DNA Stability

[dad]

For 99.9999999% of biology, they don't. We don't need to know anything about abiogenesis in order to work out phylogenies for mammals or vertebrates. Even for work on reconstructing LUCA (last universal common ancestor), it really doesn't enter into the equation much.

Right, you just need immense faith in an imaginary tree whose branches all got same state past sap. Good luck with that! Additionally, one has to start off omitting a creator, and assuming that life produced it's little self! So called science is mental rigor mortis.

 

[Loudmouth]

Right, you just need immense faith in an imaginary tree whose branches all got same state past sap. Good luck with that! Additionally, one has to start off omitting a creator, and assuming that life produced it's little self! So called science is mental rigor mortis.

You don't even understand what a phylogeny is. Why should any of us take you seriously?

 

[Loudmouth]

Sure. Everybody and their mother thinks they have found the secret sauce, but rarely do any of those ideas yield anything. Still, recognizing and understanding patterns are a very important step in predicting behavior.

Before the roll of a pair of dice in craps, you can predict that the most likely outcome is 7. The distribution of results is a bell curve around the number 7. It has a pattern, yet it is random. I guess I don't understand why you are contrasting patterns and randomness.

I'm asking if the stability of DNA is related to the sequence such that we could put a measure on it and conclude sequence A is x% more stable than sequence B.

If by stability you mean less prone to mutation, you would first need to know if the sequence is functional, at least in prokaryotes. Wright et al. (1999) has a really nice paper demonstrating that actively transcribed genes in E. coli experience a higher rate of mutation. This is due to DNA being single stranded during transcription. I don't know if this extends to eukaryotes or not.

Hypermutation in derepressed operons of Escherichia coli K12

If that same stretch of DNA is not being transcribed, then it is more stable. So you can't score the stability of a DNA sequence simply by its sequence. There is more to it than that.

Second, if that were possible, I would be interested in comparing the stability of junk DNA to coding DNA.

For eukaryotes, I think it would hinge more on CpG content than anything else.

Of all the papers I've read about prediciting patterns in DNA, your claim seems the most confident. If I thought I could do it myself, I would. I'd like to better understand what BLAST does. My impression is that it uses some sort of fuzzy (statistical/empirical) basis similar to a neural net, but I'm not sure.

They are simple algorithms that find the best matches to your query.

But since you seem to think it an easy thing, maybe you could try a few things for us here at CF:
1) What % confidence is there that BLAST will predict the next base correctly?

For human coding regions that have orthologs in chimps, more than 99%.

2) Does the prediction improve as you give it more related sequences?

Yes.

3) Is the % confidence different for coding and junk DNA?

There is more divergence in junk DNA, so the confidence would be lower in junk DNA.

 

[dad]

You don't even understand what a phylogeny is. Why should any of us take you seriously?

The basis for your reinventing the kinds is clear and not rocket science. Pretend it is more than religion all you like. I know.

 

[dad]

For human coding regions that have orthologs in chimps, more than 99%.

Prove that these are related by linear descent?

 

[sfs]

So ... do you have a coding sequence and a junk sequence from the same genome I could use see what happens?

What you'll find will depend greatly on what kind of junk you pick. Here's some junk sequence. It's the consensus sequence for the Alu-Y family of SINE elements. All told, there are ~1 million Alu copies in the human genome. (Assuming I typed it in correctly -- I couldn't find a copy I could cut and paste.)

GGCCGGGCGCGGTGGCTCACGCCTGTAATCCCAGCACTTTGGGAGGCCGAGGCGGGCGGATCACGAGGTCAGGAGATCGAGACCATCCTGGCTAAC
ACGGTGAAACCCCGTCTCTACTAAAAATACAAAAAATTAGCCGGGCGTGGTGGCGGGCGCCTGTAGTCCCAGCTACTCGGGAGGCTGAGGCAGGAGA
ATGGCGTGAACCCGGGAGGCGGAGCTTGCAGTGAGCCGAGATCGCGCCACTGCACTCCAGCCTGGGCGAGAGCGAGACTCCGTCTCA

Here's some non-junk. It's the gene hemoglobin B (without introns); coding sequence is in caps.

acatttgcttctgacacaactgtgttcactagcaacctcaaacagacaccATGGTGCATCTGACTCCTGAGGAGAAGTCTGCCGTTACTGCCCTGTGGGGCAAGGTGAA
CGTGGATGAAGTTGGTGGTGAGGCCCTGGGCAGGTTGGTATCAAGGTTACAAGACAGGTTTAAGGAGACCAATAGAAACTGGGCATGTGGAGACAGA
GAAGACTCTTGGGTTTCTGATAGGCACTGACTCTCTCTGCCTATTGGTCTATTTTCCCACCCTTAGGCTGCTGGTGGTCTACCCTTGGACCCAGAGGTTC
TTTGAGTCCTTTGGGGATCTGTCCACTCCTGATGCTGTTATGGGCAACCCTAAGGTGAAGGCTCATGGCAAGAAAGTGCTCGGTGCCTTTAGTGATGGC
CTGGCTCACCTGGACAACCTCAAGGGCACCTTTGCCACACTGAGTGAGCTGCACTGTGACAAGCTGCACGTGGATCCTGAGAACTTCAGGGTGAGTC
TATGGGACGCTTGATGTTTTCTTTCCCCTTCTTTTCTATGGTTAAGTTCATGTCATAGGAAGGGGATAAGTAACAGGGTACAGTTTAGAATGGGAAACAGA
CGAATGATTGCATCAGTGTGGAAGTCTCAGGATCGTTTTAGTTTCTTTTATTTGCTGTTCATAACAATTGTTTTCTTTTGTTTAATTCTTGCTTTCTTTTTTTTT
CTTCTCCGCAATTTTTACTATTATACTTAATGCCTTAACATTGTGTATAACAAAAGGAAATATCTCTGAGATACATTAAGTAACTTAAAAAAAAACTTTACACA
GTCTGCCTAGTACATTACTATTTGGAATATATGTGTGCTTATTTGCATATTCATAATCTCCCTACTTTATTTTCTTTTATTTTTAATTGATACATAATCATTATACA
TATTTATGGGTTAAAGTGTAATGTTTTAATATGTGTACACATATTGACCAAATCAGGGTAATTTTGCATTTGTAATTTTAAAAAATGCTTTCTTCTTTTAATATAC
TTTTTTGTTTATCTTATTTCTAATACTTTCCCTAATCTCTTTCTTTCAGGGCAATAATGATACAATGTATCATGCCTCTTTGCACCATTCTAAAGAATAACAGTG
ATAATTTCTGGGTTAAGGCAATAGCAATATCTCTGCATATAAATATTTCTGCATATAAATTGTAACTGATGTAAGAGGTTTCATATTGCTAATAGCAGCTACAA
TCCAGCTACCATTCTGCTTTTATTTTATGGTTGGGATAAGGCTGGATTATTCTGAGTCCAAGCTAGGCCCTTTTGCTAATCATGTTCATACCTCTTATCTTCCT
CCCACAGCTCCTGGGCAACGTGCTGGTCTGTGTGCTGGCCCATCACTTTGGCAAAGAATTCACCCCACCAGTGCAGGCTGCCTATCAGAAAGTGGTGG
CTGGTGTGGCTAATGCCCTGGCCCACAAGTATCACTAAgctcgctttcttgctgtccaatttctattaaaggttcctttgttccctaagtccaactactaaactgggggatattatgaag
ggccttgagcatctggattctgcctaataaaaaacatttattttcattgc

(broken into arbitrary lines for avoid messing up the thread)

 

[sfs]

Note that there are all kinds of patterns in DNA. Some of them are caused by the source of the sequence, e.g. transposons that copy themselves produce lots of (nearly) identical DNA segments. Many of them are functional: transcription factor binding motifs, for example, or PRDM9 binding sites. The functional ones may not be significantly overrepresented in the genome -- in fact, may well be underrepresented -- but they're the ones that biologists spend time teasing out, since they're the interesting ones.

 

[Loudmouth]

Prove that these are related by linear descent?

Already done in multiple threads.

 

[Loudmouth]

The basis for your reinventing the kinds is clear and not rocket science. Pretend it is more than religion all you like. I know.

Do you even know how phylogenies are constructed? It doesn't appear that you do.

 

[dad]

Already done in multiple threads.

Not one ever actually, despite what you may think. Simply blathering on about how something was linear in Noah's day is religion. Not based on any knowledge at all.

 

[dad]

Do you even know how phylogenies are constructed? It doesn't appear that you do.

Any dolt can google that. The darn thing is that real life did not work that way, and you assume it did and draw silly trees. Not impressed.

 

[Resha Caner]

What you'll find will depend greatly on what kind of junk you pick. Here's some junk sequence. It's the consensus sequence for the Alu-Y family of SINE elements. All told, there are ~1 million Alu copies in the human genome. (Assuming I typed it in correctly -- I couldn't find a copy I could cut and paste.)

GGCCGGGCGCGGTGGCTCACGCCTGTAATCCCAGCACTTTGGGAGGCCGAGGCGGGCGGATCACGAGGTCAGGAGATCGAGACCATCCTGGCTAAC
ACGGTGAAACCCCGTCTCTACTAAAAATACAAAAAATTAGCCGGGCGTGGTGGCGGGCGCCTGTAGTCCCAGCTACTCGGGAGGCTGAGGCAGGAGA
ATGGCGTGAACCCGGGAGGCGGAGCTTGCAGTGAGCCGAGATCGCGCCACTGCACTCCAGCCTGGGCGAGAGCGAGACTCCGTCTCA

Here's some non-junk. It's the gene hemoglobin B (without introns); coding sequence is in caps.

acatttgcttctgacacaactgtgttcactagcaacctcaaacagacaccATGGTGCATCTGACTCCTGAGGAGAAGTCTGCCGTTACTGCCCTGTGGGGCAAGGTGAA
CGTGGATGAAGTTGGTGGTGAGGCCCTGGGCAGGTTGGTATCAAGGTTACAAGACAGGTTTAAGGAGACCAATAGAAACTGGGCATGTGGAGACAGA
GAAGACTCTTGGGTTTCTGATAGGCACTGACTCTCTCTGCCTATTGGTCTATTTTCCCACCCTTAGGCTGCTGGTGGTCTACCCTTGGACCCAGAGGTTC
TTTGAGTCCTTTGGGGATCTGTCCACTCCTGATGCTGTTATGGGCAACCCTAAGGTGAAGGCTCATGGCAAGAAAGTGCTCGGTGCCTTTAGTGATGGC
CTGGCTCACCTGGACAACCTCAAGGGCACCTTTGCCACACTGAGTGAGCTGCACTGTGACAAGCTGCACGTGGATCCTGAGAACTTCAGGGTGAGTC
TATGGGACGCTTGATGTTTTCTTTCCCCTTCTTTTCTATGGTTAAGTTCATGTCATAGGAAGGGGATAAGTAACAGGGTACAGTTTAGAATGGGAAACAGA
CGAATGATTGCATCAGTGTGGAAGTCTCAGGATCGTTTTAGTTTCTTTTATTTGCTGTTCATAACAATTGTTTTCTTTTGTTTAATTCTTGCTTTCTTTTTTTTT
CTTCTCCGCAATTTTTACTATTATACTTAATGCCTTAACATTGTGTATAACAAAAGGAAATATCTCTGAGATACATTAAGTAACTTAAAAAAAAACTTTACACA
GTCTGCCTAGTACATTACTATTTGGAATATATGTGTGCTTATTTGCATATTCATAATCTCCCTACTTTATTTTCTTTTATTTTTAATTGATACATAATCATTATACA
TATTTATGGGTTAAAGTGTAATGTTTTAATATGTGTACACATATTGACCAAATCAGGGTAATTTTGCATTTGTAATTTTAAAAAATGCTTTCTTCTTTTAATATAC
TTTTTTGTTTATCTTATTTCTAATACTTTCCCTAATCTCTTTCTTTCAGGGCAATAATGATACAATGTATCATGCCTCTTTGCACCATTCTAAAGAATAACAGTG
ATAATTTCTGGGTTAAGGCAATAGCAATATCTCTGCATATAAATATTTCTGCATATAAATTGTAACTGATGTAAGAGGTTTCATATTGCTAATAGCAGCTACAA
TCCAGCTACCATTCTGCTTTTATTTTATGGTTGGGATAAGGCTGGATTATTCTGAGTCCAAGCTAGGCCCTTTTGCTAATCATGTTCATACCTCTTATCTTCCT
CCCACAGCTCCTGGGCAACGTGCTGGTCTGTGTGCTGGCCCATCACTTTGGCAAAGAATTCACCCCACCAGTGCAGGCTGCCTATCAGAAAGTGGTGG
CTGGTGTGGCTAATGCCCTGGCCCACAAGTATCACTAAgctcgctttcttgctgtccaatttctattaaaggttcctttgttccctaagtccaactactaaactgggggatattatgaag
ggccttgagcatctggattctgcctaataaaaaacatttattttcattgc

(broken into arbitrary lines for avoid messing up the thread)

Thanks. Hopefully it wasn't too much effort or you'll make me feel guilty. At first glance I don't really see what I was looking for ... but maybe it was worth it just for that.

 

[sfs]

Thanks. Hopefully it wasn't too much effort or you'll make me feel guilty.

Nah. Just did a little looking around during a slack period during a conference I'm at.

 

[sfs]

Note that there are all kinds of patterns in DNA. Some of them are caused by the source of the sequence, e.g. transposons that copy themselves produce lots of (nearly) identical DNA segments. Many of them are functional: transcription factor binding motifs, for example, or PRDM9 binding sites. The functional ones may not be significantly overrepresented in the genome -- in fact, may well be underrepresented -- but they're the ones that biologists spend time teasing out, since they're the interesting ones.

I heard a talk last night that happened to be about both underrepresented patterns in the genome and PRDM9 binding sites. Outline:

1) The gene PRDM9 produces a protein that binds to a particular motif in DNA. When it binds, it initiates recombination, so PRDM9 binding sites become hotspots of recombination.
2) Intense recombination, though, has a good chance of changing the DNA at the site, causing the motif (and hotspot) to disappear. So the number of recombination hotspots tends to decline over time.
3) Since recombination is good for organisms, (2) means that there is selection pressure for changes to PRDM9 that will bind to a new motif. PRDM9 does in fact change frequently on evolutionary timescales. (All of this is already known.)
4) Previous versions of PRDM9 should be detectable because their motifs are still underrepresented in the genome, having been destroyed by the process in (2). The talk was about searching the genomes of humans and other primates for the underrepresented motifs. They identified many.
5) Because recombination drives the loss of motifs, the degree of depletion of old motifs at different places in the genome provides a map of recombination rates at earlier points in the species' history; a region with stronger depletion means the recombination rate was high in that region
6) When they reconstruct the map of ancient recombination rates for the human genome, it mostly looks very similar to modern recombination maps. In particular, it reveals the characteristic increase in recombination near the ends of chromosomes. The only place where the old maps and current maps really disagree? Chromosome 2, where the reconstructed ancient rate had a big spike in the middle of the chromosome, one that is lacking today. It occurs (of course) at the fusion point between the two ancestral chromosomes that joined to form our chromosome 2. In other words, they're reconstructing recombination rates from before the famous fusion occurred.

Very cool analysis -- and a good illustration of the kinds of biologically meaningful patterns that geneticists are interested in.

 

[Loudmouth]

Any dolt can google that. The darn thing is that real life did not work that way, and you assume it did and draw silly trees. Not impressed.

Then google it. Show us what those phylogenies are based on. You will find that you can construct those trees without assuming common descent.

If life did not evolve, then you need to explain why the evidence is consistent with evolution. If all you have is mockery, then you have lost the debate.

 

[Loudmouth]

Not one ever actually, despite what you may think. Simply blathering on about how something was linear in Noah's day is religion. Not based on any knowledge at all.

I can't force you to look at the evidence. When you are ready to be honest, we can discuss the evidence.

 

[PsychoSarah]

Exactly. So what about 6 codes? 100 codes? 1000 codes? What is the shortest DNA (or RNA) sequence you know of that has been observed to replicate and produce an organism?



But what must be included in the system that allows these things to replicate? If you subtract something from the system, and the entity henceforth fails to replicate, then it's not a viable system. So what is the minimum system that will replicate?



Only because they can cannibalize another system. So, if you want to define a "viral system" per the question I'm asking, it would need to include the host.

This question is irrelevant, because the first item capable of replicating probably wouldn't be considered alive, and anything we observe doing so today has had billions of years to develop adaptations to get better at it, all of which would lengthen their genomes, even nonliving ones such as viruses. Prions are the smallest I know of, and they consist of about 150 amino acids. And that is it, nothing else. But they aren't DNA. As for DNA, I suppose the shortest sequence possible would be ATGTAA , which would produce just 1 amino acid. As signals, DNA sequences in triplets called codons, so ATG is a start codon that also signals the production of an amino acid, and TAA is one of 3 stop codons. But, this is a matter of function, technically, it doesn't matter how long the DNA is so long as replicating proteins are present. And nothing would prevent a protein produced by one strand from interacting with other nearby strands.

No, DNA would just replicate slower and have more errors in the process. All of the energy we produce and use goes to making such things go faster, most of the processes of a cell are chemical reactions that happen outside of living things, just slower.

The service a host provides to a virus is material for replication, a virus contains the means to force replication to occur. A cell nucleus has a high concentration of nucleic acids, which is what a virus needs in order to replicate. In an environment with a high concentration of nucleic acids, an early virus could have simply released its genetic material to the outside in order to replicate.

 

[Papias]

sfs wrote:

GATTTCTCGAA.....

Cool, thanks for posting actual DNA.

it reveals the characteristic increase in recombination near the ends of chromosomes. The only place where the old maps and current maps really disagree? Chromosome 2, where the reconstructed ancient rate had a big spike in the middle of the chromosome, one that is lacking today. It occurs (of course) at the fusion point between the two ancestral chromosomes that joined to form our chromosome 2. In other words, they're reconstructing recombination rates from before the famous fusion occurred.

Wow! How cool is that! yet another confirmation of our earlier ape ancestry.

-Papias

 

[dad]

Then google it. Show us what those phylogenies are based on. You will find that you can construct those trees without assuming common descent.

Great construct one for us. I will point out in new York minute how there is no basis for the connection at all.

If life did not evolve, then you need to explain why the evidence is consistent with evolution.

It did evolve..AFTER God created it! Nothing you have says otherwise. Make like a clam.

 

[dad]

I can't force you to look at the evidence.

I can't force you to post said evidence. But I can expose whatever you post as religion and not evidence.




When you are ready to be honest, we can discuss the evidence.