Posted on 09/11/2008 9:55:10 AM PDT by GodGunsGuts
You have to put it in your equation and that, along with my short astronomy lesson, disprove your statement that the incoming rays ALWAYS point back exactly to the source (sun).
Maybe. It doesn't specify how they were burned.
The earliest Waldensians believed in poverty and austerity, promoting true poverty, public preaching and the personal study of the scriptures.[1] The sect originated in the late 12th century as the Poor Men of Lyons, a band organized by Peter Waldo, a wealthy merchant of Lyon, who gave away his property around 1177 and went about preaching apostolic poverty as the way to perfection.[1]
In 1179, they went to Rome, where Pope Alexander III blessed their life but forbade preaching without authorization from the local clergy.[7] They disobeyed and began to preach according to their own understanding of scripture. Seen by the Roman Catholic Church as unorthodox, they were formally declared heretics by Pope Lucius III in 1184 and by the Fourth Lateran Council in 1215.[7] In 1211 more than 80 were burned as heretics at Strasbourg[who?], beginning several centuries of persecution that nearly destroyed the sect. Part of their legacy is recognized as works of the writer Henri Arnaud. The Waldensian Church of Italy has survived to the present day.
And yes, error prone DNA polymerase increases mutations throughout the bacterial genome. How could it not? It is more error prone than regular DNA polymerase.
Put it this way, I can’t find anything that would support such a thing in the New Testament.
Tell that to Giordano Bruno :(
=Christians weren’t burning people at the stake.
Uh huh. Go to the following and search for “stake”
http://www.religionfacts.com/christianity/charts/protestant_reformers.htm
That's not what real scientists are finding:
http://www.ncbi.nlm.nih.gov/pubmed/9926936
"Mutation hotspots were identified by comparing the observed distribution of mutations to the pattern expected from a random multinomial distribution."..."Both high evolutionary constraint and mutation hotspots are noted at amino acids close to the protein-DNA interface and at others more distant from DNA, often buried within the core of the folded protein but sometimes on its surface."
Oops, not random...
http://mmbr.asm.org/cgi/content/full/70/3/830
Like many eukaryotes, bacteria make widespread use of postreplicative DNA methylation for the epigenetic control of DNA-protein interactions. Unlike eukaryotes, however, bacteria use DNA adenine methylation (rather than DNA cytosine methylation) as an epigenetic signal. DNA adenine methylation plays roles in the virulence of diverse pathogens of humans and livestock animals, including pathogenic Escherichia coli, Salmonella, Vibrio, Yersinia, Haemophilus, and Brucella. In Alphaproteobacteria, methylation of adenine at GANTC sites by the CcrM methylase regulates the cell cycle and couples gene transcription to DNA replication. In Gammaproteobacteria, adenine methylation at GATC sites by the Dam methylase provides signals for DNA replication, chromosome segregation, mismatch repair, packaging of bacteriophage genomes, transposase activity, and regulation of gene expression. Transcriptional repression by Dam methylation appears to be more common than transcriptional activation. Certain promoters are active only during the hemimethylation interval that follows DNA replication; repression is restored when the newly synthesized DNA strand is methylated. In the E. coli genome, however, methylation of specific GATC sites can be blocked by cognate DNA binding proteins. Blockage of GATC methylation beyond cell division permits transmission of DNA methylation patterns to daughter cells and can give rise to distinct epigenetic states, each propagated by a positive feedback loop. Switching between alternative DNA methylation patterns can split clonal bacterial populations into epigenetic lineages in a manner reminiscent of eukaryotic cell differentiation. Inheritance of self-propagating DNA methylation patterns governs phase variation in the E. coli pap operon, the agn43 gene, and other loci encoding virulence-related cell surface functions.
Now where do you think that says that mutation is random?
All I see is confirmation of what I have already said.
The ENTIRE citation.....
Missense mutations in p53 frequently occur at ‘hotspot’ amino acids which are highly conserved and represent regions of structural or functional importance. Using the p53 mutation database and the p53 DNA sequences for 11 species, we more precisely defined the relationships among conservation, mutation frequency and protein structure. We aligned the p53 sequences codon-by-codon and determined the degree of substitution among them. As a whole, p53 is evolving at an average rate for a mammalian protein-coding gene. As expected, the DNA binding domain is evolving more slowly than the carboxy and amino termini. A detailed map of evolutionary conservation shows that within the DNA binding domain there are repeating peaks and valleys of higher and lower evolutionary constraint. Mutation hotspots were identified by comparing the observed distribution of mutations to the pattern expected from a random multinomial distribution. Seventy-three hotspots were identified; these 19% of codons account for 88% of all reported p53 mutations. Both high evolutionary constraint and mutation hotspots are noted at amino acids close to the protein-DNA interface and at others more distant from DNA, often buried within the core of the folded protein but sometimes on its surface. The results indicate that targeting highly conserved regions for mutational and functional analysis may be efficient strategies for the study of cancer-related genes.
I have spoken to you of earthly things and you do not believe; how then will you believe if I speak of heavenly things?
I think you're wasting your time. The usual response to those kinds of facts is "no real Christian would do such a thing, so therefore they weren't Christians, QED and heads I win, tails you lose."
“You have to put it in your equation and that, along with my short astronomy lesson, disprove your statement that the incoming rays ALWAYS point back exactly to the source (sun).”Sorry, the equation was a hypothetical one that did not involve the atmosphere.
And neither is mutation.
Here's an easier one for you. From an evolutionist. Maybe you will believe him.
"Mutations in DNA are clearly probabilistic, but they aren't random."
http://www.geocities.com/lclane2/mut
But that wasn't a response to your “Charlie Gibson” of the Science paper you mangled to try to claim that mutations are not random, it was a response to your incorrect claims about gene activity meaning mutation and epigenetics expression constraint means mutation constraint. Lets try to keep all your incorrect claims straight; were dealing with three so far.
The Correct answers:
a) Mutations are observed to be random from error prone DNA polymerase and mutagens (although some mistakes are more likely than others).
b) Gene activity doesn't include mutation as part of its activity.
c) Epigenetic constraint of expression doesn't mean constraint of mutation.
Are you trying to say that genetic mutation is 'random' prior to error-correction?
Is that what you are saying? LOL!
Probabilistic doesn't help you.
Error prone DNA polymerase given the same segment of DNA to copy doesn't make the same mistakes every time or even most the time. It makes mistakes randomly with some mistakes being a bit more likely than others due to the molecular nature of DNA and DNA polymerase.
So done mangling pubmed citations (they cannot possibly help you in context) and now quoting geocities?
Oh, I get it. You don't understand what the word 'random' means or are using a special definition.
"b) Gene activity doesn't include mutation as part of its activity."
You're the only one saying that it does.
"c) Epigenetic constraint of expression doesn't mean constraint of mutation."
From your post 1183: "DNA methylation or histones do not to prevent mutation (although DNA methylation DOES have a role in DNA repair)."
So obviously epigenetic expression does impact mutation by marking errors for repair. Either you're talking about 'random' mutation being a pre-correction phenomenon or you just contradicted yourself wrt epigenetic impacts on 'random' mutation.
You still don't seem to understand that light isn't instantaneous : (
I can't afford to go buy books. (Unemployed)
Then quit wasting time on FR and get a job.
I am fully aware that light is not instantaneous.
From your questions you seem to sometimes be ignorant of that fact. Specifically when I ask you 'When' something occurs.
Where you go wrong is in assuming that there is no difference between the Earth spinning in place or the sun orbiting the earth.
Not if you are using the Earth as your frame of reference. We already went though this with a two body example.
based on your assertion that “There is no difference between the Earth spinning in place or the sun orbiting the earth, the suns apparent position vs actual position is the same.”, I would conclude that you have no idea what your talking about.
For the purposes of this example, there is no difference between the Earth orbiting the Sun or the Sun orbiting the earth. You don't seem to be able to grasp the idea of frames of reference very well.
I'm starting to feel like a bully beating up a cripple in a wheel chair.
Sadly I fear that you will never know how wrong you are. Your almost complete and utter failure to answer my questions and look at the concept from a different perspective indicates a closed and fixed mindset.
Yeah, you're using a special definition of random. If some thing is more likely than another thing, the outcome may be probabilistic but it certainly isn't random.
Random means equal chance for each outcome. By definition, if some outcomes are more likely then it isn't random.
They looked at the p53 protein in eleven different species and saw which sections were “allowed” to change and which “HAD” to be the same based upon which were evolutionarily conserved and which were different.
Because p53 is under extreme selective pressure, if it doesn't perform its function the animal doesn't survive to reproduce. p53 has a DNA binding domain. It detects damaged DNA as part of its function. Many of the highly conserved amino acids in the p53 protein are in that DNA binding domain.
That isn't what I am saying, that is what the paper you “Gibson’d” says that you sourced despite all the clear warnings that they were talking about evolution and how USEFUL it is to finding out what parts of a protein are actually doing the work and are thus highly conserved between species.
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