About New Lamarckian Synthesis Theory

Because it has been falsified by the evidence. There is nothing to protect. The evidence points to random mutations which is why we conclude that mutations are random. You, on the other hand, ignore the evidence and keep pushing guided mutations which are not supported by evidence. Why do you do that? Epigenetic inheritance does not change DNA sequence nor does it explain the differences between species (e.g. the differences between humans and chimps). I really don't see how it is on topic in a discussion dealing with the question of random vs. guided mutations. Mutations are caused by mechanisms that are incapable of determining if the mutation will be harmful, neutral, or beneficial. That is why these mechanisms will produce mutations that confer antibiotic resistance when no antibiotics are present. Hardly. You really need to read this paper:http://www.genetics.org/content/28/6/491.full.pdf+htmlLuria and Delbruck tested for both random and guided mutations. The results of the experiment pointed to random mutations. The somatic hyper-mutation that produced those sequences were random with respect to fitness. That is epigenetics. It does not involve a change in DNA sequence.

Beneficial mutations occur in the absence of the environment in which they are beneficial. For example, mutations conferring antibiotic and bacteriophage resistance occur in the absence of antibiotics and bacteriophage. Even more, we can study the exact mechanisms that are producing these mutations. In the following study, they measured the fit between the incoming nucleotide and polymerase responsible for extinding the DNA molecule. They found that there is a loose fit between the substrate and the enzyme resulting in the random production of mutations.

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Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):15803-8. Epub 2005 Oct 25.

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Probing the active site tightness of DNA polymerase in subangstrom increments.

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Kim TW, Delaney JC, Essigmann JM, Kool ET.
SourceDepartment of Chemistry, Stanford University, Stanford, CA 94305-5080, USA.

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Abstract
We describe the use of a series of gradually expanded thymine nucleobase analogs in probing steric effects in DNA polymerase efficiency and fidelity. In these nonpolar compounds, the base size was increased incrementally over a 1.0-A range by use of variably sized atoms (H, F, Cl, Br, and I) to replace the oxygen molecules of thymine. Kinetics studies with DNA Pol I (Klenow fragment, exonuclease-deficient) in vitro showed that replication efficiency opposite adenine increased through the series, reaching a peak at the chlorinated compound. Efficiency then dropped markedly as a steric tightness limit was apparently reached. Importantly, fidelity also followed this trend, with the fidelity maximum at dichlorotoluene, the largest compound that fits without apparent repulsion. The fidelity at this point approached that of wild-type thymine. Surprisingly, the maximum fidelity and efficiency was found at a base pair size significantly larger than the natural size. Parallel bypass and mutagenesis experiments were then carried out in vivo with a bacterial assay for replication. The cellular results were virtually the same as those seen in solution. The results provide direct evidence for the importance of a tight steric fit on DNA replication fidelity. In addition, the results suggest that even high-fidelity replicative enzymes have more steric room than necessary, possibly to allow for an evolutionarily advantageous mutation rate.

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Guess what gene they used to measure the mutation rate? That would be the tonB gene, the gene that was responsible for bacteriophage resistance in the Luria and Delbruck paper that I referenced above. We understand down to the angstrom why mutations are random. What do you have to show for guided mutations? The Baldwin effect is selection only. It does not deal with how mutations occur. The Baldwin effect results in selection for variants that are able to learn a behavior more quickly or more effectively. The production of those variants is still reliant on random mutations. Real scientists do not push ideas that are not backed by evidence, and even worse, ideas that are contradicted by evidence. They also do not confuse epigenetics and random mutagenesis as you do.Edited by Taq, : No reason given.

First off, "deep DNA" is a throw away term. It really doesn't mean anything. There is no such thing as shallow and deep DNA. There is just DNA.Second, you are not addressing the real problem. Why are chimps and humans different? Why are humans and horses different? I can tell you right now that these differences are NOT due to differences in DNA methylation or histone packaging. Epigenetics is not an explanation for the problem that we are trying to answer.So why are humans and horses different? It is because the DNA sequence of our genomes is different. Therefore, your synthesis must explain how DNA sequence changes over time. So far, you have failed to explain this. Epigenetics is completely off topic unless you can show how it influences sequence changes over time.

In order to have a theory, you need to show how it DOES happen. It is your theory. You need to present the evidence that it does happen as you claim it does. How does epigenetics guide mutations so that they are not random with respect to fitness?

Science is always open to new evidence. The history of modern science shows this to be true.What we need now is that evidence. What scientists are really interested in his how nature DOES work, not how it COULD work. You need to bring evidence to bear. You need to demonstrate your claims, not merely make them. More importantly, you need to have a better understanding of modern genetics so you can know when your ideas have already been falsified.

Scientists accept the theory of random mutations because that is what the evidence indicates:http://www.genetics.org/content/28/6/491.full.pdf+htmlhttp://profiles.nlm.nih.gov/ps/access/BBABFJ.pdfThey don't blindly accept random mutations. Notice how I posted two peer reviewed papers that contain evidence that backs my claims. Notice how you do not do this. They are many, but you refuse to even acknowledge the ones that I do put forth. When will be reviewing the Luria and Delbruck paper or the Lederberg's paper? There is no difficulty in determining that mutations are random in metazoans, you just refuse to go over the evidence.

Fair enough. The Luria and Delbruck paper along with the Lederbergs' paper linked above are the classic experiments demonstrating how mutations are random. This was done in prokaryotes, but the same processes that produce mutations in prokaryotes are occuring in eukaryotes. This includes chemical mutagenesis, incorporation of the incorrect base during replication, radiation, recombination, and indels.For metazoans with long generation times it is difficult to do these same experiments. However, we can use genomic comparisons and the appearance of disease alleles to help us reach a conclusion. First, we observe that the processes of mutagenesis in metazoans produces deleterious mutations. These processes are the same ones that produce beneficial mutations. If mutations are being guided, then why do we get detrimental mutations. Second, when we compare genomes between species we observe that there are many neutral changes that have occurred since common ancestry. These changes are seen in pseudogenes and introns, to name two commonly used examples. Once again, the same mechanisms that produce neutral mutations and detrimental mutations are also producing beneficial mutations.

The same processes that produce detrimental and neutral mutations are the same processes that produce beneficial mutations. They are one in the same. If they are random processes when they produce detrimental and neutral mutations then they are random when they produce beneficial mutations. You are simply using post hoc rationalizations to claim that mutations are random.Let's use an analogy. Let's say that I have a rabbit's foot that I claim guides the roll of the dice so that I win. I also claim that it doesn't always work, but it does sometimes. I then go to the craps table. Everytime I lose I claim that the rabbit's foot just wasn't working on that roll. When I win I claim that the rabbit's foot was working. When I compare 1,000 of my rolls with someone who does not have my rabbit's foot it turns out that we won at the same rate. Would you say that my claims about the rabbit's foot are supported or not supported by the evidence?

Those are not mutations.

"Epigenetic changesstable but potentially reversible alterations in a cell’s genetic information that result in changes in gene expression but do not involve changes in the underlying DNA sequencemay mediate some of the detrimental effects of prenatal alcohol exposure and contribute to the deficits and abnormalities associated with fetal alcohol spectrum disorders."
Alcohol Res Health Volume 34(1);  2011 - PMC"IGT during pregnancy was associated with leptin gene DNA methylation adaptations with potential functional impacts. These epigenetic changes provide novel mechanisms that could contribute to explaining the detrimental health effects associated with fetal programming, such as long-term increased risk of developing obesity and type 2 diabetes."
Leptin Gene Epigenetic Adaptation to Impaired Glucose Metabolism During Pregnancy - PMCSo we have detrimental epigenetic effects seen in both fetal alcohol syndrome and type 2 diabetes. Obviously, they do go astray and cause detrimental changes.

Based on what evidence?

Based on what evidence? Yes, because the results of the roll will still be random with respect to the bet made. The only thing that would change is the payout for the bets as judged by the odds of randomly hitting specific results. Reducing the number of slots on the roulette wheel does not make the results non-random. They are still random. Reducing the number of ping pong balls in the lottery hopper does not make the lottery non-random. It is still random.

No, it is the accurate term to describe the relationship between mutagenesis and fitness. It perfectly describes the disconnect between how variation is produced and the variation that the organism needs. If I am holding a lottery ticket with a specific set of numbers did the act of printing off those numbers increase the chances that those ping pong balls will show up in the results? NO!!! It is the same for mutations. Are they permanent or dynamic? You need to choose one.Also, how does the environment make mutations non-random with respect to fitness. Perhaps you could describe and experiment or specific potential evidence that would rule it out. What evidence would you have to see in order to admit that mutations are not guided.

Then please show how the process of mutagenesis is different in metazoans and how that results in non-random mutations.

You are obviously wrong since I have pointed to two examples of epigenetic changes that are not only useless but detrimental.