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originally posted by: cooperton
originally posted by: JameSimon
a reply to: cooperton
Only evolution could allow a gene to switch off an on.
The good ol' evolution gods haha. But no it is not evolution. Turning genes on and off is epigenetic. Epigenetic alterations occur within the lifetime of an organism.
Please address everything else I said (and that you so carefully choose to ignore).
I am going one at a time, you still seem to stubbornly think evolution is responsible for epigenetic mechanisms.
originally posted by: JameSimon
I didn't say such thing, so please refrain from making personal statements when the only argument you have is to distort the message.
Your blanket statement was "wrong", and my claim was the involvement of epigenetics. I stand by what I said.
originally posted by: JameSimon
Epigenetics is the study of heritable phenotype changes that do not involve alterations in the DNA sequence.
originally posted by: cooperton
originally posted by: JameSimon
Epigenetics is the study of heritable phenotype changes that do not involve alterations in the DNA sequence.
haha you literally copy and pasted the first sentence of the wikipedia page for epigenetics. Riveting.
"Epigenetics is the study of heritable phenotype changes that do not involve alterations in the DNA sequence"
Wiki page for epigenetics
originally posted by: AngryCymraeg
And that makes it less true because....?
originally posted by: Noinden
a reply to: cooperton
Ahh so you can prove this? Lets talk SNP alterations of hemoglobin. Assuming you understand what the SNP does. I will hint, its a structural change (for the most part) to the function of the proteins which make Hemoglobin.
originally posted by: Noinden
a reply to: cooperton
I said prove it is the primary form. Also the SNPs for hemoglobin are not all about malaria resistance (its not prevention). It includes greater oxygen uptake for example.
So once again. Prove your statement.burdon of proof and all that Jazz
originally posted by: Zanti Misfit
a reply to: watchitburn
Basic Chemicals can be Combined to Create Biological Life . This is Old News.....
originally posted by: Noinden
a reply to: cooperton
That is not proof. That is supposition. QED show proof it is the primary mode of heritibility, as per your statement. Further more, based on your statement, show that it is not involved in the evolutionary process.
Burden of proof remains yours.
Mutations in Epigenetic Regulation Genes Are a Major Cause of Overgrowth with Intellectual Disability. Tatton-Brown K1, Loveday C2, Yost S2, Clarke M2, Ramsay E2, Zachariou A2, Elliott A2, Wylie H2, Ardissone A3, Rittinger O4, Stewart F5, Temple IK6, Cole T7; Childhood Overgrowth Collaboration, Mahamdallie S2, Seal S2, Ruark E2, Rahman N8. Author information
Abstract To explore the genetic architecture of human overgrowth syndromes and human growth control, we performed experimental and bioinformatic analyses of 710 individuals with overgrowth (height and/or head circumference ≥+2 SD) and intellectual disability (OGID). We identified a causal mutation in 1 of 14 genes in 50% (353/710). This includes HIST1H1E, encoding histone H1.4, which has not been associated with a developmental disorder previously. The pathogenic HIST1H1E mutations are predicted to result in a product that is less effective in neutralizing negatively charged linker DNA because it has a reduced net charge, and in DNA binding and protein-protein interactions because key residues are truncated. Functional network analyses demonstrated that epigenetic regulation is a prominent biological process dysregulated in individuals with OGID.Mutations in six epigenetic regulation genes-NSD1, EZH2, DNMT3A, CHD8, HIST1H1E, and EED-accounted for 44% of individuals (311/710). There was significant overlap between the 14 genes involved in OGID and 611 genes in regions identified in GWASs to be associated with height (p = 6.84 × 10-8), suggesting that a common variation impacting function of genes involved in OGID influences height at a population level. Increased cellular growth is a hallmark of cancer and there was striking overlap between the genes involved in OGID and 260 somatically mutated cancer driver genes (p = 1.75 × 10-14). However, the mutation spectra of genes involved in OGID and cancer differ, suggesting complex genotype-phenotype relationships. These data reveal insights into the genetic control of human growth and demonstrate that exome sequencing in OGID has a high diagnostic yield.
How Genetics Affect Epigenetics While epigenetics and genetics can cooperate in cancer initiation and progression, the interconnectedness between of these two processes is becoming increasingly apparent with the realization that several epigenetic modifiers are mutated in human cancers(Kasinski and Slack, 2011b; Rodriguez-Paredes and Esteller, 2011; Schuettengruber et al., 2011; Wilson and Roberts, 2011).
Some examples of genetic mutations of epigenetic modifiers are shown in Table 1 and Figure 2. The mutation of epigenetic modifiers presumably leads to profound epigenetic changes, including aberrant DNA methylation, histone modifications and nucleosome positioning although this remains to be demonstrated. These epigenetic alterations can lead to abnormal gene expression and genomic instability, which may predispose to cancer(Rodriguez-Paredes and Esteller, 2011; Wilson and Roberts, 2011).
originally posted by: Noinden
a reply to: cooperton
You have read all those studies have you? Or perhaps done a key word search
You are missing the point, that mutations are still happening with the epigenetic modifications.
originally posted by: Phantom423
a reply to: cooperton
Mutations are part of the process. There's no getting around this fact.
There are no repeatable, observable examples of a gene making a leap to another gene function. Lactase genes produce lactase, HBB genes produce beta-globin, etc. To assume that these SNPs could make a functional leap from an old gene to a new one is unfounded in scientific literature
There are no repeatable, observable examples of a gene making a leap to another gene function. Lactase genes produce lactase, HBB genes produce beta-globin, etc. To assume that these SNPs could make a functional leap from an old gene to a new one is unfounded in scientific literature
originally posted by: Phantom423
I'm not clear on what you mean. If a gene undergoes mutation, it is changed. Are you saying that the functional DNA in that gene doesn't jump to another gene and change it permanently? I must have missed it, but I didn't see any paper posted which suggested that. And I don't know the answer to that question. I have to research it. I've heard of "jumping genes" but not sure it applies to lactase.