The Nature of Mutations II

salty, I have to point out to you that schrafinator asked you several relevant questions and you have evaded answering her and claimed she has insulted you. Do you consider it an insult for someone to question you? you claim you will take Darwinism to task but are you claiming that you yourself are above question? If so, is that not extremely hypocritical?You would do yourself a great service if you would attempt to answer her specific questions....where in your papers are the answers to her specific questions?cheers,
M

Hi WK,
I am thinking specifically of thisCloned lambs--lessons from pathologyS M Rhind, T J King, L M Harkness, C Bellamy, W Wallace, P DeSousa & I Wilmut
Nature Biotechnology 21, 744 - 745 (2003).and thisBiol Reprod. 2003 May 14 [Epub ahead of print]. Disruption of Imprinted Gene Methylation and Expression in Cloned Preimplantation Stage Mouse Embryos.
Mann MR, Chung YG, Nolen LD, Verona RI, Latham KE, Bartolomei MS.Cloning by somatic cell nuclear transfer requires that epigenetic information possessed by the donor nucleus be reprogrammed to an embryonic state. Little is known, however, about this remodeling process, including when it occurs, its efficiency, and how well epigenetic markings characteristic of normal development are maintained. Examining the fate of epigenetic information associated with imprinted genes during clonal development offers one means of addressing these questions. We examined transcript abundance, allele-specificity of imprinted gene expression, and parental allele-specific DNA methylation in cloned mouse blastocysts. Striking disruptions were seen in total transcript abundance and allele-specificity of expression for 5 imprinted genes. Only 4% of clones recapitulated a blastocyst mode of expression for all 5 genes. Cloned embryos also exhibited extensive loss of allele-specific DNA methylation at the imprinting control regions of the H19 and Snprn genes. Thus, epigenetic errors arise very early in clonal development in the majority of embryos, indicating that reprogramming is inefficient, and that some epigenetic information may be lost.Though Dolly herself appeared to be relatively normal (though I am not aware if they tested all imprinted genes of Dolly), there are imprinting associated problems in failed lamb clones according to Wilmut's group.

wj will certainly come back with his own comments but I will address some points that need elaborating.

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I do not understand Intelligent Design but that it exists is beyond any doubt. I feel the same way and for the same reasons about gravitation.

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If intelligent design exists beyond a doubt, please demonstrate a single biological system of your choosing that can unequivically be a result of intelligent design to the exclusion of a natural process.

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It is the height of arrogance to insist that we understand all of nature.

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It is actually the height of arrogance to insist that one knows more than anybody else about a certain topic i.e. your grasp of evolution and biology has been shown to be very tenuous.

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I cannot answer metaphysical questions but I can maintain that my convictions about preformed developmental and evolutionary information remain completely compatible with the facts as revealed by both paleontology and developmental biology.

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Please give a concise list of the facts that you here claim are so readily at your disposal that would reconcile preformed developmental and evolutionary information with reality.

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Evolution has been very largely the expression of preformed rudiments as claimed by both Berg and Grasse.

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Considering the vast amount of information that has been accumulated via the genomics revolution and the study of molecular biology and genetics..can you demonstrate a single study that supports the "expression of pre-formed rudiments"?

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The environment remains unable to alter what has been the inexorable expression of forces far beyond our understanding.

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Perhaps beyond your understanding but not everyones. There are clear examples of the impact of environment on genetics and the association is pretty well understood by those doing the research. Is the entire basis of your argument that because you do not understand modern research that your conclusions are therefore correct?

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If the members of this or any other forum think they have an insight into how evolution took place, they are fantasizing.

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Actually, many of us do have an insight that you apparently do not possess and no, people who do not agree with your assertions are not necessarily fantasizing.I have to point out salty that you are being extremely hypocritical in claiming you are being insulted all the time on this forum yet you conduct yourself in the manner of a small child.You will no doubt take this post as an insult and complain. Not a single point I raise is an attack on you but an attempt to get you to actually attempt to answer some of the questions to you...you have thus far not made the slightest effort...what are you afraid of?cheers,
M[This message has been edited by Mammuthus, 07-07-2003]

The last question is easy..if you had not read anything in 50 years then you would not know that anything new had happened
At least he is not arguing blended inheritance like Symansu

Two problems again with this Peter. First off, what is the chemical difference between a mutation in a somatic cell versus a germ cell? Mutation is a mutation is a mutation...to quote Scott. One is inherited because it occurs in a specific cell type (germline) the other is not inherited. That is why one is usually called somatic mutation and the other germline mutation...i.e. both are called mutation.Imprinting in itself is not a mutation. But since you have restricted mutation to DNA copy error, what about gross phenotypic abnormalities caused by errors in imprinting where the DNA sequence remains unchanged? i.e. Prader Willi syndrome? What would you call heritable errors in imprinting if not mutation?Copy error in regards to chromsomal replication errors i.e. non disjunction makes your term "coopy" vague. Is this a replication error i.e. point mutation? Failure of the chromsomes to separate but the replication itself is flawless?A broad definition of mutation like that presented by Wounded King is the best with specific mutations discussed in their detail in my opinion. Calling the same event in differnt cell types mutation in one case and not the other is uncessesarily complicated.
cheers,
M

Unfortunately, your conduct, your inability to define your position, and your absolute reluctance to substantiate your claims makes all of your publications extremely suspect. (Remember, Scott is not the only one who has read some of your work, I have, Quetzal has, Taz has) and when questioned about specific points you have resorted to evasion, indignation, and insult. Your work is also suspect because you have failed to define "Darwinian". Your apparent claim in this last post is that all who accept the theory of evolution are atheists also demonstrates a complete lack of even tangential information on the subject you claim to be so passionate about.You also in this post claim that we should not ask you questions...then what is the point of entering a DEBATE FORUM? You do understand the concept of this website? Have you bothered to read the mission statement of the site or did you just log in blindly? This is not the "pat salty on the back club"...you can get that at Terry Trainor's site where you as a member and not administrator don't know what one can or cannot get away with on Terry's site since he bans anyone who actually supports their claims.It is a pity salty that you are to afraid to actually address the questions posted to you like schrafinators regarding determining the difference between intelligent design and a system that evolved..though you yourself claim that not being able to see this makes one insane...one would think you could whip up a post in no time to enlighten the masses but instead you evade...again, salty, what are you so scared of?

Hi Peter,
Imprinting occurs in the genome and is heritable. The other examples provided by Wounded King are as well. An error in any of these systems that is passed from parent to offspring would be called what if not mutation?cheers,
M

I am highly skeptical that many C's would take the necessary time to reflect on anything scientific such that they would come to such a realization.

However, by making a distinction between the nature of somatic versus germline mutations i.e. one is a mutation and the other is not according to your definition, one makes things more complicated and certainly less parsimonious if you call the same chemical change something different depending on the cell type.The second part of your post as I have tried to explain is wrong...individuals can have identical DNA sequence yet one inherits an imprinting mutation which is not a DNA copy error. Different enyzmes replicate DNA and methylate it. Both are capable of making errors leading to mutation.

I think when you say somatic mutation versus germline mutation that makes it pretty clear which can be inherited.

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The second part was what I thought you were telling me, then I
thought it wasn't, now I KNOW it is what you are telling me

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I think this was my exact response when salty first brought up semi-meiosis Imprinting is not very well understood i.e. how it is regulated.Bioessays. 2003 Jun;25(6):577-88. Related Articles, LinksImprinting evolution and the price of silence.Murphy SK, Jirtle RL.Department of Radiation Oncology, Duke University Medical Center, Durham.In contrast to the biallelic expression of most genes, expression of genes subject to genomic imprinting is monoallelic and based on the sex of the transmitting parent. Possession of only a single active allele can lead to deleterious health consequences in humans. Aberrant expression of imprinted genes, through either genetic or epigenetic alterations, can result in developmental failures, neurodevelopmental and neurobehavioral disorders and cancer. The evolutionary emergence of imprinting occurred in a common ancestor to viviparous mammals after divergence from the egg-laying monotremes. Current evidence indicates that imprinting regulation in metatherian mammals differs from that in eutherian mammals. This suggests that imprinting mechanisms are evolving from those that were established 150 million years ago. Therefore, comparing genomic sequence of imprinted domains from marsupials and eutherians with those of orthologous regions in monotremes offers a potentially powerful bioinformatics approach for identifying novel imprinted genes and their regulatory elements. Such comparative studies will also further our understanding of the molecular evolution and phylogenetic distribution of imprinted genes. BioEssays 25:577-588, 2003. Copyright 2003 Wiley Periodicals, Inc....but DNA is replicated by DNA polymerases..DNA is methylated by DNA methyltransferases.

yeah..what Wounded King said

Are you going to post anything substantive or answer any of the multiple questions addressed to you or are you going to obsess about Scott for the rest of your stay here?cheers,
M

J Pediatr Endocrinol Metab. 2002 Dec;15 Suppl 5:1279-88. Related Articles, LinksImprinting disorders: non-Mendelian mechanisms affecting growth.Butler MG.Section of Medical Genetics and Molecular Medicine, Children 's Mercy Hospitals and Clinics and The University of Missouri-Kansas City School of Medicine, Kansas City, MO 64108, USA. mgbutler@cmh.eduMost autosomal genes are expressed from both maternal and paternal alleles. However, imprinted genes are an example of non-Mendelian genetics, in which only one member of the gene pair is expressed and expression is determined by the parent of origin. Imprinted genes may account for 0.1-1% of all mammalian genes. At least 50 imprinted genes have been identified in humans, and imprinted genes frequently cluster under the control of an imprinting center. Many imprinted genes contribute to growth, either as growth factors, such as insulin-like growth factors (IGF2 in Beckwith-Wiedemann syndrome), or as growth inhibitors, such as the GRB10 gene in Russell-Silver syndrome. Imprinted genes have evolved over time in mammals to fine-tune the growth of the fetus. Paternally expressed genes generally enhance growth, whereas maternally expressed genes appear to suppress growth. In addition, normal and abnormal genomic imprinting and loss of heterozygosity contribute to a wide range of malignancies. A common process for controlling gene activity is methylation, which can be changed during male or female gametogenesis. Examples of classic human disorders related to genomic imprinting are Beckwith-Wiedemann syndrome (chromosome 11), Prader-Willi/Angelman syndromes (chromosome 15), Russell-Silver syndrome (chromosome 7), and Albright hereditary osteodystrophy (chromosome 20). Several of these disorders are discussed and illustrated.If you look in the abstract, it says that methylation can be changed during gametogenesis...so like a DNA mutation, methylation mutations can occur during gametogenesis and cause phenotypic change.

Certain sequences are more likely to be imprinted than others is all. so that is the association with a "switch" or a DNA sequence. However, an imprinting mutation would not be observable as a change in DNA sequence.

Very cool...that simplifies things a bit.