Potential falsifications of the theory of evolution

If an organism were to simply start increasing its random mutation rate-where would the net gain come from?

If every type of mutation is equally likely, why would you ever expect this to be a winning formula?

Organism would be receiving lethal mutations left and right, so you would quickly expect to see a decrease in the number of viable organisms, not an increase.

It would be as if you had a new contagious disease enter the premises of a large factory of quarantined workers, and you didn't have a cure yet, but you had a big warehouse full of chemicals for making medicines. So you told everyone in the building, all 1000 people to just start eating all the chemicals around, and hopefully one of you will stumble upon one that is useful. In the meantime most everyone who ate the chemicals would die from ingesting the wrong toxins. Maybe someone would get lucky eventually, and eat just the right mix of things, but that would be extremely inefficient, and very unlikely.

We are not seeing extreme inefficiencies, we are seeing extreme efficiencies. The organisms he is talking about aren't experiencing rapid declines and sudden drops in the fitness levels of the population as one would expect from your scenario ...

Your premise just doesn't stand up to reason.

Bolder-dash writes:I can not respond- because that will of course cause you to once again slobber something unsubstantiated, asinine, insidious and unimaginative; and that will be my fault for forcing you to attempt to write something.I think I am allowed to say "Go read a book, dodo." though.That appears to be an approved retort here.

I think I am allowed to say "Go read a book, dodo." though.

I can not respond ...

I think I am allowed to say "Go read a book, dodo." though.

It would be much more appropriate to point to a peer reviewed research paper, preferrably a primary source and not a review article. If you think mutations are non-random then find papers that specifically demonstrate this non-random nature complete with the actual data from experiments. This is exactly what I did to demonstrate that the genetic engineering systems in E. coli produce a higher rate of random mutations through upregulation of DNA polymerase IV, if you need an example.

I believe that Shapiro in "Mobile DNA and evolution in the 21st century", Mobile DNA 2010, 1:4 has stated that that biasing retrovirus insertion upstream of coding regions has shown that certain changes are non-random.

I believe that Shapiro in "Mobile DNA and evolution in the 21st century", Mobile DNA 2010, 1:4 has stated that that biasing retrovirus insertion upstream of coding regions has shown that certain changes are non-random.

Taq writes:PLoS One. 2010 May 27;5(5):e10862.Competition of Escherichia coli DNA polymerases I, II and III with DNA Pol IV in stressed cells.
Hastings PJ, Hersh MN, Thornton PC, Fonville NC, Slack A, Frisch RL, Ray MP, Harris RS, Leal SM, Rosenberg SM.Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, United States of America. hastings@bcm.eduAbstract
Escherichia coli has five DNA polymerases, one of which, the low-fidelity Pol IV or DinB, is required for stress-induced mutagenesis in the well-studied Lac frameshift-reversion assay. Although normally present at approximately 200 molecules per cell, Pol IV is recruited to acts of DNA double-strand-break repair, and causes mutagenesis, only when at least two cellular stress responses are activated: the SOS DNA-damage response, which upregulates DinB approximately 10-fold, and the RpoS-controlled general-stress response, which upregulates Pol IV about 2-fold. DNA Pol III was also implicated but its role in mutagenesis was unclear. We sought in vivo evidence on the presence and interactions of multiple DNA polymerases during stress-induced mutagenesis. Using multiply mutant strains, we provide evidence of competition of DNA Pols I, II and III with Pol IV, implying that they are all present at sites of stress-induced mutagenesis. Previous data indicate that Pol V is also present. We show that the interactions of Pols I, II and III with Pol IV result neither from, first, induction of the SOS response when particular DNA polymerases are removed, nor second, from proofreading of DNA Pol IV errors by the editing functions of Pol I or Pol III. Third, we provide evidence that Pol III itself does not assist with but rather inhibits Pol IV-dependent mutagenesis. The data support the remaining hypothesis that during the acts of DNA double-strand-break (DSB) repair, shown previously to underlie stress-induced mutagenesis in the Lac system, there is competition of DNA polymerases I, II and III with DNA Pol IV for action at the primer terminus. Up-regulation of Pol IV, and possibly other stress-response-controlled factor(s), tilt the competition in favor of error-prone Pol IV at the expense of more accurate polymerases, thus producing stress-induced mutations. This mutagenesis assay reveals the DNA polymerases operating in DSB repair during stress and also provides a sensitive indicator for DNA polymerase competition and choice in vivo.

I believe that Shapiro in "Mobile DNA and evolution in the 21st century", Mobile DNA 2010, 1:4 has stated that that biasing retrovirus insertion upstream of coding regions has shown that certain changes are non-random.

Shapiro writes:That coregulated loci have arisen in this way during evolution has been documented in mice, where similar retroviral promoters initiate transcription of different loci in oocytes and preimplantation embryos [71].

You have understood my position pretty well. I have written a book entitiled "Evolution: A View from the 21st Century," and I expect it to come out this summer or fall. That will expand on my 2010 review.and lay out many other considerations. Note that you can also view a public lecture I gave in October on "Revisiting evolution in the 21st Century" at James A. Shapiro - Revisiting evolution in the 21st Century on Vimeo .I will answer your questions below.Has NATURAL GENETIC ENGINEERING changed the modern Darwinian theory of evolution as we know it today?Of course. Going from random accidents to regulated biochemical systems as the source of genetic variation is a fundamental change. It allows us to understand how outside events can trigger change (see table in my 2006 "Genome Informatics" article), makes it clear how combinatorial change can occur using established adaptive components (e.g. protein domains, regulatory modules), and provides a way to investigate what kind of heuristic guidance may be operating in genome change.Is the modern Darwinian theory outdated and being replaced by Natural Genetic Engineering? And if so in both micro and macro evolution?Yes, it is outdated. What would make Darwinian Evolution the one exceptional case of theoreticalr immortality in the history of science? Darwin knew nothing of horizontal transfer, whole genome doublings or natural genetic engineering capabilities and neglected symbiosis. His ideas were based strictly on vertical inheritance, and he insisted on gradualism. Neither position is supported by genome sequencing.Do you have an opinion whether mutations are random with respect to fitness per the modern Darwinian Theory?I gave examples in my 2010 article (e.g. biasing retrovirus insertion upstream of coding regions) where certain changes are non-random with respect to their potential biological utility.Do you have an opinion whether natural selection per the modern Darwinian Theory is a primary means of evolution today?The neo-Darwinian Modern Synthesis could not account for the evolution of antibiotic resistance in the latter 20th Century. It also does not explain much in the genome sequence record.Can genetic change come about other than by means of random mutation and natural selection?The genome sequence databases are full of examples, and I cite many of them in my papers.When you use the term non-random do you mean evolution can be non random in regards to fitness?Evolution is a process that produces adaptive inventions with a spontaneous probability of occurrence that is vanishingly small. How can that be anything other than non-random? Remember, non-random and strictly deterministic are not synonymous. There can be tremendous variability within non-random processes, such as the generation of distinct antibody specificities.When you use the term intelligent do you mean that the cells in some way are evolving w/o random mutations?I try to avoid the term "intelligent" because it carries too much philosophical and anthropocentric baggage. I prefer terms like cognitive or sentient, meaning based up the acquisition and utilization of information. There are many such processes we can now specify in molecular detail.Without natural selection?Selection is unavoidable, but in my view it is a purifying rather than creative process.When you use the term sentient do you mean that the cells are capable of making decisions that affect their evolution?Yes, such as when they activate mobile elements in response to DNA damage, starvation or interspecific hybridization.

Here's the cited paper.71. Peaston AE, Evsikov AV, Graber JH, de Vries WN, Holbrook AE, Solter D, Knowles BB: Retrotransposons regulate host genes in mouse oocytes and
preimplantation embryos. Dev Cell 2004, 7:597-606.

Do you have an opinion whether mutations are random with respect to fitness per the modern Darwinian Theory?I gave examples in my 2010 article (e.g. biasing retrovirus insertion upstream of coding regions) where certain changes are non-random with respect to their potential biological utility.

When you use the term non-random do you mean evolution can be non random in regards to fitness?Evolution is a process that produces adaptive inventions with a spontaneous probability of occurrence that is vanishingly small. How can that be anything other than non-random? Remember, non-random and strictly deterministic are not synonymous. There can be tremendous variability within non-random processes, such as the generation of distinct antibody specificities.

Selection is unavoidable, but in my view it is a purifying rather than creative process.

When you use the term sentient do you mean that the cells are capable of making decisions that affect their evolution?Yes, such as when they activate mobile elements in response to DNA damage, starvation or interspecific hybridization.

At the same time, they also have a higher chance of causing deleterious change, but he doesn't mention that.

Like new mutations produced by any mutator mechanism, the majority of new TE-induced mutations are expected to be deleterious to their hosts. Those mutations that survive over long periods of evolutionary time are expected to be a small subsample of newly induced mutations.

On average, TEs that insert within the exons of genes are most likely to result in null mutations because of the sensitivity of these regions to frame shift mutations and the lack of tolerance of highly conserved regions to most mutations of any kind. However, those mutations that are not simply inviable can provide interesting and sometimes spectacular phenotypic variability.