusion was also carried out on six antibiotics (ampicillin, gentamicin, apramycin, sulpho-namides, cefotaxime and cephradine). Overall, 90% were ampicillin resistant, as a result of beta-lactamase expression in more than half the cases (as determined by hydrolysis of a chromogenic cephalosporin, nitrocefin). The level of resistance to apramycin was low, at 12–33%, whereas resistance to the other antibiotics was comparable, at 33–73%.


The authors conclude:

Our results show that resistance to antibiotics is widespread in at least some wild populations, even though these have never to our knowledge been exposed to antibiotics, and they undermine the presumption that resistance will decline in the absence of antibiotic treatment. The origin(s) of the resistance and the selection mechanisms (if indeed such mechanisms are necessary) responsible for maintaining a high prevalence of resistance are unknown. It is important to address these questions, not least because similar mechanisms may operate in farm animals and humans, in which case the management of antibiotic resistance may need to be reconsidered.


You see, scientists are actually honest. The origin of resistance is stated as unknown. Although this resistance was evolved, the authors do not speculate on how this resistence was selected for. It could be, quite easily, that some antibiotics have entered the natural system, (the rodent's diet), or it could be, once again, that the resistance, as stated in the introduction, may have come around as part of the bacteria's natural intraspecific and interspecific competition. Given that the tested antibiotics in question, although semi-synthetic, have a natural fungi/bacteria base, this is very likely. Its not something you can work out easily; but it is still an evolved character.

The point is, you can explain "Phd's mystery", that vexing question, if you try to. You can find, somewhere, some alternative hypothesis, other than the the whole of evolutionary theory being wrong. You seriously believe that "Phd" has questioned each and avenue of investigation?

Think about that. The whole of evolution. Falsified. Because some bacteria have antibiotic resistance.

But hes not trying, and his audience isnt trying; it isnt even questioning.

#23 jason777

jason777

    Moderator

  • Moderator Team
  • PipPipPipPip
  • 2,670 posts
  • Gender:Male
  • Interests:Machining, Engine Building, Geology, Paleontology, Fishing
  • Age: 40
  • Christian
  • Young Earth Creationist
  • Springdale,AR.

Posted 29 March 2010 - 04:28 PM

The point is, you can explain "Phd's mystery", that vexing question, if you try to. You can find, somewhere, some alternative hypothesis, other than the the whole of evolutionary theory being wrong. You seriously believe that "Phd" has questioned each and avenue of investigation?


No McStone, we do something you never could do. We devolop our hypothesis from the empirical data instead of trying to claim "It must be evolution". The scientists in the referenced articles knew that their hypothesis had to be wrong, but they did'nt know the mechanism was wrong as well.

http://www.evolution...indpost&p=53021


That leaves you in the position you started at. Equivocating after the prediction fails and your left with nothing but rhetoric.




Enjoy.

#24 Guest_McStone_*

Guest_McStone_*
  • Guests

Posted 30 March 2010 - 03:26 AM

The point is, you can explain "Phd's mystery", that vexing question, if you try to. You can find, somewhere, some alternative hypothesis, other than the the whole of evolutionary theory being wrong. You seriously believe that "Phd" has questioned each and avenue of investigation?


No McStone, we do something you never could do. We devolop our hypothesis from the empirical data instead of trying to claim "It must be evolution". The scientists in the referenced articles knew that their hypothesis had to be wrong, but they did'nt know the mechanism was wrong as well.

http://www.evolution...indpost&p=53021
That leaves you in the position you started at. Equivocating after the prediction fails and your left with nothing but rhetoric.
Enjoy.

View Post



But what empricial data? What data are you talking about? Antibiotic resistance? Yes. It evolves... from mutation. From your second article:

Several antibiotics act by targeting protein biosynthesis,
interacting with ribosomal structural proteins, rRNAs,
and ribosomal-associated proteins (23). Understanding more
about the precise interactions between antibiotics and ribosomal
proteins will be especially informative as more detailed
information is revealed in higher-resolution structures of the
ribosome (4, 9, 11, 15). In particular, mutations in ribosomal
proteins L22, S5, and S12 have been observed to confer resistance
to erythromycin (10), spectinomycin (7, 14), and streptomycin
(1, 24, 25), respectively, in Escherichia coli. As bacteria
are exposed to these drugs, the specific changes in ribosomal
proteins are incorporated. Patterns of mutations at the particular
sites in various strains of E. coli emerge for each drug (10,
14, 25). A method to rapidly screen bacteria for mutations in
proteins would be a valuable tool for evaluating antibiotic
mechanisms and for determining an appropriate treatment of
an infection. Further insights into the antibiotic mechanism
could be gleaned from the details of the mutation. For example,
knowing which specific amino acid alterations in ribosomal
proteins L4 and L22 result in resistance to erythromycin as well
as sites in 23S rRNA whose mutations also confer resistance
provides information not only on details on the mechanism of
erythromycin function but also on details of functional interactions
between ribosomal proteins and rRNA
(10)


(After Wilcox et al. 2001)

What are you trying to say? Seriously? Are you just looking for any instances of "antibiotic resistance" on google? Are you even reading the work?

The authors understand that the relatively simple process:

mutation -> change in amino acid sequence -> change in protein -> change in function ----->Natural selection --- = evolution

is occurring in bacteria, therby confering resistance to antibiotics. Its so easy to understand!!! There are pictures in the article showing the consequences on mass spectrometry feedbacks.

It is even the point. The original point in "PhDs" example was that resistance to antibiotics was found in bacteria isolated (to the best of his knowledge) from anthroprogenic antibiotics. He implies, stupidly, that this is because antibiotic resistance is not evolving in bacteria; that it is, somehow, an instinctive trait in any and all bacteria. Its presented - even more rediculous - as a test of evolution, when all thats tested is his audience's ignorance, and nothing more.


But his hypothesis is wrong, because, as we have established, many - most- antibiotics have a natural fungal/bacterial base, and anthroprogenic semi-synthetic antitbiotics share this base. There are tanks - full to the brim of bacteria - producing antibiotics, quite literally drained by a tap. But he neglected to say this; he neglected to say that antibiotics are naturally-occurring compounds; in soils, in the human digestive tract. Anywhere there are bacteria and fungi, in fact. Because bacteria use them to kill other bacteria. We exploit his happily genocidal relationship, and we do it well.

If i was at "PhDs" conference, i would say, during his seminar:

"But antibiotics are naturally occurring. Is is not possible that these bacteria evolved resistance to naturally occurring antibiotics, and that modern antibiotics share some simliarity to these?"

What possible answer could he have?

"i guess"
"yes"
"No"

It doesnt matter what answer he could provide, his claim, his method and his conclusions are as sloppy as a pile of manure, and, although his audience to too ignorant to realise otherwise, i dont think you are, and you shouldnt degrade yourself by associating with them.

Why do YECs set so low standards for themselves?

This guy is taking quotes from people in a scientific conference, and presenting them as science. He is not a scientist, he is a theologian, with the methods of one studying humanities.

#25 jason777

jason777

    Moderator

  • Moderator Team
  • PipPipPipPip
  • 2,670 posts
  • Gender:Male
  • Interests:Machining, Engine Building, Geology, Paleontology, Fishing
  • Age: 40
  • Christian
  • Young Earth Creationist
  • Springdale,AR.

Posted 30 March 2010 - 03:39 AM

But what empricial data? What data are you talking about? Antibiotic resistance? Yes. It evolves... from mutation. From your second article:


Anybody with a scroll bar can see that you yourself pointed out that the authors did'nt know the reason for antibotic resitance in post#22

You see, scientists are actually honest. The origin of resistance is stated as unknown. Although this resistance was evolved, the authors do not speculate on how this resistence was selected for.


It is also easy for anybody to follow my link in post#23 and see that antiobiotic resitance has been empirically established, by Mass spectrometry, as a protein change, which falisifies your prediction of genetic mutation.


"Mutations in several ribosomal proteins are known to be related to antibiotic resistance. For several strains of Escherichia coli, the mutated protein is known but the amino acid actually altered has not been documented. Characterization of these determinants for antibiotic resistance in proteins will further the understanding of the precise mechanism of the antibiotic action as well as provide markers for resistance. Mass spectrometry can be used as a valuable tool to rapidly locate and characterize mutant proteins by using a small amount of material. We have used electrospray and matrix-assisted laser desorption ionization–time of flight (MALDI–TOF) mass spectrometry to map out all 56 ribosomal proteins in E. coli based on intact molecular masses. We used this fingerprinting approach to locate variants of ribosomal proteins displaying a change in mass. In particular we have studied proteins responsible for streptomycin, erythromycin, and spectinomycin resistance in three strains of E. coli, and then we characterized each mutation responsible for resistance by analyzing tryptic peptides of these proteins by using MALDI-TOF and nanoelectrospray tandem mass spectrometry. The results provided markers for antibiotic resistance and demonstrated that mass spectrometry can be used to rapidly investigate changes in individual proteins from a complex with picomole amounts of protein."



Enjoy.

#26 Guest_McStone_*

Guest_McStone_*
  • Guests

Posted 30 March 2010 - 03:59 AM

Anybody with a scroll bar can see that you yourself pointed out that the authors did'nt know the reason for antibotic resitance in post#22


Yes.... thats because that particular study did not address the mechanism of where the antibiotics came from. It could have been an external (inflitration of the rodents' diet) or internal source (competition between bacteria). Both routes have been independantly observed. Scroll up and see the references.

It is also easy for anybody to follow my link in post#23 and see that antiobiotic resitance has been empirically established, by Mass spectrometry, as a protein change, which falisifies your prediction of genetic mutation.


Oh my god, Jason, you've really put your foot in this one. How do you suppose proteins are made in the first place?

They are made from the transcription and translation of DNA into a sequence of AMINO ACIDS. Your arguing with that now? If you are, then things really have gotten bad.

Lol, your quote even says as much:

Mutations in several ribosomal proteins are known to be related to antibiotic resistance. For several strains of Escherichia coli, the mutated protein is known but the amino acid actually altered has not been documented. Characterization of these determinants for antibiotic resistance in proteins will further the understanding of the precise mechanism of the antibiotic action as well as provide markers for resistance. Mass spectrometry can be used as a valuable tool to rapidly locate and characterize mutant proteins by using a small amount of material. We have used electrospray and matrix-assisted laser desorption ionization–time of flight (MALDI–TOF) mass spectrometry to map out all 56 ribosomal proteins in E. coli based on intact molecular masses. We used this fingerprinting approach to locate variants of ribosomal proteins displaying a change in mass. In particular we have studied proteins responsible for streptomycin, erythromycin, and spectinomycin resistance in three strains of E. coli, and then we characterized each mutation responsible for resistance by analyzing tryptic peptides of these proteins by using MALDI-TOF and nanoelectrospray tandem mass spectrometry. The results provided markers for antibiotic resistance and demonstrated that mass spectrometry can be used to rapidly investigate changes in individual proteins from a complex with picomole amounts of protein

Yes, antibiotic resistance may indeed be expressed in a protein, but thats because

DNA -> Amino acids -> Protein

Its kind of simple - real simple. Real basic genetics right there.
And before you chase up "documented amino acid", thats because its beyond the scope (and probably funding) of this particular study.

#27 Mankind

Mankind

    Member

  • Veteran Member
  • PipPipPip
  • 212 posts
  • Age: 50
  • Christian
  • Young Earth Creationist
  • Southeast

Posted 30 March 2010 - 08:42 AM

That's a good video thanks. It makes me wonder about evolutionists claim that "all fossils are transitional" or "humans are transitional forms", or something to that affect. I know I have heard something similar to that many times but that might just be a false argument. However if that is supposed to be the case the fruit fly destroys that. The fruit fly hasn't transformed into any other form for all of those millions of generations.

#28 Guest_McStone_*

Guest_McStone_*
  • Guests

Posted 30 March 2010 - 10:06 AM

That's a good video thanks.  It makes me wonder about evolutionists claim that "all fossils are transitional" or "humans are transitional forms", or something to that affect.  I know I have heard something similar to that many times but that might just be a false argument.  However if that is supposed to be the case the fruit fly destroys that.  The fruit fly hasn't transformed into any other form for all of those millions of generations.

View Post



....because, as ive said, being a fruitfly is a very successful lifestyle, with a very wide niche. Theres no reason for it evolve any further.

#29 Mankind

Mankind

    Member

  • Veteran Member
  • PipPipPip
  • 212 posts
  • Age: 50
  • Christian
  • Young Earth Creationist
  • Southeast

Posted 30 March 2010 - 10:20 AM

....because, as ive said, being a fruitfly is a very successful lifestyle, with a very wide niche. Theres no reason for it evolve any further.

View Post



Right, I'm sure it's not because the creator put in specific boundaries of change within each form, it has to be from the ToE. ;) However this is what I was referring to concerning the statement that I have heard that "all forms are transitional". If that statement is true then the fruit fly goes against that statement because it is the same form after millions of generations and bacterial also. But if what you are saying that the fruit fly doesn't have a big enough reason to change to another form then the statement that "all forms are transitional" is false and I need to make sure I tell the people that say that to me of the falscivity of it. B)

#30 Guest_McStone_*

Guest_McStone_*
  • Guests

Posted 30 March 2010 - 01:05 PM

Right, I'm sure it's not because the creator put in specific boundaries of change within each form, it has to be from the ToE. ;) However this is what I was referring to concerning the statement that I have heard that "all forms are transitional".  If that statement is true then the fruit fly goes against that statement because it is the same form after millions of generations and bacterial also.  But if what you are saying that the fruit fly doesn't have a big enough reason to change to another form then the statement that "all forms are transitional" is false and I need to make sure I tell the people that say that to me of the falscivity of it. B)

View Post



Yes, Im sure its not too. What "boundaries" are you thinking of, exactly?

The boundary stopping DNA coding for an amino acid?
The boundary stopping amino acids making protein?
The boundary stopping proteins constructing cells, and cells tissues?

Care to elaborate? What exactly stops evolution. We're just making it all up, obviously, so we must be wrong. Logically.

How is genetic change limited, how is protein construction limited and how is cell structure and function limited?

If your right, there must be a mechanism - something-that kicks in once variation has reached a certain level that goes:

"hang on lads, hang on. Ribosome, put that wrench down, your a danger to yourself and others. More trouble than your worth. Now boys, it seems to me like that this genome has got a little too much variation for our tastes. Lets just take this allele out, and swap it with this one. Phew! That was close, i mean, we dont want to start off evolution here or something"

God being god, he creates fruitflies with apparent stasis, but makes chimp and humans (or rather adam) more than >98% identical. I mean what could be clearer?

There is no unseen mechanism regulating the magnitude of change in genomes at all. Nothing. Mutation, ironically, enough, is the only thing that can, and as we know, mutations are random, both temporally and spatially. Thats why evolution happens. There is abundant evidence to suggest that mutation can explain evolution, bacterial resistance being just one example.

#31 jason777

jason777

    Moderator

  • Moderator Team
  • PipPipPipPip
  • 2,670 posts
  • Gender:Male
  • Interests:Machining, Engine Building, Geology, Paleontology, Fishing
  • Age: 40
  • Christian
  • Young Earth Creationist
  • Springdale,AR.

Posted 30 March 2010 - 01:46 PM

Oh my god, Jason, you've really put your foot in this one. How do you suppose proteins are made in the first place?


Because every gene has the ability to make several different proteins. A gene in the fruit fly is the record holder for the ability to produce more than 30,000 different proteins. When adaptation is needed it simply selects the protein that helps it survive.


They are made from the transcription and translation of DNA into a sequence of AMINO ACIDS. Your arguing with that now? If you are, then things really have gotten bad.


The genes produce the proteins and the DNA produce the genes, all of which are pre-existing. I'm not arguing with that, i'm trying to educate you, if you don't want to accept the fact that protein replacement does'nt support antibiotic resistance by genetic mutation, then remain ignorant. ;) If you have an empirical observation of genetic mutation producing antibiotic resistance without assuming, then we would all be glad to see it. Until then, i'll stick with the known facts.

There is no unseen mechanism regulating the magnitude of change in genomes at all. Nothing. Mutation, ironically, enough, is the only thing that can, and as we know, mutations are random, both temporally and spatially. Thats why evolution happens. There is abundant evidence to suggest that mutation can explain evolution



True, but genetic mutation is almost always neutral and sometimes detramental. How that supports evolution is absurd.

Once again we'll stick to empirical observation. Here is a list of genetic disorders. If evolution were true, then we should be able to produce a list of "observed" benefical "genetic mutations" that out number that list 100:1. Good luck because even sickle cell is neutral because it deforms the red blood cells making them less efficient at carrying oxygen, meaning that it is benefical at a cost.

God being god, he creates fruitflies with apparent stasis, but makes chimp and humans (or rather adam) more than >98% identical. I mean what could be clearer?


Indels alone account for 12% difference and if you compare proteins they only share 20% homology.

However, if one looks at proteins, which are mainly responsible for phenotypic differences, the picture is quite different, and about 80% of proteins are different between the two species. Still, the number of proteins responsible for the phenotypic differences may be smaller since not all genes are directly responsible for phenotypic characters.. However, if one looks at proteins, which are mainly responsible for phenotypic differences, the picture is quite different, and about 80% of proteins are different between the two species. Still, the number of proteins responsible for the phenotypic differences may be smaller since not all genes are directly responsible for phenotypic characters.


http://linkinghub.el...378111904006705


Thanks.

#32 Guest_McStone_*

Guest_McStone_*
  • Guests

Posted 31 March 2010 - 02:23 AM

Because every gene has the ability to make several different proteins. A gene in the fruit fly is the record holder for the ability to produce more than 30,000 different proteins. When adaptation is needed it simply selects the protein that helps it survive.


Yes, thats not actually what you said though, is it Jason?:

It is also easy for anybody to follow my link in post#23 and see that antiobiotic resitance has been empirically established, by Mass spectrometry, as a protein change, which falisifies your prediction of genetic mutation.


Proteins sequences are coded by genes, you missed this point (or ignored it), and are now trying to escape your blunder. The more i read it, the more silly it is.

Curious fact of fruitfly aside, (and your wrong, by-the-way, about every gene making more than one protein... Oh, and the fruitfly having the largest number of proteins made from a single gene. Nice fact) you have answered your own question. Adaptation is primarily a chemical process, if a chemical solution can be found, it will be. Evolving a large number of reading frames on a gene can greatly enhance the number of proteins produced. So its not that the fruitfly hasnt evolved, it just hasnt evolved new limbs or eyes. Its evolved, with simple genetic changes, the ability to produce more protein for some other purpose.

The genes produce the proteins and the DNA produce the genes, all of which are pre-existing. I'm not arguing with that, i'm trying to educate you, if you don't want to accept the fact that protein replacement does'nt support antibiotic resistance by genetic mutation, then remain ignorant. tongue.gif If you have an empirical observation of genetic mutation producing antibiotic resistance without assuming, then we would all be glad to see it. Until then, i'll stick with the known facts.


Jason, forgive me if i decline your particular brand of education just at the moment.

Proteins -every protein - are made by amino acids, themselves coding by a sequence of DNA nucleotides. So a protein, replaced by another, is still a reflection of genetics. Something as been replaced or changed at the genetic level as well. What you are saying defies logic. The known facts are out there for you take, but you cant do it. As for examples of:

mutation -> antibiotic resistance

have a look yourself, there are plenty (even with a google search). But im going to do your work for you, you have to look and read - entire articles - yourself.

mutation -> protein -> antibiotic resistance

is the same thing.

True, but genetic mutation is almost always neutral and sometimes detramental. How that supports evolution is absurd.

Once again we'll stick to empirical observation. Here is a list of genetic disorders. If evolution were true, then we should be able to produce a list of "observed" benefical "genetic mutations" that out number that list 100:1. Good luck because even sickle cell is neutral because it deforms the red blood cells making them less efficient at carrying oxygen, meaning that it is benefical at a cost.


Doesnt that rather depend on the selective environment and the strength of selection pressures? Again, observational evidence suggests otherwise.

Indels alone account for 12% difference and if you compare proteins they only share 20% homology.


Yes jason, this is because evolution has happened since. They still share frightening levels of genetic homology.

#33 deadlock

deadlock

    Veteran Member

  • Veteran Member
  • PipPipPipPip
  • 1,196 posts
  • Age: 43
  • Christian
  • Creationist
  • Rio de Janeiro

Posted 31 March 2010 - 03:00 AM

....because, as ive said, being a fruitfly is a very successful lifestyle, with a very wide niche. Theres no reason for it evolve any further.

View Post


Are you saying that frutflies have 100% of fitness ?

#34 deadlock

deadlock

    Veteran Member

  • Veteran Member
  • PipPipPipPip
  • 1,196 posts
  • Age: 43
  • Christian
  • Creationist
  • Rio de Janeiro

Posted 31 March 2010 - 03:05 AM

Yes, Im sure its not too. What "boundaries" are you thinking of, exactly?

The boundary stopping DNA coding for an amino acid?
The boundary stopping amino acids making protein?
The boundary stopping proteins constructing cells, and cells tissues?

Care to elaborate? What exactly stops evolution. We're just making it all up, obviously, so we must be wrong. Logically.

How is genetic change limited, how is protein construction limited and how is cell structure and function limited?


Dont you know ? Whay dont you ask fruitfly ? it seems it discovered a way.

There is no unseen mechanism regulating the magnitude of change in genomes at all. Nothing. Mutation, ironically, enough, is the only thing that can, and as we know, mutations are random, both temporally and spatially. Thats why evolution happens. There is abundant evidence to suggest that mutation can explain evolution, bacterial resistance being just one example.


Dont equivocate the meaning of the word evolution. Dont use an example of micro-evolution as evidence of macro-evolution.

#35 scott

scott

    Veteran Member

  • Veteran Member
  • PipPipPipPip
  • 1,749 posts
  • Age: 21
  • Christian
  • Young Earth Creationist
  • mississippi

Posted 31 March 2010 - 05:45 AM

McStone has to use examples of Micro-evolution as evolution because that's all he has. Micro-evolution is not evolution McStone... it's using existing genes to create different breeds using existing genes.

I'm sorry McStone, but you simply do not understand genetics, or the breeding process. Neither require evolution, and neither have ever shown evolution.

#36 Guest_McStone_*

Guest_McStone_*
  • Guests

Posted 31 March 2010 - 12:24 PM

Are you saying that frutflies have 100% of fitness


Fitness isnt measured as a percentage. Fitness is a measure of a given allele's proliferation relative to any other; most often as expressed in a number of offspring. Natural selection cannot produce perfect organisms (how do we even judge perfect?); that said, the fruitfly is well adapted to its niche. It will not be exposed to selective pressures strong enough to make it evolve into a new genera or evolve dramatic new body parts. Evolution works on what came previously. To evolve new limbs would require millions of years of a constant selective pressure. The fruitfly can generate billions of descendants in a single summer period. If limb number was selected for and against in these descendants, then we would expect to see limbs evolving (either more or less limbs). As it happens, the first insects were able to survive with 6 limbs; no more or less. They have been able to survive with 6 limbs. Since this time, fruitflies, and the entire insect group, havent encountered an environment (or ecological niche), which selects strongly enough to evolve more limbs.

An insect with 6 legs can walk just as easily if it had 8 legs.
An insect with 6 legs might even fly better with only 6 legs.

See what im getting at?

Evolution is all about trade-offs. If new limbs would effect survival (and natural selection can detect this), then we would predict evolution of new limbs. If not, any individual hatched with 8 limbs, by chance, would have no greater chance of reproduction than any other (perhaps reduced odds). Their particular genome would not enter the population; the allele or mutation responsible would not proliferate, and the population would not evolve; the species would not evolve. Evolution would not occur.

Dont you know ? Whay dont you ask fruitfly ? it seems it discovered a way.


Again, not really. As demonstrated above, things dont have to evolve. They evolve only when necessary. When the wind is blowing the right direction.

Dont equivocate the meaning of the word evolution. Dont use an example of micro-evolution as evidence of macro-evolution.


But its the same thing. Maybe your definition is wrong.


McStone has to use examples of Micro-evolution as evolution because that's all he has. Micro-evolution is not evolution McStone... it's using existing genes to create different breeds using existing genes.

I'm sorry McStone, but you simply do not understand genetics, or the breeding process. Neither require evolution, and neither have ever shown evolution


...that coming from the man who thinks that the every single one of the 7 billion people on this planet descended from two people, and every species of animal likewise. Scott, your in no position to lecture me about the "breeding process". Good lord, even rearing a child with a cousin can produce lethal disease; let alone with your sister/mother/daughter, generation after generation. But of course, it was "different back then".

Your not getting it, and i understand evolution, and genetics, alot better than you do. Micro and macro are the same thing. They have the same mechanism. I can show you evidence of macroevolution too, you say its evidence of common design:

Posted Image

common design?

Posted Image

common design?

Posted Image

common design?

theres alot more out there scott, alot more.

Common design? What does that even mean? That god is somehow "human" in the way he designs things? He's god!!!, "economy of design" has no relevance for him. Its the only thing you can cling too, the vague hope that god recycled "parts". If god is real, hes alot brighter than you give him credit for.

#37 scott

scott

    Veteran Member

  • Veteran Member
  • PipPipPipPip
  • 1,749 posts
  • Age: 21
  • Christian
  • Young Earth Creationist
  • mississippi

Posted 31 March 2010 - 04:59 PM

Incorrect McStone, I am in every position to lecture you in the breeding process, because you simply do not understand it.

Of course you know what common design is, and as I have already shown that it totally refutes your argument. I'm not be-littleing the design, because if you knew me, then you'd know complexity, and I sure do see it. Why? It's an attribute for one that builds/ paints cars, and studies the complexity of nature. Did you know that all the animals that you present or could present will have a certain amount of common design?

Hmmm??? I think you know.

And you believe that 7 billion people came from only a few or 1, or 2 ape ancestors... yes McStone, evolution demands that these traits come from parent to offspring... So McStone... when did the breeding process contain more than Male and Female to produce an offspring??? By default and as an evolutionist you have to believe an Adam and Eve like story for apes anyways. ( of course it must have been different back then, I mean humans were randomly popping up everywhere).

Hmmm McStone, you thought you showed me evidence of Macro-evolution, and you quite possibly thought you showed me evidence of Micro-evolution. Point in case, you only showed me a few pictures which prove nothing towards evolution and actually show signs of common design.

The mere fact that you claim Macro-evolution and Micro-evolution are the same thing proves that you do not infact know more about evolution than I do, sorry McStone but your posts show this.

#38 jason777

jason777

    Moderator

  • Moderator Team
  • PipPipPipPip
  • 2,670 posts
  • Gender:Male
  • Interests:Machining, Engine Building, Geology, Paleontology, Fishing
  • Age: 40
  • Christian
  • Young Earth Creationist
  • Springdale,AR.

Posted 31 March 2010 - 09:51 PM

Proteins sequences are coded by genes, you missed this point (or ignored it), and are now trying to escape your blunder. The more i read it, the more silly it is.


Your completely rejecting the empirical observation because it falsifies your assumption of antibiotic resistance being an example of evolution by genetic mutation. Would you like me to produce a list of other empirical sciences one must reject to be an evolutionists - I would be here all day.

True, but genetic mutation is almost always neutral and sometimes detramental. How that supports evolution is absurd.

Once again we'll stick to empirical observation. Here is a list of genetic disorders. If evolution were true, then we should be able to produce a list of "observed" benefical "genetic mutations" that out number that list 100:1. Good luck because even sickle cell is neutral because it deforms the red blood cells making them less efficient at carrying oxygen, meaning that it is benefical at a cost.

Doesnt that rather depend on the selective environment and the strength of selection pressures? Again, observational evidence suggests otherwise.


No Mcstone. Your inability to produce an observed list of beneficial genetic mutations that outnumber the accumulation of deleterious mutations already falsifies your hypothesis. If you care to produce any scientific facts in this conversation, then were all ears.

Indels alone account for 12% difference and if you compare proteins they only share 20% homology.

Yes jason, this is because evolution has happened since. They still share frightening levels of genetic homology. 


Your wrong estimate of 98% genetic homology is proven wrong, but it must be evolution anyway. What a way to test a theory, falsify the prediction, and keep the theory by simply changing the prediction to fit the data. Evolution is like trying to pin jello to the wall.

Your not getting it, and i understand evolution, and genetics, alot better than you do. Micro and macro are the same thing. They have the same mechanism. I can show you evidence of macroevolution too, you say its evidence of common design:


Sure McStone. Are you now suggesting "common descent by means of protein substitution"? :( Charles Darwin must be rolling in his grave. Ofcoarse it is evidence of common desing because, the more genomes that are mapped and compared, it contradicts common descent.

http://www.evolution...indpost&p=51580









Thanks.

#39 deadlock

deadlock

    Veteran Member

  • Veteran Member
  • PipPipPipPip
  • 1,196 posts
  • Age: 43
  • Christian
  • Creationist
  • Rio de Janeiro

Posted 01 April 2010 - 05:08 AM

Fitness isnt measured as a percentage. Fitness is a measure of a given allele's proliferation relative to any other; most often as expressed in a number of offspring. Natural selection cannot produce perfect organisms (how do we even judge perfect?); that said, the fruitfly is well adapted to its niche. It will not be exposed to selective pressures strong enough to make it evolve into a new genera or evolve dramatic new body parts. Evolution works on what came previously. To evolve new limbs would require millions of years of a constant selective pressure. The fruitfly can generate billions of descendants in a single summer period. If limb number was selected for and against in these descendants, then we would expect to see limbs evolving (either more or less limbs). As it happens, the first insects were able to survive with 6 limbs; no more or less. They have been able to survive with 6 limbs. Since this time, fruitflies, and the entire insect group, havent encountered an environment (or ecological niche), which selects strongly enough to evolve more limbs.

An insect with 6 legs can walk just as easily if it had 8 legs.
An insect with 6 legs might even fly better with only 6 legs.

See what im getting at?

Evolution is all about trade-offs. If new limbs would effect survival (and natural selection can detect this), then we would predict evolution of new limbs. If not, any individual hatched with 8 limbs, by chance, would have no greater chance of reproduction than any other (perhaps reduced odds). Their particular genome would not enter the population; the allele or mutation responsible would not proliferate, and the population would not evolve; the species would not evolve. Evolution would not occur.
Again, not really. As demonstrated above, things dont have to evolve. They evolve only when necessary. When the wind is blowing the right direction.


You are completelly wrong. Selective pressure cannot guide mutations. Mutations happen randomly and Natural Selection choose what will survive. So, if no organism is perfect then it always can have its fitness improved.I can easily guess many changes that would improve the frutfly fitness.

But its the same thing. Maybe your definition is wrong.


No it´s not. If you cant understand the difference so you aren´t prepaired to discuss the matter.

#40 Guest_McStone_*

Guest_McStone_*
  • Guests

Posted 01 April 2010 - 01:22 PM

Incorrect McStone, I am in every position to lecture you in the breeding process, because you simply do not understand it.


We could do this forever scott, we really could. Lets just concede that "present" reality is in my favour (you know, things like people not coming from ribs), because it sure as hell aint in yours.

Of course you know what common design is, and as I have already shown that it totally refutes your argument. I'm not be-littleing the design, because if you knew me, then you'd know complexity, and I sure do see it. Why? It's an attribute for one that builds/ paints cars, and studies the complexity of nature. Did you know that all the animals that you present or could present will have a certain amount of common design?


Scott, if you had shown me any sort of argument - let alone a convincing one - id stop and listen. As it happens, you couldnt argue your way out of a wet paper bag.

Biologists dont study "complexity" they study "function" and how and why "function" changes. Complexity is an irrelevent side-effect.

Stop endlessly repeated YEC dogma, just for a moment. Common design means that god thought it fitting to make other animals >98% identical to humans; genetics, behaviour, conciousness... Not sure where "adam" fits in? Come to think of it, im not even sure where adam got his DNA from. It shares so much, well, with everything else. Any suggestions?

And you believe that 7 billion people came from only a few or 1, or 2 ape ancestors... yes McStone, evolution demands that these traits come from parent to offspring... So McStone... when did the breeding process contain more than Male and Female to produce an offspring??? By default and as an evolutionist you have to believe an Adam and Eve like story for apes anyways. ( of course it must have been different back then, I mean humans were randomly popping up everywhere).


Oh my god, someone please get this boy a NEW book. Seriously!!! Scott, with as much respect as one stranger can give to another (and i do respect you) you really, really dont understand anything about evolution - absolutely nothing. This is going too far, way too far. Im being completely honest with you.

Evolution does not stipulate that a given species descended from just two individuals; quite the contrary. THIS IS IMPOSSIBLE, and modern biology (except YEC for some reason) understands this. An isolated population of even 100 individuals will likely face genetic meltdown through increased homozygozity.

Scott, evolution works on POPULATIONS; whole populations. Thousands of individuals. Whilst it is true that mutation is ultimately an individual process (or at least, in a small number of individuals), a new species is not formed by one mutation. Two individuals cannot contain enough meaningful variation for their progeny to be a new species or bear some macroevolutionary development. The mutation rate in humans, for example, is around 3 mutations per individual. But not one of these mutations have had enough effect to induce speciation in homo sapiens

Evolution is a cumulative process; it builds on all prior variation. The alleles (and new genes), involved, say, in the evolution of a wing, are built up over time, from many different sources. The change happens like this:

this community of flightless birds, in this particular woodland, seem to have significantly (not necessarily massively) longer forelimbs than conspecifics. There may not be any particular reason for this lengthening, but its just natural variation - microevolution. If there is a genetic cause, and its not deleterious, then their offspring will also have slightly longer limbs. If there is a clear reproductive benefit to having slightly longer limbs (e.g. being able to signal more effectively), than we would expect the number of individuals with longer limbs to increase. This is because even minutely perceptible increases in signalling ability are highly attractive (because it is energetically more costly) to females. So, if females are selecting males with slightly longer limbs, then we would rightly predict the frequency of the responsible alleles to increase in the general population:


Females prefer longer limbs = more s@x with longer-limbed males = more offspring with longer limbs


At the same time, a community of flightless birds, from the same species but in a different patch of woodland down the road, have slightly thicker feathers. Again, this a consequence of small-scale variation (perhaps perpetuating from one individual). This wood is warmer, and consequently has denser populations of biting invertebrates. If having slightly thicker feathers helps it bearer, for example, in resisting mite infection (the mites find it harder burrowing into skin), then, again, we would predict the frequency of the responsible alleles to increase in the general population:

Individuals with slightly thicker feathers = reduced parasite loads = higher fecundity = more offspring with slightly thicker feathers.

So, we have two populations; one with slightly longer limbs, one with slightly thicker feathers. If these populations meet, and reproduce, we would see, through mendielian inheritence, some with with longer limbs and normal feathers, some with normal limbs and thicker feathers, some with both longer limbs and thicker feathers and some with neither longer limbs or thicker feathers.

If one of these combinations has its own benefit (perhaps having both thicker feathers and longer limbs increases reproductive success better than either alone), then the frequency of the responsible alleles will again increase in the general population:

Individuals with slightly longer limbs and slightly thicker feathers = reduced parasite loads and greater signalling capability = glossier feathers, higher fecundity and mating chances = more offspring with both traits.

Thus macroevolution - evolution above species level - is in actuality a long series of microevolutionary events. Individual variation in traits, latched onto the genome of an entire species. A wing is not a new appendage; its is a modified form of an arm. The same modification that is apparent between individuals.

"He has long arms" "She has small arms".

But evolution does not result from two individuals; it results from the cumulative variation in numberless individuals.
Where as some might have slightly longer arms, others might have slightly looser joints. These things all add up to something. Only when enough individuals have all this variation (and they will, if its selected for) will macroevolution occur. The change is almost inperceptible at any period in time.

Speciation might occur when a viable future population is isolated; never at any other time.

Hmmm McStone, you thought you showed me evidence of Macro-evolution, and you quite possibly thought you showed me evidence of Micro-evolution. Point in case, you only showed me a few pictures which prove nothing towards evolution and actually show signs of common design.



Scott, you dont choose to accept evolution, i get it. I just hope your happy with:

Naoh shall take two of every organism (except the ones that we think might have survived in saltwater and resisted osmotic and pressure changes many thousand times greater than today)
"Every organism lord?"
"Yes Noah. Every organism" The lord laughed.

So noah embarked on a round the world cruise, though jungle and desert, through swamps and the poles, from the highest mountain to the lowest cave. From John O' Groats to Antartica.
He started off when he was 300, and he was still at it when he was 900. He trekked, he climbed, he skied, and he caught two of every terrestrial organism; insects and athropods (and lots of other invertebrates), mammals (including other human species and apes), reptiles and dinosaurs, amphibians, birds and samples of every plant too, and of microbial soil communities, fungi and viruses, and they all lived in a big boat.

The lord went absolutely berserk on the earth.


The said thing is, its not even a charicature.

The mere fact that you claim Macro-evolution and Micro-evolution are the same thing proves that you do not infact know more about evolution than I do, sorry McStone but your posts show this.


No scott, they dont.

Your completely rejecting the empirical observation because it falsifies your assumption of antibiotic resistance being an example of evolution by genetic mutation. Would you like me to produce a list of other empirical sciences one must reject to be an evolutionists - I would be here all day



Sigh, i AM going to have to read for you.

here:
http://www.pnas.org/.../14607.abstract

here:
http://linkinghub.el...14067369390417F

here:
http://www.jstor.org/pss/30061627

here:
http://www.sciencedi...c7a308149317409

here:
http://bmb.oxfordjou...stract/54/1/207

here:
http://linkinghub.el...368764603000037

here:
http://www.sciencedi...a29a5c8e21d0c40

....... Im not doing this all night. Do yourself a favour, go on google scholar, type in mutation antibiotic resistance.
You'll find that most, indeed, all, scientific papers these days recognise that:

DNA -> amino acids -> Protein

They dont keep having to repeat it to reassure the general public that antibiotic resistance is an evolved trait (by mutation).

Your wrong estimate of 98% genetic homology is proven wrong, but it must be evolution anyway. What a way to test a theory, falsify the prediction, and keep the theory by simply changing the prediction to fit the data. Evolution is like trying to pin jello to the wall.

Sure McStone. Are you now suggesting "common descent by means of protein substitution"? Charles Darwin must be rolling in his grave. Of coarse it is evidence of common desing because, the more genomes that are mapped and compared, it contradicts common descent.


No, its not. Chimps and humans are >98% genetically identical, it doesnt mean they produce exactly the same proteins.

How does it contradict common descent? Isnt shared genetic components - including non sequencing junk - exactly what common descent predicts?


You are completelly wrong. Selective pressure cannot guide mutations. Mutations happen randomly and Natural Selection choose what will survive. So, if no organism is perfect then it always can have its fitness improved.I can easily guess many changes that would improve the frutfly fitness.


Selective pressure (same thing as natural selection) can actually guide mutations, thats what a selective pressure does. It selects mutations which promote themselves (by increasing reproductive fitness) from the background variation.

Can you? Having another set of wings, another head, these sort of things dont do anything. They dont increase reproductive fitness, if anything, they are a hinderence to it. Also, evolution is limited by what came previously.




2 user(s) are reading this topic

0 members, 2 guests, 0 anonymous users