The Scientific Impossibility of Evolution

a reply to: cooperton

You know you really don't understand zip about molecular biology. You're so wrapped up in your cult that there's no room or desire to learn anything.

Here's an article from NATURE reconfirming what I posted previously. This and many other articles wipe out your theory that there are no mutations like a wet mop. And please don't respond with one of your epigenetic diatribes because you don't understand that either.

www.nature.com...

Molecular mechanisms of antibiotic resistance
Jessica M. A. Blair, Mark A. Webber, Alison J. Baylay, David O. Ogbolu & Laura J. V. Piddock
Nature Reviews Microbiology volume 13, pages 42–51 (2015) | Download Citation

Abstract
Antibiotic-resistant bacteria that are difficult or impossible to treat are becoming increasingly common and are causing a global health crisis. Antibiotic resistance is encoded by several genes, many of which can transfer between bacteria. New resistance mechanisms are constantly being described, and new genes and vectors of transmission are identified on a regular basis. This article reviews recent advances in our understanding of the mechanisms by which bacteria are either intrinsically resistant or acquire resistance to antibiotics, including the prevention of access to drug targets, changes in the structure and protection of antibiotic targets and the direct modification or inactivation of antibiotics.

Key points
Antibiotic resistance is a global health emergency.

Resistance mechanisms exist for all current antibiotics, and few new drugs are in development.

Resistance can occur via a reduction in the intracellular concentration of drug, by target site alteration or protection and by the direct inactivation of antibiotics.

The mobilization of resistance genes into pathogens is making the treatment of severe infections challenging owing to a lack of effective antibiotics.

Our understanding of the molecular mechanisms of resistance has recently increased as a result of advances in systems biology, genomics and structural biology.

New knowledge about antibiotic resistance should be used to inform the design of novel therapeutic agents that might not be subject to, or can circumvent, mechanisms of resistance.


Here's a few more papers:

Molecular mechanism of drug resistance newly discovered in clinical isolated pathogenic bacteria
Junichi Watoshino

www.jstage.jst.go.jp...

Spontaneous mutation frequency and molecular mechanisms of Shigella flexneri fluoroquinolone resistance under antibiotic selective stress

link.springer.com...


There's a wealth of information out there which turns all your "theories" upside down. Do you ever get tired of being ignorant for the sake of your cult?

originally posted by: Phantom423
a reply to: cooperton

You know you really don't understand zip about molecular biology.

Yikes, so what part of my statement demonstrates a lack of understand of molecular biology? You have to defend these statements you say against me with actual examples, and a demonstration of why it is empirically incorrect:

Recent evidence shows that antibiotic resistance in microbes is due to epigenetic inheritance. The most compelling evidence to demonstrate this, is the fact that antibiotic resistant lines will eventually fade back to non-antibiotic resistance after multiple generations of not administering antibiotic resistance. This is evidence that it is not hard-wired mutations, but epigenetic alterations that are responsible. But don't take my word for it, I am just reiterating this paper:

"Adaptive resistance emerges when populations of bacteria are subjected to gradual increases of antibiotics. It is characterized by a rapid emergence of resistance and fast reversibility to the non-resistant phenotype when the antibiotic is removed from the medium. Recent work shows that adaptive resistance requires epigenetic inheritance... In contrast with the standard assumption, our model predicts that adaptive resistance cannot be explained by increased mutation rates."

source

originally posted by: Phantom423

Does calling other people idiots make you feel better about your self?

a reply to: cooperton

That's one paper. There are many papers which show definitive mutation. How many papers refute mutation and attribute antibiotic resistance to epigenetic changes? None - not the source you posted or any other paper I could find. As Peter said in his post here:
www.abovetopsecret.com..., you conveniently slipped over the relationship between epigenetic impact and mutational events. The paper you cited says that adaptive features are part of the process. It DOES NOT say it is the entire process, leaving out mutational changes.

Here once again you demonstrate your ignorance of molecular biology. You don't understand the intent of that paper nor can you interpret the results. Look at the references. If epigentic changes were the single cause of antibiotic resistance, the author WOULD NOT be referencing work that INCLUDES mutational changes.

I don't know who you think you're fooling - but it ain't us.

originally posted by: Phantom423
a reply to: cooperton

That's one paper. There are many papers which show definitive mutation. How many papers refute mutation and attribute antibiotic resistance to epigenetic changes? Answer: One.

The difference between a scientist and a dogmatic evolutionist is that when new evidence appears, the scientist does not hide from the evidence, they go searching to discover new ideas based on empirical data. The dogmatic evolutionist closes their ears and shouts insults.

If you searched for more papers regarding this truth, you would have found many that discovered the same result:

more proof:
"In the absence of selective pressure, resistances fell to low levels within 100 generations of growth"



In other words, it is the variable levels of the expression of genes that creates the antibiotic resistant effect.


further demonstration
"Overall, this work provides evidence for a complex nongenetic response, encompassing shifts in gene expression and gene expression variability, which underlies adaptive resistance."

a reply to: cooperton

Once again, you demonstrate your ignorance - read the entire paper - what does the conclusion say? It does not say that epigenetic changes are the single cause of antibiotic resistance. You can slice it any way you want. It simply does not say that.

a reply to: cooperton

"Coincident with the emergence of resistance was the appearance of a previously cryptic energy-dependent efflux system for tetracycline. The expression of resistance phenotypes and the tetracycline efflux system were temperature sensitive at 42 degrees C."

Do you know what an efflux system is?

originally posted by: Phantom423
a reply to: cooperton

Once again, you demonstrate your ignorance - read the entire paper - what does the conclusion say? It does not say that epigenetic changes are the single cause of antibiotic resistance. You can slice it any way you want. It simply does not say that.

It's directly in the abstract, claiming that it is alterations in genetic expression, and not alterations to the genes themselves, that are resulting in the change:

further demonstration
"Overall, this work provides evidence for a complex nongenetic response, encompassing shifts in gene expression and gene expression variability, which underlies adaptive resistance."

These are not my words, these are their words.

originally posted by: Phantom423
a reply to: cooperton

Do you know what an efflux system is?

Yes it is the degree of expression of these efflux pumps that are primarily responsible for antibiotic resistance. Essentially the microbe increases the number of these efflux pumps (through inheritable epigenetic alteration) which allows a higher degree of detoxification capabilities, and thus antibiotic resistance. This is an energetically burdensome increase in expression, so once the antibiotic threat is removed, the epigenetic markers return the genetic expression of the efflux pumps to baseline levels

a reply to: cooperton
Here's a link to the Antibiotic Resistance Gene Database. Have a ball finding a single paper that says that epigenetic changes are responsible for antibiotic resistance.


ARDB-Antibiotic Resistance Genes Database

Introduction
Antibiotic Resistance Genes Database
Resistance Genes Search Database
Resistance Genes BLAST Database
Mutational Resistance Identification
Search
Analysis & Tools
ardb.cbcb.umd.edu...



Introduction
Efforts on identifying new antibiotics were once a top research and development priority among pharmaceutical companies. However, the treatment of infections is increasingly compromised by the ability of bacteria to develop resistance to antibiotics through mutation or acquisition of resistance genes. Treatment failure can have serious consequences in patients with infections of some pathogens, such as methicillin-resistant Staphyococcus aureus or vancomycin-resistant Enterococcus. Antibiotic resistance genes are also potentially be used by bio-terrorists in genetically modified organisms. In order to facilitate identification and characterization of antibiotic resistance genes, we have created a manually curated database (ARDB) unifying most of the publicly available resistance genes and related information. Resistance genes are further categorized to resistance types by their resistance profiles and sequence similarity. Each gene or type is annotated with rich information, including resistance profile, resistance mechanism, resistance requirement, epidemiology, GO term, COG and CDD. ARDB allows the user to browse and search antibiotic resistance information from a view of gene, type, organism and antibiotic. Regular BLAST and RPS-BLAST tools would help the user to identify and annotate new potential resistance genes by blasting against ARDB DNA or protein sequences. ARDB can help user to identify mutational resistance for 12 antibiotic target genes by BLAST. Currently, ARDB contains resistance information for 13293 genes, 377 types, 257 antibiotics, 3369 species and 124 genera.

a reply to: cooperton

Here's another one:

aac.asm.org...


The Comprehensive Antibiotic Resistance Database


Individual Antibiotic Resistance Ontology (ARO) terms in the CARD have been associated with specific computational tools and models via Chado's cvtermprop table. The majority of ARO terms have text mining of regular expressions (RegEx) to correctly assign ARO terms to molecular sequences imported into the CARD based on the text annotations provided in the GenBank records. These RegEx entries are actively curated. The resulting tagged sequences, particularly those of polypeptides, form the underlying BLAST database used by the Resistance Gene Identifier (RGI) to identify antibiotic resistance genes in raw sequence data as outlined below. For antibiotic resistance involving specific mutations (i.e., single nucleotide polymorphisms [SNPs]), ARO terms are additionally associated with hidden Markov models (HMMs), alignment reference sequences, and position-specific SNPs for positional alignment of sequences and detection of position-specific SNPs. HMMs are constructed by the CARD curators and utilized by the CARD software using the HMMer software (19).

a reply to: cooperton




www.ncbi.nlm.nih.gov...
Detection of antimicrobial resistance genes associated with the International Space Station environmental surfaces
C. Urbaniak,1 A. Checinska Sielaff,1,5 K. G. Frey,2 J. E. Allen,3 N. Singh,1 C. Jaing,3 K. Wheeler,4 and K. Venkateswarancorresponding author1
Author information ► Article notes ► Copyright and License information ► Disclaimer



Abstract
Antimicrobial resistance (AMR) is a global health issue. In an effort to minimize this threat to astronauts, who may be immunocompromised and thus at a greater risk of infection from antimicrobial resistant pathogens, a comprehensive study of the ISS “resistome’ was conducted. Using whole genome sequencing (WGS) and disc diffusion antibiotic resistance assays, 9 biosafety level 2 organisms isolated from the ISS were assessed for their antibiotic resistance. Molecular analysis of AMR genes from 24 surface samples collected from the ISS during 3 different sampling events over a span of a year were analyzed with Ion AmpliSeq™ and metagenomics. Disc diffusion assays showed that Enterobacter bugandensis strains were resistant to all 9 antibiotics tested and Staphylococcus haemolyticus being resistant to none. Ion AmpliSeq™ revealed that 123 AMR genes were found, with those responsible for beta-lactam and trimethoprim resistance being the most abundant and widespread. Using a variety of methods, the genes involved in antimicrobial resistance have been examined for the first time from the ISS. This information could lead to mitigation strategies to maintain astronaut health during long duration space missions when return to Earth for treatment is not possible.

a reply to: cooperton
card.mcmaster.ca...

The Comprehensive Antibiotic Resistance Database
A bioinformatic database of resistance genes, their products and associated phenotypes.

3999 Ontology Terms, 2727 Reference Sequences, 1210 SNPs, 2446 Publications, 2776 AMR Detection Models

Resistome predictions: 79 pathogens, 4264 chromosomes, 4780 plasmids, 66402 WGS assemblies, 146946 alleles

The CARD is a rigorously curated collection of characterized, peer-reviewed resistance determinants and associated antibiotics, organized by the Antibiotic Resistance Ontology (ARO) and AMR gene detection models.

a reply to: cooperton

Antibiotic resistance genes from the environment: a perspective through newly identified antibiotic resistance mechanisms in the clinical setting

www.sciencedirect.com...

Abstract
Soil bacteria may contain antibiotic resistance genes responsible for different mechanisms that permit them to overcome the natural antibiotics present in the environment. This gene pool has been recently named the ‘resistome’, and its components can be mobilized into the microbial community affecting humans because of the participation of genetic platforms that efficiently facilitate the mobilization and maintenance of these resistance genes. Evidence for this transference has been suggested or demonstrated with newly identified widespread genes in multidrug-resistant bacteria. These resistance genes include those responsible for ribosomal methylases affecting aminoglycosides (armA, rtmB), methyltransferases affecting linezolid (cfr) or plasmid-mediated efflux pumps conferring low-level fluoroquinolone resistance (qepA), all of which are associated with antibiotic-producing bacteria. In addition, resistance genes whose ancestors have been identified in environmental isolates that are not recognized as antibiotic producers have also been recently detected. These include the qnr and the blaCTX genes compromising the activity of fluoroquinolones and extended-spectrum cephalosporins, respectively. The application of metagenomic tools and phylogenetic analysis will facilitate future identification of other new resistance genes and their corresponding ancestors in environmental bacteria, and will enable further exploration of the concept of the resistome as being a unique reservoir of antibiotic resistance genes and genetic elements participating in resistance gene transfer.

a reply to: cooperton

Come back when you've read all that.

a reply to: cooperton

It is NOT what the paper is saying. It is also a solitary paper, not a body of work. QED you need to go back to university.

originally posted by: Phantom423
a reply to: cooperton
Here's a link to the Antibiotic Resistance Gene Database. Have a ball finding a single paper that says that epigenetic changes are responsible for antibiotic resistance.

originally posted by: Noinden
a reply to: cooperton

It is NOT what the paper is saying. It is also a solitary paper, not a body of work. QED you need to go back to university.

You guys are zealots. The paper I gave demonstrated the epigenetic facet of antibiotic resistance:

"Adaptive resistance emerges when populations of bacteria are subjected to gradual increases of antibiotics. It is characterized by a rapid emergence of resistance and fast reversibility to the non-resistant phenotype when the antibiotic is removed from the medium. Recent work shows that adaptive resistance requires epigenetic inheritance...In contrast with the standard assumption, our model predicts that adaptive resistance cannot be explained by increased mutation rates."

source

Epigenetic control increases the expression of efflux pumps to allow greater detoxification rates - this can be passed on to subsequent generations. It's ironic that you guys are the ones who are anti-science whenever it disrupts your beloved belief system.

a reply to: cooperton

“You guys are zealots. The paper I gave demonstrated the epigenetic facet of antibiotic resistance”

What are the other “facets”? How about mutation.

“The empirical evidence shows that epigenetic inheritance is the source of antibiotic resistance. If this is the case, then already set genes are the cause of the resistance, and not some novel genetic mutation. This is demonstrated by the fact that the population returns to non-resistance after the antibiotic is removed. Think for your self, and actually analyze those implications.”

Neither your source, nor any other reference material which you posted say that. However, all the papers which I posted cite specific, unique mutations associated with antibiotic resistance.
Of course, we don't expect that you'll read those papers any time soon – they're above your pay grade.

“I can understand you disagree with my conclusions that this is evidence against evolutionary theory, but you can't argue that the paper is demonstrating that population adaptation is orchestrated by epigenetic inheritance.”

No, the paper did NOT characterize epigenetic inheritance as the only causal agent for antibiotic resistance. Recommendation: Take an English language course.

“Obviously evolutionary theorists will move the goalposts again, because "evolution did it". No real empirical due process, just the magical wand. "it was done, therefore evolution did it" “

Please link to a quote posted by me or anyone else who said: “evolution did it”, “no real empirical due process”, “just the magical wand” or “it was done, therefore evolution did it”.

“The quick return to non-resistance demonstrates that it is epigenetic inheritance, and not classical mutation inheritance as theorized by evolutionists. Don't go on about other topics, focus. The study shows that it is epigenetic inheritance, and even succinctly shows that it is the methylation of a particular efflux pump. It is totally epigenetic - no new genes, no mutations. If this is how adaptation works, then it relies totally on genes that are already present in an organism and cannot go outside those bounds.”

Then what are those gene mutations cited in the numerous papers I posted? Are they all wrong? Did you repeat their experiments? Did you write them a letter telling them that they don't know what the hell they're doing?

“They call it evolution but it is not evolution in the traditional sense, or any sense for that matter. There are no mutations, which is the core tenet of how novel traits arise according to evolutionary theory. They can call it evolution all they want, but they proved otherwise. They demonstrated Lamarckism, which is antithetical to evolutionary theory. Epigenetics work on already existent genes, any generational alterations due to epigenetics are reversible, and therefore could not culminate in new species, because it is always working off the original gene template.

What is a mutation?

“Yeah the common misconception is that a mutation in a gene, and voila, you now have wings, or half wings, or the first bone in creating a wing. But a genetic mutation would only alter the protein that it codes for, and the symphony of effects which that protein has. This makes it troublesome to say evolution occurs through genetic mutations, because the old gene gets ruined, along with the multitude of other functions that it had in synchrony with the rest of the physiology of the organism. The implications of this cannot be realized if you are zealously attached to the idea that "evolution did it". It is an anchor to the progress of philosophical thought.”

The old gene gets ruined?? OMG.................

“Here's a dilemma: which came first, the protein coding gene, or the factors that maintains its homeostatic expression?”

That question symbolizes how little you understand about molecular biology or anything else in related sciences. Not worthy of an answer, however.

originally posted by: Phantom423

“Here's a dilemma: which came first, the protein coding gene, or the factors that maintains its homeostatic expression?”


Not worthy of an answer, however.

No, it is desperately in need of an answer. You nor anyone else can explain how the gene and its homeostatic mechanisms could evolve in a synchronized manner. If you could actually answer that dilemma, you would be one of the greatest biological scientists of all time.

No, the paper did NOT characterize epigenetic inheritance as the only causal agent for antibiotic resistance. Recommendation: Take an English language course.

The fact that they found epigenetic inheritance as the causal agent for antibiotic resistance is literally the title of the paper

"Adaptive Resistance in Bacteria Requires Epigenetic Inheritance, Genetic Noise, and Cost of Efflux Pumps"

Are you anti-science now?

a reply to: cooperton

Ahh so reading comprehension is Zealotry is it? Yeah try again.

a reply to: cooperton

The "dilemma" as you put it, is reproduced day after day in labs around the world. There is no mystery here. The only mystery is why you're even interested in a subject that completely eludes you and have no intuitive capability for.