There is no selective advantage demonstrated for large populations given the parameters in the study. More mutations translate into less of a selective advantage, that is why they are deletreous.
this makes no sense, and is certainly not a conclusion of the paper
no, its a simple and obvious fact to those who can read and understand the scientific literature
I can't decide if you are really reading this article or just writing the first thing that comes to mind.
no, i'm accurately portraying it, to counter your bizzare conclusions
With all the documentation that goes into a paper like this I would suggest you follow the bibliography. I did and found that this is perfectly consistant with related studies, no selective advantage so it is still an unsolved mystery why such a transition would occure. The obvious conclusion, except to the most adamant apologist for Darwinian evolution, is that it never happened.
thats a ridiculous conclusion, for at least two major reasons
1) organisms capable of both sexual and asexual reproduction actually do reproduce sexually - so there MUST be some advantage
2) the paper only adresses a single hypothesis on the reasons for the origin of sex
The evidence is abundant and yet you have yet to offer a shred of proof. This is exactly what you guys accuse creationists of and you are worse.
yeast genome duplication, mosquito esterase duplication, hox expansion, the nylonase bacteria, the drosophila sperm axoneme protein etc..
you've clearly figured out how to use pubmed - go search
You cited nothing, ever, not even once.
1: Nature. 2004 Apr 8;428(6983):617-24. Epub 2004 Mar 07. Related Articles, Links
Click here to read
Proof and evolutionary analysis of ancient genome duplication in the yeast Saccharomyces cerevisiae.
Kellis M, Birren BW, Lander ES.
The Broad Institute, Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts 02138, USA.
manoli@mit.edu
Whole-genome duplication followed by massive gene loss and specialization has long been postulated as a powerful mechanism of evolutionary innovation. Recently, it has become possible to test this notion by searching complete genome sequence for signs of ancient duplication. Here, we show that the yeast Saccharomyces cerevisiae arose from ancient whole-genome duplication, by sequencing and analysing Kluyveromyces waltii, a related yeast species that diverged before the duplication. The two genomes are related by a 1:2 mapping, with each region of K. waltii corresponding to two regions of S. cerevisiae, as expected for whole-genome duplication. This resolves the long-standing controversy on the ancestry of the yeast genome, and makes it possible to study the fate of duplicated genes directly. Strikingly, 95% of cases of accelerated evolution involve only one member of a gene pair, providing strong support for a specific model of evolution, and allowing us to distinguish ancestral and derived functions.
PMID: 15004568 [PubMed - indexed for MEDLINE]
1: Genetica. 2003 Jul;118(2-3):233-44. Related Articles, Links
Origin and evolution of a new gene expressed in the Drosophila sperm axoneme.
Ranz JM, Ponce AR, Hartl DL, Nurminsky D.
Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 33143, USA.
Sdic is a new gene that evolved recently in the lineage of Drosophila melanogaster. It was formed from a duplication and fusion of the gene AnnX, which encodes annexin X, and Cdic, which encodes the intermediate polypeptide chain of the cytoplasmic dynein. The fusion joins AnnX exon 4 with Cdic intron 3, which brings together three putative promoter elements for testes-specific expression of Sdic: the distal conserved element (DCE) and testes-specific element (TSE) are derived from AnnX, and the proximal conserved element (PCE) from Cdic intron 3. Sdic transcription initiates within the PCE, and translation is initiated within the sequence derived from Cdic intron 3, continuing through a 10 base pair insertion that creates a new splice donor site that enables the new coding sequence derived from intron 3 to be joined with the coding sequence of Cdic exon 4. A novel protein is created lacking 100 residues at the amino end that contain sequence motifs essential for the function of cytoplasmic dynein intermediate chains. Instead, the amino end is a hydrophobic region of 16 residues that resembles the amino end of axonemal dynein intermediate chains from other organisms. The downstream portion of Sdic features large deletions eliminating Cdic exons v2 and v3, as well as multiple frameshift deletions or insertions. The new protein becomes incorporated into the tail of the mature sperm and may function as an axonemal dynein intermediate chain. The new Sdic gene is present in about 10 tandem repeats between the wildtype Cdic and AnnX genes located near the base of the X chromosome. The implications of these findings are discussed relative to the origin of new gene functions and the process of speciation.
1: Proc Natl Acad Sci U S A. 2004 Nov 8 [Epub ahead of print] Related Articles, Links
Click here to read
Evolving protein functional diversity in new genes of Drosophila.
Zhang J, Dean AM, Brunet F, Long M.
Department of Ecology and Evolution, University of Chicago, Chicago, IL 60637.
The mechanism by which protein functional diversity expands is an important evolutionary issue. Studies of recently evolved chimeric genes permit direct investigation of the origin of new protein functions before they become obscured by subsequent evolution. Found in several African Drosophila species, jingwei (jgw), a recently evolved gene with a domain derived from the still extant short-chain alcohol dehydrogenase (ADH) through retroposition, provides an opportunity to examine this previously undescribed process directly. We expressed JGW proteins in a microbial expression system and, after purification, investigated their enzymatic properties. We found that, unexpectedly, positive Darwinian selection for amino acid replacements outside the active site of JGW produced a novel dehydrogenase with altered substrate specificity compared with the ancestral ADH. Instead of detoxifying and assimilating ethanol like its Adh parental gene, we observe that JGW efficiently utilizes long-chain primary alcohols found in hormone and pheromone metabolism. These data suggest that protein functional diversity can expand rapidly under the joint forces of exon shuffling, gene duplication, and natural selection.
PMID: 15534206 [PubMed - as supplied by publisher]
hows that for starters
Mutations are eliminated by natural selection, they are not accumulated. You are continueing to talk in circles which makes my part in this discussion so easy it's embarassing.
utter garbage that even a first year biology student could refute
natural selection acts on phenotype, not genotype - so it depends completely on what effect on phenotype a given mutation has, as to its fate decided by selection
Get this through you're head, no selective advantage = extinction. Read Darwins Origin of Species or anything on the modern synthesis...anything at all.
get this through your head - sexually reproducing species aren't extinct - so what you think is so obvious is quite obviously wrong
the paper DID NOT demonstrate that sex provides no selective advantage, it demonstrated that synergistic epistasis is not a selective advantage
again, this is simply you extrapolating unwarranted conclusions
I did address that point and the antagonistic effects equal the synergestic one blowing you're argument to pieces.
it does nothing to my argument - sex exists, and occurs - so clearly you've made some bad conclusions somewhere along the way
whether epistasis is antagonistic or synergistic really doesn't adress the fact that sex occurs in organisms capable of both types of reproduction
What part of natural selection is too hard for you to understand. Try to concentrate...no selective advantage = extinction.
try to understand mark
-the paper did not say there was no selective advantage in sex
-organisms which reproduce sexually are not extinct
-no selective advantage for any particular trait does not = extinct, because a trait may be selectively neutral and also because selection acts on the whole phenotype, not just one particular trait, meaning that populations can (and actually do) carry selectively deleterious traits
Logic requires a yes or no response and the selective advantage question for the transition from asexual to sexual evolution of living organisms is no.
no IT ISN'T
this paper only answers no to the following question
"Is synergistic epistasis as an explanation for the selective advantage for sex?"
Thus no demonstrated mechanism which is what I would expect for conceptual theory that is based in presumption.
you've confused "mechanism" for "selective advantage". They're not the same thing
Oh right, you prefer the ones that keep producing one null hypothesis after another.
I prefer the theory which has numerous confirmed hypotheses and predictions, as opposed to the one which makes neither
I understand the science, the paper and I know why you are not interested in the actual evidence. There has not been one shred of evidence offered to counter me and I had a ton of stuff to support what I am saying. What happened is no one could counter the argument so I just let you guys argue in circles.
You clearly don't understand the paper, or even the process of science
you don't really have an argument, you have a bunch of muddled up assertions
That's right most mutations are either deletreous or harmfull. The rare beneficial mutation is not capable of making evolutionary changes on a macro scale.
this is one of those muddled up assertions
And again the hypothesis is found to be null so we have no demonstrated mechanism for evolutionary change
again, this is an unwarranted generalization from a paper which is specifically only dealing with a question of selective advantage for a particular trait - and not the mechanism by which it arose
I am glad you are enjoying the discussion, for me its fish in a barrel.
everybody here who knows the slightest bit about biology and genetics knows that you're completely out of your depth in these arguments mark
Because there are just as many antagonisitic ones as synergestic ones.
confirming that you are erroneously referring to mutations as antagonistic or synergistic, and furthermore, confusing antagonistic and synergistic with harmful and beneficial respectively
Right, and so we can discard deleterious mutations as having what it takes to evolve single celled organisms from asexual to sexual organisms.
yes of course mark - sometimes the sun shines through the clouds and theres a ray of logic and coherence in your posts
nobody was ever suggesting that deleterious mutations were responsible for the evolution of sex
Mendel's laws are the exact opposite of the Darwinian concept of a single common ancestory. The key difference is in demonstrated proof, stasis is the rule and evolution as it is drawn up in evolutionary trees is a myth.
mendel's laws are about allelic inheritance, they're not really the opposite of evolution - in fact, they provide a mechanism for evolution to occur
stasis is not the rule in evolution
and mendel's laws do not actually hold in real life
It should be embarassing that the only substantive proof for evolution is found in the work of a creationist and the largest bundle of null hypothesis is being produced by an agnostic secularist.
its embarassing that your knowledge of genetics hasn't managed to make it past mendel - else you'd know that substantive proof of evolution is provided by modern genetics
Darwin was wrong and this is being proven in so many ways it boggles the mind that his model is so popular amoung secular apologists for evolution.
you're talking out of your nether regions - its utterly amazing that you think you have more insight into evolution that vastly more qualified biologists