Darwin and Mendel

[Papias]

LM wrote:

You don't see the significance of mutations producing a beneficial phenotype? Really?

Wow, ..... yet......again.....

Thanks, sfs and Loudmouth, for taking the time and effort to help everyone here learn some really cool genetics. Your intelligence, knowledge, and expertise are recognized by myself and others, even if some prefer to continue to deny reality and act as if they have a clue as to the topic under discussion.



Thanks mark, for posting your posts here in this open forum where there are several experts on genetics who can help you learn.

In Jesus' name-

Papias

 

[mark kennedy]

If you have two alleles for a gene, this means that the alleles have different DNA sequences. Guess what produces differences in DNA sequence? Mutations.

The only directly observed or demonstrated effect with a known cause is an artificial amino acid substitution, the rest are simple comparisons. Nothing conclusive or consistent with random mutations.

It is very conclusive. Please address it.

The genetic basis of adaptive melanism in pocket mice

That's just a link, your begging the question based on a random paper you haven't even quoted.

You don't see the significance of mutations producing a beneficial phenotype? Really?

It's not a phenotype, it's a changing trait at best.

The mechanisms of mutagenesis are well understood. Are you denying that mutations occur?

Of course not, epigentics is far more a reliable explanation. Changing the actual DNA is not always the explanation.

That is false. Substitutions are more common than indels. We have shown you this many many times. It also doesn't change the fact that I just showed you that they are substitution mutations. You are trying to deny the facts.

That is an absolute statistical fact, the effect of mutations will be deleterious at least 98% of the time, at least. What we are talking about is an amino acid substitution, that is a triplet codon, artificially substituted, producing the color change. That's your problem, you never learned the basics, you don't appreciate the danger of frameshifts if protein coding genes and as far as I can tell you have no idea that we are talking about an amino acid substitution, not a point mutation.

You have major problems with the basics, a failing you cloud with semantics. I've seen you do this too many times LM, this time is a fundamental misunderstanding of an amino acid substitution because you have no appreciation for what an amino acid actually is:

How do you get an amino acid substitution by means other then artificial selection?

A non-synonymous substitution mutation.

Still you have no cause which is the fallacious nature of Darwinian logic.

Have a nice day
Mark

 

[Loudmouth]

The only directly observed or demonstrated effect with a known cause is an artificial amino acid substitution, the rest are simple comparisons. Nothing conclusive or consistent with random mutations.

Are you seriously denying that mutations have been observed in the lab? I can come up with tons of papers demonstrating that random mutations occur, including in humans.

That's just a link, your begging the question based on a random paper you haven't even quoted.

"Both alleles of the entire Mc1r gene (954 bp) were sequenced in the 69 mice in Fig. 1. Twenty-four single-nucleotide polymorphisms were observed: 15 were synonymous and 9 were nonsynonymous. Four of the nine amino acid polymorphisms were observed only in the dark mice from the Pinacate locality (Arg-18 → Cys, Arg-109 → Trp, Arg-160 → Trp, and Gln-233 → His). These four amino acid variants were present at high frequency (82%) among the Pinacate dark mice and were in complete linkage disequilibrium with one another. All other Mc1r amino acid polymorphisms were present at low frequencies and showed no association with mouse color. The distribution of Mc1r nucleotide variation among light and melanic mice from the Pinacate site is shown in Table 1. "
The genetic basis of adaptive melanism in pocket mice

It's not a phenotype, it's a changing trait at best.

And here I thought you knew how Mendelian genetics works. It seems that you can't even do simple Punnett squares.

Of course not, epigentics is far more a reliable explanation. Changing the actual DNA is not always the explanation.

Are humans different from elephants because of epigenetics? Do you even know what epigenetics is? Here you are talking about Mendelian genetics, and you want to throw it all away for epigenetics.

That is an absolute statistical fact, the effect of mutations will be deleterious at least 98% of the time, at least.

Reference please.

What we are talking about is an amino acid substitution, that is a triplet codon, artificially substituted, producing the color change.

You only need to change one base in order to have a chance to change the amino acid sequence at one position.

That's your problem, you never learned the basics, you don't appreciate the danger of frameshifts if protein coding genes and as far as I can tell you have no idea that we are talking about an amino acid substitution, not a point mutation.

Substitutions don't produce frameshifts. Again, you are getting the basics wrong.

You have major problems with the basics, a failing you cloud with semantics. I've seen you do this too many times LM, this time is a fundamental misunderstanding of an amino acid substitution because you have no appreciation for what an amino acid actually is:

I know exactly what it is. I have experience working with DNA, including the introduction of synonymous restriction sites for downstream diagnostics through the use of PCR mutagenesis.

I am not the one who is continually confusing indels with substitutions.

I am not the one who keeps failing to understand that substitutions are more common than indels.

I am not the one who keeps failing to understand the difference between synonymous and nonsynonymous substitution reactions.

I am not the one who doesn't understand what epigenetics is.

I am not the one who doesn't understand how a Punnett square works.

All of these are things you keep failing to understand.

How do you get an amino acid substitution by means other then artificial selection?

A perfect example of what I am talking about. Mutagenesis and selection ARE DIFFERENT THINGS.

Still you have no cause which is the fallacious nature of Darwinian logic.

Have a nice day
Mark

The cause is mutations which you keep ignoring.

 

[Loudmouth]

Just so everyone is on the same page, there are two sequences below. Sequence A is the original sequence, and sequence B is the mutated sequence.

A synonymous substitution mutation at the 3rd position.

sequence A: ATTATTATT
sequence B: ATAATTATT

The ATT and ATA codons both produce isoleucine, so it is considered a synonymous mutation.

A nonsynonymous substitution mutation at the 3rd position:

sequence A: ATTATTATT
sequence B: ATGATTATT

The change to the ATG codon produces methionine which is a different amino acid, so this makes it a nonsynonymous mutation.

A single base indel at the 3rd position

sequence A: ATTATTATT
sequence B: AT-ATGATG

This is a frameshift mutation which produces a different amino acid sequence in the second and third codons.

 

[Loudmouth]

Mr. Kennedy also tries to make the false claim that indels are more common than singl nucleotide subsitutions. This is completely false. For example, the very recent paper looked at 10 parent-offspring trios and found that single nucleotide substitutions are about 10 times more common than indel mutations:

"In addition, we use trio information to identify de novo mutations and use a probabilistic method to provide direct estimates of 1.27e−8 and 1.5e−9 per nucleotide per generation for SNVs and indels, respectively."
Novel variation and de novo mutation rates in population-wide de novo assembled Danish trios : Nature Communications : Nature Publishing Group

There is a substitution every 130 million bases and an indel about every 1.5 billion bases.

Mr. Kennedy also claims that the vast majority of mutations (~97%) are deleterious because they change amino acid sequence. Since only 2% of the genome is translated into proteins, this claim is completely false even on the face of it.

 

[mark kennedy]

Fallacy mongering is not a crime, your free to go.

Mr. Kennedy also tries to make the false claim that indels are more common than singl nucleotide subsitutions. This is completely false.

I never said that, I guess this is where the ad hominem kicks in.

For example, the very recent paper looked at 10 parent-offspring trios and found that single nucleotide substitutions are about 10 times more common than indel mutations:

"In addition, we use trio information to identify de novo mutations and use a probabilistic method to provide direct estimates of 1.27e−8 and 1.5e−9 per nucleotide per generation for SNVs and indels, respectively."
Novel variation and de novo mutation rates in population-wide de novo assembled Danish trios : Nature Communications : Nature Publishing Group

Indels, that is insertions and deletions in comparing the Chimpanzee and Human Genomes dwarf the single base pair differences. I appreciate the fact that you have abandoned all substantive discussion, it's a fun little straw man argument.

There is a substitution every 130 million bases and an indel about every 1.5 billion bases.

Mr. Kennedy also claims that the vast majority of mutations (~97%) are deleterious because they change amino acid sequence. Since only 2% of the genome is translated into proteins, this claim is completely false even on the face of it.

Who are you talking to and more importantly, what did that poor strawman ever do to you?

Have a nice day
Mark

 

[mark kennedy]

Are you seriously denying that mutations have been observed in the lab? I can come up with tons of papers demonstrating that random mutations occur, including in humans.

What I said was the amino acid substitution observed, which was sufficient to produce the color change, was artificially induced. Your not even watching your own argument just going straight to the derailment.

"Both alleles of the entire Mc1r gene (954 bp) were sequenced in the 69 mice in Fig. 1. Twenty-four single-nucleotide polymorphisms were observed: 15 were synonymous and 9 were nonsynonymous. Four of the nine amino acid polymorphisms were observed only in the dark mice from the Pinacate locality (Arg-18 → Cys, Arg-109 → Trp, Arg-160 → Trp, and Gln-233 → His). These four amino acid variants were present at high frequency (82%) among the Pinacate dark mice and were in complete linkage disequilibrium with one another. All other Mc1r amino acid polymorphisms were present at low frequencies and showed no association with mouse color. The distribution of Mc1r nucleotide variation among light and melanic mice from the Pinacate site is shown in Table 1. "
The genetic basis of adaptive melanism in pocket mice

Which simply describes the different sequences. Standard genomics.

And here I thought you knew how Mendelian genetics works. It seems that you can't even do simple Punnett squares.

Whatever that means.

Are humans different from elephants because of epigenetics? Do you even know what epigenetics is? Here you are talking about Mendelian genetics, and you want to throw it all away for epigenetics.

Changes without mutations, dominant and recessive traits, the 3:1 ratio. Any of this ringing any bells?

Reference please.

If you would decide on an actual topic I can do that.

You only need to change one base in order to have a chance to change the amino acid sequence at one position.

What you need is an amino acid substitution in order to produce the trait artificially.

Substitutions don't produce frameshifts. Again, you are getting the basics wrong.

A single base substitution in an amino acid sequence could, if you substitute another amino acid it could work in a lab. The odds of it happening as the result of a spontaneous mutation is about zip. Then there are those Arctic Cod fish...you probably wouldn't be interested in an actual adaptation though...

I know exactly what it is. I have experience working with DNA, including the introduction of synonymous restriction sites for downstream diagnostics through the use of PCR mutagenesis.

Yea, that was random.

I am not the one who is continually confusing indels with substitutions.

No your the one who plays fast and loose with the semantic shell game. Indels are generally two or more in length, while what your calling substitutions are single base substitutions, aka point mutations, in the general terminology of basic genetics. I have never gotten any indication that you cared what the terms mean.

I am not the one who keeps failing to understand that substitutions are more common than indels.

More frequent. This is what your talking about whether you know it or not:

On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions. (Initial Sequence of the Chimpanzee Genome, Nature 2005)​

The size of the indels, some of which are over a million base pairs, dwarf the single base substitutions. Steve likes to argue that even an indel a million base pairs long counts as just one mutation. That's where your pedantic correction is coming from but Steve is talking about mutation rates, which is actually a true statement, weak argument, but actual fact. If you ever bothered to learn a little about the subject matter, these discussions could be a lot more interesting.

I am not the one who keeps failing to understand the difference between synonymous and nonsynonymous substitution reactions.

Not that it matters in this discussion.

I am not the one who doesn't understand what epigenetics is.

Yea, actually, you are.

I am not the one who doesn't understand how a Punnett square works.

Which has nothing to do with anything.

All of these are things you keep failing to understand.

No, you just make condescending remarks in circles

A perfect example of what I am talking about. Mutagenesis and selection ARE DIFFERENT THINGS.

So are cause and effect.

The cause is mutations which you keep ignoring.

In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair. Mutations

I've pointed it out repeatedly, your the one who ignores basic biology, in circles, endlessly.

Have a nice day
Mark

 

[mark kennedy]

Thanks, sfs and Loudmouth, for taking the time and effort to help everyone here learn some really cool genetics. Your intelligence, knowledge, and expertise are recognized by myself and others, even if some prefer to continue to deny reality and act as if they have a clue as to the topic under discussion.

Steve, aka sfs really does work in the field and is an accomplished scientist. LM is trolling the boards a lot like your so fond of doing. There is really not that much going on in the discussion except some unidentified beneficial mutations and LM's standard semantic shell games.

Thanks mark, for posting your posts here in this open forum where there are several experts on genetics who can help you learn.

I've been playing intellectual ping pong with these guys for years. But if you think LM is an expert your pretty badly mistaken.

In Jesus' name-

Papias

Grace and peace,
Mark

 

[Loudmouth]

What I said was the amino acid substitution observed, which was sufficient to produce the color change, was artificially induced.

How was it artificially induced? It was found in wild populations.

Which simply describes the different sequences. Standard genomics.

It describes the MUTATIONS that separate them, the mutations that are responsible for the change in fur color.

Whatever that means.

You don't even know how to use Punnett squares?

Changes without mutations, dominant and recessive traits, the 3:1 ratio. Any of this ringing any bells?

Yeah, it should ring bells with you too. The light allele is recessive. The dark allele is dominant. Therefore, the dark phenotype could not have been hiding in the original population as a recessive allele.

The basalt lava where the dark mice are found is much younger than the surrounding light colored desert. As you can see, the black mice can not survive on the light colored desert. No black mice are found between the black basalt lava fields in the light colored desert, even thought the black phenotype is dominant. Therefore, the black allele had to come about through mutations in the light color allele after the black lava fields came to be.

What you need is an amino acid substitution in order to produce the trait artificially.

Why can't it happen naturally?

A single base substitution in an amino acid sequence could, if you substitute another amino acid it could work in a lab. The odds of it happening as the result of a spontaneous mutation is about zip. Then there are those Arctic Cod fish...you probably wouldn't be interested in an actual adaptation though...

I just showed you the single base substitutions that did produce a change in the amino acid sequence.

No your the one who plays fast and loose with the semantic shell game. Indels are generally two or more in length, while what your calling substitutions are single base substitutions, aka point mutations, in the general terminology of basic genetics. I have never gotten any indication that you cared what the terms mean.

You are the one who continually confuses indels and substitutions.

More frequent. This is what your talking about whether you know it or not:

On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions. (Initial Sequence of the Chimpanzee Genome, Nature 2005)​

A 10 base indel is one indel. A 100 base indel is one indel. A 2 base indel is one indel. That is what you fail to understand. From that same paper:

"•Insertion and deletion (indel) events are fewer in number than single-nucleotide substitutions, but result in ~1.5% of the euchromatic sequence in each species being lineage-specific."

"The analysis of modest-sized insertions reveals ~32 Mb of human-specific sequence and ~35 Mb of chimpanzee-specific sequence, contained in ~5 million events in each species (Supplementary Information ‘Genome evolution’ and Supplementary Fig. S5). "

That's 35 million substitutions and 5 million indels. Substitutions are 6 times more common than indels when comparing the chimp and human genomes. You get this wrong EVERY time even though we correct you EVERY time.

Steve likes to argue that even an indel a million base pairs long counts as just one mutation.

That's because it does. An indel event can add/remove a single base or millions of base pairs IN A SINGLE EVENT.

Not that it matters in this discussion.

How does it not matter? You are the one stressing mutations that change amino acid sequences and those that don't. Are you saying that the amino acid sequence doesn't matter?

Yea, actually, you are.

I understand that the major mechanisms of epigenetics are DNA methylation and histone ubiquitination. I also know that the changes in gene expression caused by epigenetics only lasts 3 generations or fewer, and can not explain the larger differences between species. I also know that the difference in fur color between the mice in the paper is not due to epigenetics since it is due to a DIFFERENCE IN DNA SEQUENCE.

You understand none of this. You throw out the word "epigenetics" in an attempt to ignore the genetics.

Which has nothing to do with anything.

The interplay between recessive and dominant alleles has nothing to do with Mendellian genetics? Seriously?

So are cause and effect.

More avoidance to hide that fact you don't understand the basics of genetics.

In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair. Mutations

I've pointed it out repeatedly, your the one who ignores basic biology, in circles, endlessly.

Have a nice day
Mark

Not all changes are repaired, which you ignore at every turn. I even referenced a paper where they look at 10 families, and found the mutations that have occurred in the children. 10 families, mark. They found the mistakes that weren't fixed. They found the mutations.

 

[Split Rock]

That is an absolute statistical fact, the effect of mutations will be deleterious at least 98% of the time, at least. What we are talking about is an amino acid substitution, that is a triplet codon, artificially substituted, producing the color change. That's your problem, you never learned the basics, you don't appreciate the danger of frameshifts if protein coding genes and as far as I can tell you have no idea that we are talking about an amino acid substitution, not a point mutation.

You have major problems with the basics, a failing you cloud with semantics. I've seen you do this too many times LM, this time is a fundamental misunderstanding of an amino acid substitution because you have no appreciation for what an amino acid actually is:

Where do you get this number of 98% of mutations being deleterious?

How do you get an amino acid substitution by means other then artificial selection?

By a natural mutation. Either an un-repaired DNA replication error or a chemical reaction, or ionization, etc.

 

[Split Rock]

More frequent. This is what your talking about whether you know it or not:

On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions. (Initial Sequence of the Chimpanzee Genome, Nature 2005)​

The size of the indels, some of which are over a million base pairs, dwarf the single base substitutions. Steve likes to argue that even an indel a million base pairs long counts as just one mutation. That's where your pedantic correction is coming from but Steve is talking about mutation rates, which is actually a true statement, weak argument, but actual fact. If you ever bothered to learn a little about the subject matter, these discussions could be a lot more interesting. .

Are these indels located in coding or non-coding areas of the genome? If it is in a non-coding region, does it matter how long they are? Are the longer indels located primarily in non-coding regions?

 

[Loudmouth]

Are these indels located in coding or non-coding areas of the genome? If it is in a non-coding region, does it matter how long they are? Are the longer indels located primarily in non-coding regions?

We could make a list of things mark kennedy probably doesn't understand that would lead to a misunderstanding of how indels and frameshift mutations work.

1. mark kennedy probably thinks that an indel not divisible by 3 far upstream of a gene will still cause a frameshift. He is probably not aware of ribosome binding sites and how the first methionine after these sites sets the frame for that exon/protein.

2. He probably doesn't understand how introns interrupt frameshift mutations.

3. He probably thinks that RNA and proteins are the same thing, or at least that all RNA molecules are translated into proteins (which they aren't).

 

[mark kennedy]

Are these indels located in coding or non-coding areas of the genome? If it is in a non-coding region, does it matter how long they are? Are the longer indels located primarily in non-coding regions?

Those indels and neither insertions nor deletions, they are gaps in the comparison, sequences in one genome but not in the other. They are assumed to be the result of indels, something that has never been quantified or qualified.

This is all over the genomic comparisons, for example:

Indeed, 83% of the 231 coding sequences, including functionally important genes, show differences at the amino acid sequence level...Taken together, gross structural changes affecting gene products are far more common than previously estimated (20.3% of the PTR22 proteins). DNA sequence and comparative analysis of chimpanzee chromosome 22
​

If it's non-coding does it matter how long they are? You really want to ask me that when some of them are like a million base pairs long? The truth is they are all over the place and of course the size matters, does the size of the truck that hits you matter?

Have a nice day
Mark

 

[mark kennedy]

We could make a list of things mark kennedy probably doesn't understand that would lead to a misunderstanding of how indels and frameshift mutations work.

Frameshifts don't work, they are a disruption of the reading frame, yet another fundamental misunderstanding. What is really interesting is you aren't even making a point.

1. mark kennedy probably thinks that an indel not divisible by 3 far upstream of a gene will still cause a frameshift. He is probably not aware of ribosome binding sites and how the first methionine after these sites sets the frame for that exon/protein.

Oh whatever...

A frameshift mutation (also called a framing error or a reading frame shift) is a genetic mutation caused by indels (insertions or deletions) of a number of nucleotides in a DNA sequence that is not divisible by three. Due to the triplet nature of gene expression by codons, the insertion or deletion can change the reading frame (the grouping of the codons), resulting in a completely different translation from the original. The earlier in the sequence the deletion or insertion occurs, the more altered the protein. Frameshift​

Changes on this scale are a formula for extinction not adaptive evolution and the genes involved in the human brain never respond well to mutations. That's the dirty little secret and why Darwinians like to hide behind these fallacious trolling tactics, the truth is impossible for them to answer so they bury it. I'm actually surprised sometimes when they raise a substantive point every once in a blue moon. They have never let me down yet, the inevitable ad hominem is all I really need to show me they have nothing else left. LM has been folding in the first round the last couple of times, sad really, he used to be good for at least a couple of pages.

Have a nice day
Mark

 

[Loudmouth]

Frameshifts don't work, they are a disruption of the reading frame, yet another fundamental misunderstanding.

Frameshifts are not created by substitution mutations.

Frameshifts are not created by indels in non-coding DNA.

That is what you fail to understand. About 2% of the human genome is translated into protein. This means that 98% of indels can not cause a frameshift mutation. Of the indels that do occur in coding regions, only 1 in 3 will cause a frameshift mutation if we assume that the number of bases for indels is equally distributed. An indel of 3, 6, and 9 bases will keep the same open reading frame while removing 1, 2, and 3 amino acids respectively.

What is really interesting is you aren't even making a point.

The point I am making is that it is impossible for 98% of mutations to be deleterious since only 5-10% of the genome demonstrates selectable function. The point I am making is that substitution mutations do no cause frameshifts. The point is that you don't understand what mutations are.

If you could, please try to answer this question to see if we are on the same page. If I delete 1 base from the sequence upstream of a gene (including the ribosome binding site and promoter), does this cause a frameshift mutation of the gene downstream of that 1 base deletion?

 

[Split Rock]

That is an absolute statistical fact, the effect of mutations will be deleterious at least 98% of the time, at least.

Where do you get this number of 98% of mutations being deleterious?

The point I am making is that it is impossible for 98% of mutations to be deleterious since only 5-10% of the genome demonstrates selectable function. The point I am making is that substitution mutations do no cause frameshifts. The point is that you don't understand what mutations are.

I am still waiting for Mark to explain his assertion that mutations are deleterious 98% of the time (at least) and where he gets this number from.

 

[mark kennedy]

Frameshifts are not created by substitution mutations.

They are created by insertions or deletions, thus indels. Your still swinging in the wind with the semantics shell game I see.

Frameshifts are not created by indels in non-coding DNA.

Considering we are talking about a protein coding gene, that's not a correction it's a pedantic spam filler.

That is what you fail to understand. About 2% of the human genome is translated into protein. This means that 98% of indels can not cause a frameshift mutation. Of the indels that do occur in coding regions, only 1 in 3 will cause a frameshift mutation if we assume that the number of bases for indels is equally distributed. An indel of 3, 6, and 9 bases will keep the same open reading frame while removing 1, 2, and 3 amino acids respectively.

Except we are talking about an amino acid substitution when you derailed your own remarks.

The point I am making is that it is impossible for 98% of mutations to be deleterious since only 5-10% of the genome demonstrates selectable function. The point I am making is that substitution mutations do no cause frameshifts. The point is that you don't understand what mutations are.

When they have an effect on the protein coding genes, the effects would be even more devastating in a regulatory gene. Most mutations do nothing as far as we know, your so far off on this tangent you can't be tracked on radar.

If you could, please try to answer this question to see if we are on the same page. If I delete 1 base from the sequence upstream of a gene (including the ribosome binding site and promoter), does this cause a frameshift mutation of the gene downstream of that 1 base deletion?

I'm not asking your silly circular questions, chased that around the mulberry bush way too many times. With these mice we are talking about an amino acid substitution, with the arctic cod we are talking about a protein coding gene that built a whole protein coding gene from simple repeats. Instead of talking about straight forward adaptive evolution you play this semantic shell game, that is nothing more then an ad hominem fallacy.

You not saying anything, your making disjointed remarks that disrupt the discussion and insult peoples intelligence. It's called trolling and your standing in an empty theater putting on a performance for a crowd that has left. No body here but you, me and the guy mopping the lobby and he doesn't care.

Have a nice day
Mark

 

[Split Rock]

Most mutations do nothing as far as we know, your so far off on this tangent you can't be tracked on radar.

Excuse me Mark, but this statement of yours (which I agree with) seems to contradict your earlier statement that mutations are deleterious 98% of the time (see my previous post). Could you please explain this contradiction?

 

[Loudmouth]

They are created by insertions or deletions, thus indels.

Then why do you keep talking about how frameshifts are lethal when I cite examples of substitutions?

Considering we are talking about a protein coding gene, that's not a correction it's a pedantic spam filler.

We are talking about SUBSTITUTION MUTATIONS in a mouse gene, not indels.

Except we are talking about an amino acid substitution when you derailed your own remarks.

If we were talking about substitutions, THEN WHY DID YOU BRING UP INDELS?

When they have an effect on the protein coding genes, the effects would be even more devastating in a regulatory gene. Most mutations do nothing as far as we know, your so far off on this tangent you can't be tracked on radar.

If most mutations do nothing, then why did you say that 98% are deleterious?

I'm not asking your silly circular questions, chased that around the mulberry bush way too many times. With these mice we are talking about an amino acid substitution,

Then discuss it.

You not saying anything, your making disjointed remarks that disrupt the discussion and insult peoples intelligence. It's called trolling and your standing in an empty theater putting on a performance for a crowd that has left. No body here but you, me and the guy mopping the lobby and he doesn't care.

Have a nice day
Mark

Then stop bringing up indels when we are talking about substitution mutations.

 

[Loudmouth]

Just in case mark wants peer reviewed observations of mendelian violations:

"A distinct advantage of the family-based study design is the ability to call de novo events in genomic regions with sufficient coverage in a trio. To this end, we developed the PhaseByTransmission (PBT) module in the Genome Analysis Toolkit (GATK)29. From an initial 4.5 million mendelian violations in the original calls made in the 258 independent offspring, we prioritized 29,162 autosomal de novo mutation candidates at non-polymorphic sites with PhaseByTransmission (Supplementary Note)."

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