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And my point is that DNA analysis (might) match form and function observations
not to confirm "relationships", but to confirm form and function similarities.
As I said, you get to make up the classifications anyway,
so how you classify doesn't really matter. In scripture
bats fly, so they are considered birds.
All birds have beaks, or bills. Ducks and geese have broad, flat beaks for straining food out of the water.
All birds have wings, as do insects, although not all birds fly.
-_- then I guess you'd call bacteria "creeping things" too. That'd make the "kind" of "creeping things" so broad as to be useless for descriptive purposes. It doesn't even distinguish by cell type.Both creatures were made by Lord God/Jesus as temporary creatures which are called creeping things in Scripture.
Gen 6:20 Of fowls after their kind, and of cattle after their kind, of every creeping thing of the earth after his kind, two of every sort shall come unto thee, to keep them alive.
Their kinds are the kinds which God created from water on the 5th Day. Gen 1:21
His kinds are the kinds which Lord God made temporarily such as mankind. Gen 2:7 In order to have Humans who live forever, mankind MUST be born again Spiritually by God the Trinity. Gen 1:26 Gen 5:1-2 AND John 14:16 God Bless you
-_- then I guess you'd call bacteria "creeping things" too. That'd make the "kind" of "creeping things" so broad as to be useless for descriptive purposes. It doesn't even distinguish by cell type.
Are you unaware that there are organisms which are functionally immortal and thus, barring being consumed or killed by disease, they don't die? For example, there is a species of jellyfish that cycles between being an adult and returning to it's equivalent of a child state. The Nepenthes I grow have no correlation between their age and death and the small species that don't vine could live indefinitely, as they will never grow to the point of being structurally unstable. Well, those, and ones grown in cultivation that are trimmed periodically.Amen, but here's why creeping things are different. They were made by Jesus, which means they are subject to death. From dust they are made and from dust they shall return UNLESS they are born again Spiritually by the invisible God. Amen?
Are you unaware that there are organisms which are functionally immortal and thus, barring being consumed or killed by disease, they don't die? For example, there is a species of jellyfish that cycles between being an adult and returning to it's equivalent of a child state. The Nepenthes I grow have no correlation between their age and death and the small species that don't vine could live indefinitely, as they will never grow to the point of being structurally unstable. Well, those, and ones grown in cultivation that are trimmed periodically.
-_- the jellyfish is demonstrably functionally immortal. Functional immortality means that an organism's cells do not age after a point, or that the organism has a process by which to rejuvenate cells such that aging is reversed periodically. Anything that is functionally immortal will not die of old age.No flesh is functionally immortal since everything Jesus made (His kinds) are subject to death UNTIL death is destroyed at the end of the present 6th Day. Then, those who have put on immortality, will live longer than Nepenthes. God Bless you
1Co 15:26 The last enemy that shall be destroyed is death.
-_- thanks for lumping in autistic people like myself with schizophrenics and people with bipolar disorder. None of those disorders actually limit reproduction much. Heck, all three require currently unknown environmental cues to even afflict a person. For all you know, you have a genetic predisposition to one or all three of those disorders, and you just never ended up with them by lucking out on your environment.
That's not true, in a previous debate, I listed off ones by official label. Others have done so in this very thread. I shouldn't have to keep looking up the official labels every time I bring up these mutations.
1. I'm too distracted by you ignoring the examples of beneficial brain gene mutations to want to give much thought to your continued, shallow, emotional appeal of how ridiculous you think it is for mutations to be the reason why human brains are larger than those of other apes.
2. I don't view this as "a critical point". Brains are like any other organ, you might as well be incredulous about the evolution of lizard bladders. You've failed consistently to properly defend your position that mutation can't contribute positively to human intelligence, especially when it comes to the positive brain mutations you keep deciding to ignore.
3. I'm not going to pretend that other people haven't given you official labels for positive brain mutations in humans, only for you to ignore them. You have to demonstrate that it is even worth my time to debate with you any more, by actually addressing the claimed positive mutations. You don't have to treat them as valid, I don't care how much denial you want to be in, just acknowledge people have given you examples of these positive mutations and you disagree with their claims or the studies that show them. Ignoring these points is just insulting to the people debating with you.
Don't pretend that the mutations being present in and of themselves doesn't mean a person will have the disorder is irrelevant. It is extremely relevant; why would it matter if there are more detrimental mutations than benign ones if the detrimental effect doesn't consistently happen?Those are examples of genetic mutations having a deleterious effect on the brain, nothing more.
And you keep ignoring that brain related mutations don't always result in negative effects. It's not like we'd name the conditions that result from the benign ones. We just say some people are better at math, etc.You seem to have missed the point that mutations in brain related genes have deleterious effects.
-_- the brain related genes we were discussion aren't HOX genes. Not all brain related genes are HOX genes, in fact, nearly all HOX genes are genes that guide the differentiation of organ tissues and body anatomy position. Where the brain goes, not how big it gets.But you didn't do that, you keep referring to arguments you never made. Now there was some discussion of Hox genes which hardly account for the massive overhaul of brain related genes 2 mya.
I literally Google searched this last time it came up and found out that brain related genes are some of the most mutation prone in our species. What source is telling you the opposite?The obvious fact here is we are not talking about a bladder. The human brain is developed by a large number of highly conserved genes.
https://www.scientificamerican.com/article/genetic-mutation-sleep-less/The effects of mutations on the human brain from mutations are always deleterious, when they actually have an effect.
The DEC2 gene mutation has been demonstrated to exist, and its effect in humans has been known since 2009.There have been no such proofs, arguments or even a serious suggestion. It's called begging the question of proof.
Don't pretend that the mutations being present in and of themselves doesn't mean a person will have the disorder is irrelevant. It is extremely relevant; why would it matter if there are more detrimental mutations than benign ones if the detrimental effect doesn't consistently happen?
And you keep ignoring that brain related mutations don't always result in negative effects. It's not like we'd name the conditions that result from the benign ones. We just say some people are better at math, etc.
-_- the brain related genes we were discussion aren't HOX genes. Not all brain related genes are HOX genes, in fact, nearly all HOX genes are genes that guide the differentiation of organ tissues and body anatomy position. Where the brain goes, not how big it gets.
I literally Google searched this last time it came up and found out that brain related genes are some of the most mutation prone in our species. What source is telling you the opposite?
https://www.scientificamerican.com/article/genetic-mutation-sleep-less/
The Transcriptional Repressor DEC2 Regulates Sleep Length in Mammals
Sources on the DEC2 gene mutation that, when present in humans, reduces the length of time needed to sleep. It has an effect, and it isn't detrimental or resulting in the loss of a function. This better be the last time I have to mention this.
Note that the purpose of the original study that found the mutation and its effect was to find genes that regulated sleep in humans. They noticed that all people that required less sleep to function normally had an unusual sequence, and were able to determine the function of the gene that way.
The DEC2 gene mutation has been demonstrated to exist, and its effect in humans has been known since 2009.
And my point is that DNA analysis will match form and function observations
not to confirm "relationships", but to confirm form and function similarities.
Had you considered the possibility that those 'same genes' were not sequenced to the same extent?pshun2404:
Look at this alleged “same gene” across species...an ALLEGED shared gene...
Human Gene HDLBP (uc002wba.1) a 110-kD protein that specifically binds HDL molecules, which functions in the removal of cellular cholesteral...it is a section 87,092 base pairs long
Rat Gene Hdlbp (NM_172039) which is only 68, 238 base pairs long performs a similar function but apparently not identically.
The allegedly the “SAME GENE” in Yeast, S. cerevisiae Gene SCP160 (YJL080C) functions differently and is primary to cell division, and only has 3,669 base pairs.
Finally, the alleged “SAME GENE” in D. Melongaster, Gene Dp1 (CG5170-RB). Having 9119 base pairs (3 times that of Yeast) seems to do nothing!
When I was in graduate school, we we comparing 2 introns from a gene across several species. We used the human gene - the entire coding region, plus introns, plus 3' and 5' flanking regions - as a reference. For some taxa, our genomic DNA samples were old and we had limited success in sequencing the introns. In others, we had no problems at all. The primers we used to generate PCR fragments were in exons because they were fairly well conserved, and so for some taxa we had not only the introns, but parts of exons as well. several taxa had extensive repetitions in their introns, making one, for instance, nearly 1kb larger than all of the others.
By your implicit logic, we should have concluded that these sequences were not from the SAME GENE, despite the fact that we have amplified fragments using identical primers (30+ years of reading on these subjects should be sufficient for your understanding of the above).
I suggest that the human gene you refer to includes all intronic sequence and flanking regions, whereas the others are limited to smaller regions (e.g., without the flanks, or just mRNA).
In fact, I am willing to bet on it.
What say you?
Those are examples of genetic mutations having a deleterious effect on the brain, nothing more.
You seem to have missed the point that mutations in brain related genes have deleterious effects.
I don't know why you feel the need to keep mentioning that there are mutations that result in detrimental effects on the brain. There are mutations for every organ that will mess it up to various extents.Those are examples of genetic mutations having a deleterious effect on the brain, nothing more.
BUT NOT EXCLUSIVELY. ALL MUTATIONS IN BRAIN RELATED GENES DO NOT RESULT IN DETRIMENTAL EFFECTS. So, what is the point of bringing this up all the time? I know plenty of mutations result in horrific mental defects. But not all of them do, and some are measurably benign.You seem to have missed the point that mutations in brain related genes have deleterious effects.
I will hunt down the thread so help me. Nothing irks me more than being accused of being a liar. It wasn't even that long ago, the thread is within the first two pages of the subforum.But you didn't do that, you keep referring to arguments you never made. Now there was some discussion of Hox genes which hardly account for the massive overhaul of brain related genes 2 mya.
Which are not conserved in humans at all. Before, you specified the gene area for this, making it very easy to look up the fact that it was one of the most frequently mutating gene regions in humans.The obvious fact here is we are not talking about a bladder. The human brain is developed by a large number of highly conserved genes.
So you are just going to ignore the multiple benign brain mutation examples people have given you, as well as the specific one I PROVIDED SOURCES FOR. Threads aren't fresh starts every time, you can't act as if I haven't provided sources within a currently active thread you are participating in. You can't pretend we haven't conversed on this matter before.The effects of mutations on the human brain from mutations are always deleterious, when they actually have an effect.
Genetic basis of human brain evolution overall about the genetics of human evolution, including the brain.There have been no such proofs, arguments or even a serious suggestion. It's called begging the question of proof.
There is a lot here so let me start slow....
Any study of Phylogenetics (and in our training to understand it) we see two aspects of it, one being theoretical and the other being empirical. And the opinions for or against are extant dependent on the definition of terms. This means that even though most may agree, it is largely opinion not established fact.
For example, we hear the term “relationship” being repeated over and over but when we see what we see (similarities in genetic materials, arrangement, and purpose) the question is “What does this mean?” It can mean related as in somehow similar (size, place, function, etc.) OR does it actually show we are related in the sense of demonstrating lineage (that one comes from the other)? well therein lays the dilemma that breeds discussion and debate.
What it ACTUALLY shows is some semblance of similarity, and this not nearly as exact as the rhetoric would like you to be convinced of.
If you really look at the data (void the narrative attached that explains the data according to the already accepted pre-conceived notion) we suddenly realize that the shoe does not fit the foot....
Look at this alleged “same gene” across species...an ALLEGED shared gene...
Human Gene HDLBP (uc002wba.1) a 110-kD protein that specifically binds HDL molecules, which functions in the removal of cellular cholesteral...it is a section 87,092 base pairs long
Rat Gene Hdlbp (NM_172039) which is only 68, 238 base pairs long performs a similar function but apparently not identically.
The allegedly the “SAME GENE” in Yeast, S. cerevisiae Gene SCP160 (YJL080C) functions differently and is primary to cell division, and only has 3,669 base pairs.
Finally, the alleged “SAME GENE” in D. Melongaster, Gene Dp1 (CG5170-RB). Having 9119 base pairs (3 times that of Yeast) seems to do nothing!
Now as fit as the hypothesis based explanation appears, the actual data shows us they actually are nothing alike...they are different in size AND FUNCTION...yet billed as “commonly shared” in the rhetoric.
Well since what I am telling you is true, how did they convince so many?
This process of convincing the masses of the speculative for a definite motive (to prove their theory) requires consistent:
a) Interpretation of all data (even that which could be considered contrary to that theory) though the accepted model as opposed to allowing the raw data shape and remake the model (which is good science and true critical thought)
b) Repetition over and over...early Psychologist William James discovered this characteristic of people...that if they hear, or have had modelled before them, something not really true, over and over and over, they come to believe it as if it is true. Goebbels, capitalized on this insight in the 1930’s in Germany and applying it to politics h says “If you tell a lie big enough and keep repeating it, people will eventually come to believe it. The lie can be maintained only for such time as the State can shield the people from the political, economic and/or military consequences of the lie. It thus becomes vitally important for the State to use all of its powers to repress dissent, for the truth is the mortal enemy of the lie, and thus by extension, the truth is the greatest enemy of the State.” The same is true in this matter. Those aspects which are merely opinion about the data are repeated over and over as if they are fact and the masses swallow it whole with no actual discernment taking place.
c) Appeal to Authority...the above is reinforced by this. In addition to the repetition of the COULD BE/MIGHT BE over and over (which brainwashes) when you get a bunch of alleged authorities saying “Yes It is true”....simply because of their sheepskin people say “Well it must be true after all they know”. Really? NOT!
d) And then finally through c) consensus follows (the argumentum ad populum)....which basically is that “if everyone is saying it is true then it must be true” but if history (even the history of science) has taught us one thing it is that just because a bunch believe it does not make it so.
Actually, if I had only the shallow, cherry-picked information you provided, I might be skeptical.So Phylogenetics, which says different groups and in some sense ALL living organisms share genes, this is correct (but not nearly as many as they claim...see my above “shared gene” example)...but what this means is where we enter the twilight zone of opinion and interpretation. So let me ask...
If you were NOT ALREADY CONVINCED of the theory, and you were to just view the “shared gene” data above for the first time...(please be honest here) objectively, as a scientist, would you really come to some conclusion of lineage? They do not progress and they are not in any way the same (not actually)!
Look at this alleged “same gene” across species...an ALLEGED shared gene...
Human Gene HDLBP (uc002wba.1) a 110-kD protein that specifically binds HDL molecules, which functions in the removal of cellular cholesteral...it is a section 87,092 base pairs long
Rat Gene Hdlbp (NM_172039) which is only 68, 238 base pairs long performs a similar function but apparently not identically.
The allegedly the “SAME GENE” in Yeast, S. cerevisiae Gene SCP160 (YJL080C) functions differently and is primary to cell division, and only has 3,669 base pairs.
Finally, the alleged “SAME GENE” in D. Melongaster, Gene Dp1 (CG5170-RB). Having 9119 base pairs (3 times that of Yeast) seems to do nothing!
I don't know why you feel the need to keep mentioning that there are mutations that result in detrimental effects on the brain. There are mutations for every organ that will mess it up to various extents.
BUT NOT EXCLUSIVELY. ALL MUTATIONS IN BRAIN RELATED GENES DO NOT RESULT IN DETRIMENTAL EFFECTS. So, what is the point of bringing this up all the time? I know plenty of mutations result in horrific mental defects. But not all of them do, and some are measurably benign.
I will hunt down the thread so help me. Nothing irks me more than being accused of being a liar. It wasn't even that long ago, the thread is within the first two pages of the subforum.
So you are just going to ignore the multiple benign brain mutation examples people have given you, as well as the specific one I PROVIDED SOURCES FOR. Threads aren't fresh starts every time, you can't act as if I haven't provided sources within a currently active thread you are participating in. You can't pretend we haven't conversed on this matter before.
Genetic basis of human brain evolution overall about the genetics of human evolution, including the brain.
https://www.scientificamerican.com/article/garbled-dna-might-be-good-for-you/ how widespread significant mutations in somatic cells are in healthy people. 30% or more of your liver cells have an extra chromosome or are missing one, for example.
https://www.nih.gov/news-events/nih-research-matters/gene-regulates-sleep-length DEC2 genetic mutation that allows for less sleep... again. The specific label for the mutant version of the gene being hDEC2. I will not stop mentioning this until you listen.
-_- circadian rhythm is controlled by the brain. Sleep is a brain function. But no, says the guy that acted as if metabolic disorders were the result of brain gene mutations. You like to broaden your choices when it suits you, but when it does it, you sure like to narrow your perspective. Sleep is controlled by the brain, I will not stand for your suggestion that it is not relevant to brain function when it is controlled by the brain directly.All very interesting but this one is a fairly normal protein coding gene. This mutation appears to be effecting normal circadian rhythm, not really effecting brain development or function.
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