Register | Sign In


Understanding through Discussion


EvC Forum active members: 63 (9162 total)
4 online now:
Newest Member: popoi
Post Volume: Total: 916,334 Year: 3,591/9,624 Month: 462/974 Week: 75/276 Day: 3/23 Hour: 2/0


Thread  Details

Email This Thread
Newer Topic | Older Topic
  
Author Topic:   Y.E.C. Model: Was there rapid evolution and speciation post flood?
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


Message 221 of 518 (809132)
05-16-2017 11:44 AM
Reply to: Message 218 by 14174dm
05-16-2017 11:38 AM


Re: Number of Genes for Eye Color and Skin Color
14174dm writes:
My understanding of genes and alleles is that when we say this gene controls such, we mean that we found a statistical link between the gene and the effect. We haven't traced the protein and its impacts through every cell and biochemical process.
For the specific paper on eye color, this is an accurate description. For some alleles the biochemical and physical interactions are understood at the molecular level.
When we see this allele at the gene causing blue eyes, are we also seeing what else it does? For example, adrenaline increases heart rate, opens airways and increases the emotional aspect of memories.
It is entirely possible that the alleles affeting eye color also have functions elsewhere that are being selected for.

This message is a reply to:
 Message 218 by 14174dm, posted 05-16-2017 11:38 AM 14174dm has not replied

  
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


Message 223 of 518 (809149)
05-16-2017 12:23 PM
Reply to: Message 222 by Faith
05-16-2017 11:53 AM


Re: alleles
Faith writes:
And as the Mendel squares easily demonstrate, more than two alleles per gene are not needed for all the diversity we see in living things.
How so? You seem to just assert this without any backing.

This message is a reply to:
 Message 222 by Faith, posted 05-16-2017 11:53 AM Faith has not replied

  
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


Message 228 of 518 (809185)
05-16-2017 5:55 PM
Reply to: Message 227 by Faith
05-16-2017 5:47 PM


Re: alleles: sequence and function
Faith writes:
Because the claim is that these "alleles" code for a different protein and different function of the gene than the allele whose sequence they changed, but there is no evidence that they code for anything other than the original allele did (the one at that particular locus whose sequence they changed).
Where is the evidence that they have the same function?
They aren't alleles according to what I say above, they are merely mutations, changes in the DNA sequence that do not code for a new protein or a new trait, and in my model there are lots of mutations occurring all the time, most of them neutral which is why I'm assuming that's what these are, or deleterious. Mutations ARE increasing. In my model they are not true alleles and they are not a good thing for the organism.
Do all chimp genes function exactly the same as human genes, in your model?

This message is a reply to:
 Message 227 by Faith, posted 05-16-2017 5:47 PM Faith has replied

Replies to this message:
 Message 229 by Faith, posted 05-16-2017 5:59 PM Taq has replied

  
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


Message 237 of 518 (809237)
05-17-2017 10:53 AM
Reply to: Message 229 by Faith
05-16-2017 5:59 PM


Re: alleles: sequence and function
Faith writes:
There is no evidence one way or the other, but it needs to be proved and can't be assumed that the function is not the same.
You can't assume they have the same function, either.
Faith writes:
Since most mutations are known to be neutral, others deleterious and very very few very iffily beneficial, it ought to be common sense to provide evidence that any mutation is beneficial, but no, all these on this thread are ASSUMED to be beneficial.
We don't need to assume that the genetic differences between humans and chimps are beneficial. We can directly observe that they are beneficial in both humans and chimps. Therefore, we know that changes in DNA can and are beneficial. No assumption needed.

This message is a reply to:
 Message 229 by Faith, posted 05-16-2017 5:59 PM Faith has not replied

  
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


Message 241 of 518 (809257)
05-17-2017 1:37 PM
Reply to: Message 238 by Faith
05-17-2017 1:10 PM


Re: SUMMATION OF THE USUAL FLIMFLAM
Faith writes:
I can't call a mutation a mutation, I have to call it an allele, so I can't point out that mutations are usually neutral, second deleterious, so I can't dispute the argument that I have to account for alleles that Adam and Eve didn't have on the ground that they are just neutral mutations;
No one is stopping you from saying that some alleles are detrimental, so I really don't understand what the problem is.
If you want to plant your flag on the hill labeled "mutations don't happen", go for it. However, such a position is rather hard to defend being that we can directly observe mutations happening. Alleles is just another way of saying that mutations happen. If you don't object to the observation that mutations happen, then why object to the observation that mutations produce new alleles?

This message is a reply to:
 Message 238 by Faith, posted 05-17-2017 1:10 PM Faith has not replied

  
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


(1)
Message 244 of 518 (809261)
05-17-2017 2:02 PM
Reply to: Message 242 by Percy
05-17-2017 1:38 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
Percy writes:
If I hadn't just looked it up earlier this morning I wouldn't remember what the MHC complex was - we've talked about several different genes, and to me they're still just alphabet soup. The terms polygeny and antigen are unfamiliar. I don't know what "class I" and "class II" molecules are.
The Major Histocompatibility Complex (MHC) is a complex of over 200 separate genes. That is, there is a region in your genome made up of over 200 genes that produce all of your MHC proteins. Think of it like a car manufacturer that makes over 200 different models. These models can be grouped into about 3 main categories: cars, pickups, and SUV's. Those are like the 3 MHC groups, of which MHC I and MHC II have been studied the most. They are grouped into these classes due to the type of immunity they are involved in, be it bacterial pathogens (MHC II) or cancer (MHC I).
The wide variety of MHC molecules allow them to bind to many different foreign and misformed proteins/molecules and present them on the outside of the immune cell. This allows T-cells to interact with the presented antigen and respond accordingly, either releasing cytokines to amp up the immune system to fight off infection or killing of a cell that is presenting the wrong proteins (cancer/tissue rejection).
When the article refers to "more than 200 alleles" it means across all the genes of the complex.
That's not accurate. For any single gene in the complex there can be hundreds or even thousands of alleles. For example, one of the genes in the complex is HLA-DRB1. Again, that is just a single gene. For that single gene there are hundreds if not thousands of different alleles.

This message is a reply to:
 Message 242 by Percy, posted 05-17-2017 1:38 PM Percy has replied

Replies to this message:
 Message 246 by Percy, posted 05-17-2017 3:38 PM Taq has replied

  
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


Message 248 of 518 (809270)
05-17-2017 4:15 PM
Reply to: Message 245 by Percy
05-17-2017 3:35 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
Percy writes:
Good point, but can more consistent figures be nailed down? Taq just responded that some genes of the complex "have hundreds or even thousands of alleles" all by themselves.
The genomic region has been sequenced and you can find the map here:
Complete sequence and gene map of a human major histocompatibility complex | Nature
Excel spreadsheet containing all 224 genes here:
http://www.nature.com/...01/n6756/extref/401921a0.table1.xls
If you look at the function column you will notice that not all of the genes code for actual MHC proteins (i.e. antigen presenting proteins). There are a few chaperone and and protein modifying proteins in there, such as heat shock proteins and kinases. So not all of the genes in the MHC region are directly related to immunity.
We can pick one of the MHC II molecules at random from the Excel list: HLA-DPB1. If you do a search for that molecule at Uniprot you get this page:
UniProt
If you scroll down to polymorphisms, it lists about 120 known alleles for the gene, at least by my quick count.

This message is a reply to:
 Message 245 by Percy, posted 05-17-2017 3:35 PM Percy has replied

Replies to this message:
 Message 254 by Percy, posted 05-18-2017 8:05 AM Taq has replied

  
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


Message 249 of 518 (809271)
05-17-2017 4:18 PM
Reply to: Message 246 by Percy
05-17-2017 3:38 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
Percy writes:
How do you reconcile "more than 200 alleles" across MHC I and MHC II with possibly "hundreds or even thousands" for a single gene?
Using our car manufacturing analogy from before, the MHC region is analogous to a single car manufacturer. Each gene in the region is a single vehicle model. Each vehicle model can have different trim packages, paint color, and so on. Each variant of the single type of vehicle is an allele in the analogy.
There are 224 car models in the MHC region. Each car model can possibly have just a few different variants, but some are known for having hundreds to thousands of variants.
Does this make sense?
Edited by Taq, : No reason given.

This message is a reply to:
 Message 246 by Percy, posted 05-17-2017 3:38 PM Percy has seen this message but not replied

Replies to this message:
 Message 250 by jar, posted 05-17-2017 4:29 PM Taq has not replied

  
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


Message 251 of 518 (809273)
05-17-2017 4:31 PM
Reply to: Message 247 by PaulK
05-17-2017 3:46 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
PaulK writes:
"More than two hundred" is sufficient for "hundreds". The "thousands" could conceivably be more recent and accurate figures.
The most up to date resource I could find is this one:
HLA Nomenclature @ hla.alleles.org
For HLA-DRB1 they have 2,058 alleles listed.

This message is a reply to:
 Message 247 by PaulK, posted 05-17-2017 3:46 PM PaulK has not replied

  
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


Message 262 of 518 (809442)
05-18-2017 12:11 PM
Reply to: Message 254 by Percy
05-18-2017 8:05 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
Percy writes:
What is a haplotype? The Wikipedia article on Haplotype offers several definitions.
Genes close to one another tend to stay together because fewer cross over events happen between them during meiosis. Therefore, some alleles on neighboring genes will stay together. For example, you may tend to see allele1 from gene A and allele 2 from gene B at a higher ratio than would be predicted by chance (i.e. a random shuffle).
As to a "composite of different haplotypes", I'm not sure exactly what they are talking about. They could be talking about a composite of DNA from different people, different strands of DNA (remember that human DNA is diploid so it has two strands), or a combination of both.
What does the little symbol between curly braces mean?
The Greek letter Psi is meant to denote pseudogenes (Psi ---> pseudo).
Does this mean that for some loci different people can have different genes instead of different alleles?
That is what it means. This usually indicates that some people will have a gene at a specific location while others just have a gap. It can also indicate a difference in copy number, such as one person having 1 geneA and other people have duplication of 2 geneA at the same position.
There are 118 (good "quick count" by you).
I counted the number across and the number of rows, so don't be too impressed.

This message is a reply to:
 Message 254 by Percy, posted 05-18-2017 8:05 AM Percy has seen this message but not replied

  
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


Message 263 of 518 (809447)
05-18-2017 12:28 PM
Reply to: Message 260 by Faith
05-18-2017 11:38 AM


Re: On Adam & Eve?
Faith writes:
they don't look identical to me:
They look identical to a molecular biologist.
Let's use this piece of DNA as our example:
5'--GTGGACCAGT--3'
3'--CACCTGGTCA--5'
Across from each base is it's mirror image. G is the mirror image of C, C is the mirror image of G, A is the mirror image of T, and T is the mirror image of A. Think of it like your hand being held up to a mirror. If you hold your right hand up to a mirror it isn't an identical copy of your hand, but is instead a mirror image that more resembles your left hand. Your left and right hands are mirror images of each other.
The 5' and 3' denote the ends of each DNA strand, as you will see the two DNA strands go in opposite directions. The 5' and 3' come from the number of carbon atoms on the sugar that forms the backbone of DNA:
When proteins copy DNA they start at the 5' end and stop at the 3' end.
So when we copy DNA we go from the double stranded form to the single stranded forms
5'--GTGGACCAGT--3'

3'--CACCTGGTCA--5'
DNA polymerases then copy each single strand from the 5' to 3' strand, placing the mirror image of each base on the new strand. This results in two double stranded pieces of DNA:
5'--GTGGACCAGT--3'
3'--CACCTGGTCA--5'
    ---copy-->

    <---copy--
5'--GTGGACCAGT--3'
3'--CACCTGGTCA--5'
What you end up with is two identical double strands of DNA.
Edited by Taq, : No reason given.
Edited by Taq, : No reason given.
Edited by Taq, : No reason given.

This message is a reply to:
 Message 260 by Faith, posted 05-18-2017 11:38 AM Faith has replied

Replies to this message:
 Message 264 by New Cat's Eye, posted 05-18-2017 12:37 PM Taq has replied
 Message 266 by Faith, posted 05-18-2017 12:43 PM Taq has replied

  
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


Message 265 of 518 (809456)
05-18-2017 12:43 PM
Reply to: Message 264 by New Cat's Eye
05-18-2017 12:37 PM


Re: On Adam & Eve?
New Cat's Eye writes:
Chirality!
In the case of DNA bases it isn't chirality. However, mirror image serves as a good analogy even if it can be confusing if we discuss chirality. I didn't think "complementary bases" would be as easy to understand.

This message is a reply to:
 Message 264 by New Cat's Eye, posted 05-18-2017 12:37 PM New Cat's Eye has seen this message but not replied

  
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


Message 267 of 518 (809459)
05-18-2017 12:44 PM
Reply to: Message 266 by Faith
05-18-2017 12:43 PM


Re: On Adam & Eve?
Faith writes:
That's beautiful. And you guys don't believe in intelligent design!
Not when we can watch this all happen right in front of us without any intelligent designer involved.

This message is a reply to:
 Message 266 by Faith, posted 05-18-2017 12:43 PM Faith has not replied

  
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


(1)
Message 270 of 518 (809484)
05-18-2017 1:25 PM
Reply to: Message 269 by Faith
05-18-2017 1:16 PM


Re: How to understand some but not all. Good grief
Faith writes:
Ooooooobviously I understood some of it. Sheesh.
Let's see if you are able to understand this paper:
http://www.jimmunol.org/...3/11/03/jimmunol.1302101.full.pdf
It is rather straightforward. They looked at several alleles for the HLA-A and HLA-B genes. They then tested them against multiple peptides (i.e. short proteins) from the Dengue fever virus. What they found is that different alleles bound different peptides, proof that they have different functions (table 1 from the paper).
Since they were able to show that more than two alleles for each gene bound different peptides, this demonstrates that are more than two alleles for these genes as defined by function.

This message is a reply to:
 Message 269 by Faith, posted 05-18-2017 1:16 PM Faith has not replied

Replies to this message:
 Message 271 by bluegenes, posted 05-18-2017 2:33 PM Taq has replied

  
Taq
Member
Posts: 10021
Joined: 03-06-2009
Member Rating: 5.3


Message 276 of 518 (809585)
05-19-2017 10:43 AM
Reply to: Message 274 by Percy
05-19-2017 9:28 AM


Re: On Adam & Eve?
Percy writes:
One question I've sometimes wondered about, and maybe someone here has an answer, is how geneticists decide which half of the paired DNA strands to list. For example, if they provide this short DNA sequence:
AGTTCCAGT...
They could just as easily have provided the sequence of the other strand:
TCAAGGTCA...
Which to choose?
The standard nomenclature is to label them the (+) and (-) strands. In prokaryotes with their circular chromosome, the + strand is determined by the strand containing the origin of replication which is the place at which replication of the genome begins. I'm not sure what the convention for choosing the positive strands in eukaryotes is, but I would guess that it is somewhat more arbitrary than that found in prokaryotes.
The other standard nomenclature is to always list DNA sequences in the 5' to 3' direction. Let's say we have this double strand of DNA:
5'--ATTAGGCCA--3'
3'--TAATCCGGT--5'
For the lower strand you would list the sequence as TGGCCTAAT, which is the reverse of the double strand.
As you would probably guess, some genes are found on the + strand and some on the - strand. If you are dealing with a gene then the convention is to give the sequence of the open reading frame in the 5' to 3' direction no matter what strand it is found on. Most databases will list which strand the gene is found on.
Edited by Taq, : No reason given.

This message is a reply to:
 Message 274 by Percy, posted 05-19-2017 9:28 AM Percy has seen this message but not replied

  
Newer Topic | Older Topic
Jump to:


Copyright 2001-2023 by EvC Forum, All Rights Reserved

™ Version 4.2
Innovative software from Qwixotic © 2024