Preadaptations

[alloytoo]

She is flat out wrong. IRGM is an important regulator of autophagy and disregulation of this gene is speculated to be associated with Crohn's disease. SNPs and deletions upstream of this gene (near the transcription site) are associated with Crohn's disease. Read for yourself.
McCarroll, S. A. et al. Deletion polymorphism upstream of IRGM associated with altered IRGM expression and Crohn's disease. Nature Genet. 40: 1107-1112, 2008.

Could you be a little more specific?

Is IRGM the same IRGM that we had 50 million years ago?

Does it now have an ERV LTR for a promoter?

Does it sit in a different part of the genome?

Is its surrounding genome landscape has changed dramatically?(-- 33 retrotransposons (LINES/SINES/LTRs) have taken up residence upstream of IRGM!!)?

Some people have a 20,000 base-pair deletion upstream from IRGM. This leads to expression of IRGM in wrong tissues at wrong levels, which could be a potential cause of Crohns disease

Doesn't your quote confirm this?

If you thing Abby is wrong go tell her:

The gene works fine.

Ed Wong said it produced a shorter protein? Perhaps you could ask him about that.

Dysfunctional IRGM genes are associated with Crohn's disease. From a FLE perspective, it makes sense that old genes can become functional again (junk DNA is an argument from ignorance) due to the inherent optimal properties of the genetic code, the robustness of mutation induction and subsequent repair and viewing retroviral elements as vectors of optimization .

I never made an argument for or about junk DNA, why do you keep on talking about Junk DNA? it's smelly the way you keep going on about it, fishy even, like Herring.

Which parts of this don't you understand:

The IRGM genes were mostly deleted from the monkey/ape genome, where they remain in triplicate in some other species.

The remnants of the gene is Non-functional in other monkey/ape species.

An ERV insertion in great apes caused the gene to function again.

Ed wong writes:

For 25 million years, the IRGM gene was effectively dead. But then, in the common ancestor of humans and the great apes, something unexpected happened. The gene somehow regained its ability to produce a protein, albeit a shortened one. The gene had been resurrected, and ironically enough, its saviour was another genetic hitchhiker that inserted itself in just the right place.

Ed Wong presents the facts in an accessible fashion, I recommend everyone read his article.

 

[Phronesis]

Could you be a little more specific?

Insertions and deletion near the transcription initiation site are associated with instances od Crohn's disease. A working and in tact gene plays a crucial part in autophagic processes.

Is IRGM the same IRGM that we had 50 million years ago?

Exactly the same gene? No, like the article said the promoter is ERV9 with different intronic and exonic portion. The same protein (although a little shorter) doing the same function with regards to autophagy? Yes.

Does it now have an ERV LTR for a promoter?

Yes, I did say so and if you read the article you know it is so .

Does it sit in a different part of the genome?

Yes. So what? Many genes do not sit exactly at the same spot as other genomes. Ever heard of recombination?

Is its surrounding genome landscape has changed dramatically?(-- 33 retrotransposons (LINES/SINES/LTRs) have taken up residence upstream of IRGM!!)?

Why yes, just read the article. So what?

Doesn't your quote confirm this?

Why yes it does. When it works it works like it should. Look at the p53 gene. Crucual regulator of genomic integrity. If it works it works. And just like IRGM, it can be deregulated resulting in disease.
So it does not cause disease on its own, something has to go wrong with the gene before it is the cause of disease (like Crohn's disease)

Ed Wong said it produced a shorter protein? Perhaps you could ask him about that.

It is a shorter gene and protein. So what. It still plays a role in autophagy just like the original gene does.
>IRGM Immunity-related GTPase family M protein - Length: 181 AS
MEAMNVEKASADGNLPEVISNIKETLKIVSRTPVNITMAGDSGNGMSTFISALRNTGHEGKASPPTELVKATQRCASYFS
SHFSNVVLWDLPGTGSATTTLENYLMEMQFNRYDFIMVASAQFSMNHVMLAKTAEDMGKKFYIVWTKLDMDLSTGALPEV
QLLQIRENVLENLQKERVCEY

>Irgm1 Isoform 1 of Immunity-related GTPase family M protein - Length: 409 AS
MKPSHSSCEAAPLLPNMAETHYAPLSSAFPFVTSYQTGSSRLPEVSRSTERALREGKLLELVYGIKETVATLSQIPVSIF
VTGDSGNGMSSFINALRVIGHDEDASAPTGVVRTTKTRTEYSSSHFPNVVLWDLPGLGATAQTVEDYVEEMKFSTCDLFI
IIASEQFSSNHVKLSKIIQSMGKRFYIVWTKLDRDLSTSVLSEVRLLQNIQENIRENLQKEKVKYPPVFLVSSLDPLLYD
FPKLRDTLHKDLSNIRCCEPLKTLYGTYEKIVGDKVAVWKQRIANESLKNSLGVRDDDNMGECLKVYRLIFGVDDESVQQ
VAQSMGTVVMEYKDNMKSQNFYTLRREDWKLRLMTCAIVNAFFRLLRFLPCVCCCLRRLRHKRMLFLVAQDTKNILEKIL
RDSIFPPQI

I never made an argument for or about junk DNA, why do you keep on talking about Junk DNA? it's smelly the way you keep going on about it, fishy even, like Herring.

Get a grip will you, there are still people that think streaks of DNA is junk. I was just highlighting that it is an argument from ignorance when looking at the present data.

Which parts of this don't you understand:

The IRGM genes were mostly deleted from the monkey/ape genome, where they remain in triplicate in some other species.

The remnants of the gene is Non-functional in other monkey/ape species.

An ERV insertion in great apes caused the gene to function again.

Gee, now you are just regurgitating what everyone already knows. You just don't understand how this fits nicely into a FLE perspective.

 

[rwenzori]

Dysfunctional IRGM genes are associated with Crohn's disease. From a FLE perspective, it makes sense that old genes can become functional again (junk DNA is an argument from ignorance) due to the inherent optimal properties of the genetic code, the robustness of mutation induction and subsequent repair and viewing retroviral elements as vectors of optimization .

Let's try to get this straight.

• Bebeh Jesus front-loaded the evolutionary processes with the purpose of creating man, in his own image, after some billions of years.
• Evolutionary processes took place, and made many "creatures", including often harmful nasty things called viruses, some of which work by randomly stuffing up the genetic material within cells.
• Genetic coding ( and thus the resultant "creatures" ) changes, or dies out, as a result.
• Bebeh Jesus PLANNED all this, otherwise one must assume that the purpose that has been achieved ( mankind in all his glory ) is not the one he started out with.
• Many of these viruses hit dead ends, themselves get stuffed up during replication, but random bits and pieces remain.
• Bebeh Jesus PLANNED all this, ERV by ERV, otherwise one must assume that the purpose that has been achieved ( mankind in all his glory ) is not the one he started out with.
• One of these random bits of junk from a deceased-virus gets randomly bumped half back into existence, not quite the same as the original, in a different place, resulting in it being activated at the wrong level in the wrong sequence, causing some serious suffering for some humans.
• Bebeh Jesus PLANNED all these random interactions to optimise human genetics, otherwise one must assume that the purpose that has been achieved ( mankind in all his glory ) is not the one he started out with.
• Bebeh Jesus, the master manipulator of genetics in achieving his purpose, also PLANNED retroviruses such as HIV to plague his creation presumably for his own amusement.

This is really quite bizarre thinking!

 

[rwenzori]

It is a shorter gene and protein. So what.

So you are talking crap when you use the word(s?) "in tact" - one assumes "intact".

You just don't understand how this fits nicely into a FLE perspective.

Clearly not, but since FLE is el weirdo thinking, can you blame us LOL?

 

[alloytoo]

Insertions and deletion near the transcription initiation site are associated with instances od Crohn's disease. A working and in tact gene plays a crucial part in autophagic processes.

"Crucial?" It's gene family plays an important role in defense against intracellular bacteria, but there seems to be uncertaintity as to what precise roll it plays.

Exactly the same gene? No,...

Funny that's what Abby said.......so perhaps....

She is flat out wrong.

.... is wrong?

Yes, I did say so and if you read the article you know it is so .

Abby said so too....so perhaps....

She is flat out wrong.

.... is wrong?

Yes. So what? Many genes do not sit exactly at the same spot as other genomes. Ever heard of recombination?

Yes indeed, but you said:

She is flat out wrong.

Perhaps you were mistaken?

Why yes, just read the article. So what?

She is flat out wrong.

Nuff said.

Why yes it does.....

So.....

She is flat out wrong.

Doesn't apply here either.

It is a shorter gene and protein. So what. It still plays a role in autophagy just like the original gene does.

So Ed was right too? hmmmm I'm detecting a pattern.

Get a grip will you, there are still people that think streaks of DNA is junk. I was just highlighting that it is an argument from ignorance when looking at the present data.

...still "people"....

Perhaps not herring, perhaps a strawman.

Gee, now you are just regurgitating what everyone already knows.

You seemed to have problems grasping it.

You just don't understand how this fits nicely into a FLE perspective.

You fail to grasp how it demonstrates the exact opposite.

 

[Phronesis]

This is really quite bizarre thinking!

Exactly... why would you want to think that way anyway? All these yet again show argument from ignorance and credulity are the only type of arguments you have.
Something like "I can't really understand, but if this is what you are thinking... oh no (throws toys out of cot) it can't be...".
Got any solid constructive arguments?

 

[Phronesis]

"Crucial?" It's gene family plays an important role in defense against intracellular bacteria, but there seems to be uncertaintity as to what precise roll it plays.

Can you read? Autophagic related processes and IFN-gamma signaling. FFS, open your eyes...

Funny that's what Abby said.......so perhaps....

.... is wrong?

Well then you misrepresented her by saying this:
Alloytoo:
A random event restoring a gene to functionality that may actually do more harm than good.
You forgot to add the crucial parts of "when becomes dysfunctional".
Not my problem if you cn't understand what other people write.

...still "people"....

Perhaps not herring, perhaps a strawman.

Want examples? Just go to phyrungula and say the following words:
"Hey people, junk DNA is a myth, there is no such thing as junk, functionless DNA". Watch the crazies come out of the woodwork.

You seemed to have problems grasping it.

ROFL, shame, trash talkng again. That all you got? Or do you want another lesson in the function of IRGM and how it plays a crucial role in autophagic related processes. better yet, why don't you go to mamma ERV and ask her for advice.

You fail to grasp how it demonstrates the exact opposite.

Lol, still don't get it do you?
Optimal features of the genetic code, robust replication machinery, reviva of old genes as a result of these optimal features... etc. I can go on, but what is the point, you don't even get autophagy and the role IRGM plays in ths process.
Do you want a step-by-step lesson now or what?

 

[rwenzori]

Exactly... why would you want to think that way anyway? All these yet again show argument from ignorance and credulity are the only type of arguments you have.
Something like "I can't really understand, but if this is what you are thinking... oh no (throws toys out of cot) it can't be...".
Got any solid constructive arguments?

Once again, blathering and insults instead of any constructive engagement of my criticisms or defence of your position. Do you not understand the implications of my criticisms? Must I use baby-talk?

 

[alloytoo]

Can you read? Autophagic related processes and IFN-gamma signaling. FFS, open your eyes...

In mice or humans your linkys are little funny

Well then you misrepresented her by saying this:
Alloytoo:
A random event restoring a gene to functionality that may actually do more harm than good.

Shame poor baby. You really are grasping.

Not withstanding that I linked to Abby's blog....

ERV insertions into the genome are for all intent and purpose random (unpredictable) events

The gene was indeed restored to functionality and the gene is associated with Crohn's disease. (that "may" do more harm than good)

You forgot to add the crucial parts of "when becomes dysfunctional".
Not my problem if you cn't understand what other people write.

Not my fault you don't understand the word "may" in this context. Perhaps you don't understand what people write?

You said:

She is flat out wrong.

You seem mistaken on every point.

Want examples? Just go to phyrungula and say the following words:
"Hey people, junk DNA is a myth, there is no such thing as junk, functionless DNA". What the crazies come out of the woodwork.

People like you? Since you're the only one raising the strawman.

ROFL, shame, trash talkng again. That all you got? Or do you want another lesson in the function of IRGM and ghow it plays a crucial role in autophagic related processes. better yet, why don't you go to mamma ERV and ask her for advice.

Wash Rinse repeat. Perhaps you should, since you were clearly mistaken about everything that Abby was supposedly:

...flat out wrong.

Lol, still don't get it do you?
Optimal features of the genetic code, robust replication machinery, reviva of old genes as a result of these optimal features... etc. I can go on, but what is the point, you don't even get autophagy and the role IRGM plays in ths process.
Do you want a step-by-step lesson now or what?

Deleted genes sequences, inactive for millions of years (and still so in some species), resurrected through a random HGT ERV insertion.

Frankly "Hand of God" inserting the ERV at just the right spot has more credibility than your argument.

But don't take my word for it, ask Ed or Abby

 

[Phronesis]

In mice or humans your linkys are little funny

Still not getting its function?

ERV insertions into the genome are for all intent and purpose random (unpredictable) events

Differentiate between random and unpredictable. Random to whom btw?

The gene was indeed restored to functionality and the gene is associated with Crohn's disease. (that "may" do more harm than good)

Not my fault you don't understand the word "may" in this context.

Excuse for for laughing at your "may" comment. But just about every other gene "may" be associated with a disease if massive insertions, SNPs or deletions are near the transcriptional site.

You seem mistaken on every point.

Not if you are implying that the gene contributes to disease. It only contributes to disease if something goes wrong with it. LIKE A MASSIVE DELETION. Got that?

People like you? Since you're the only one raising the strawman.

ROFL, what is your position on "junkDNA" btw? Let's hear it.

Wash Rinse repeat. Perhaps you should, since you were clearly mistaken about everything that Abby was supposedly:

She is flat out wrong if she thinks the gene is responsible for Crohn's disease. She would be right if she implies that insertions and deletions in or near the gene contributes to the development of the disease (which I think was what she wrote, but you did not get that, read YOUR STATEMENT AGAIN AND SEE HOW MISLEADING IT IS).

 

[rwenzori]

Random to whom btw?

ROFL! Random is random, old boy! No "to whom" about it - unless you mean Bebeh Jesus as I stated above ( and for which you have no counter, it seems ) LOL???

 

[Phronesis]

Kind of weird how you see randomness as an obstacle for FLE when viewed from a FLE, randomness can be viewed as a tool for optimization.
When you have a system that actively probes random space for innovation (like the immune system), it is bound to reach an optimal solution.
Life has all the necessary characteristics to do this.
1)Active mutation induction,
2) An optimal code that is highly optimal for allowing new information and it is highly robust at error minimization, although not perfect to allow for variation and innovation.
3) Controllable repair mechanisms which can bias the outcome of a repair process initiated by induced mutations.
4) Then you have vectors of optimization ... retroviral elements.

So randomness is thus just another tool for FLE to optimize future functions with the inevitable emergence of optimal structures and functions.

Now what will happen if an evolutionary algorithm reaches an optimum? Variation (diversity) will become less as it tends to stay close to the optimum (See figure).

B) Fitness landscape with local optima (A, B and D) and a global optima (C). In a memetic algorithm, the initial population of individual are randomly seeded and can be viewed as any of the arrows indicated in the figure.​

Let's see what we find in humans: Humans have a low genetic diversity when compared to other species.. There are many reasons for speculating why this is so. It makes sense from a FLE perspective.

 

[alloytoo]

Still not getting its function?

Have you fixed your of parking or mice links?

Differentiate between random and unpredictable. Random to whom btw?

Random & unpredictable (they're complimentary) to anything/anyone.

Excuse for for laughing at your "may" comment. But just about every other gene "may" be associated with a disease if massive insertions, SNPs or deletions are near the transcriptional site.

You're not excused, you're being childish. But we shall compliment you on learning a new word. Next week four letter words.

Not if you are implying that the gene contributes to disease. It only contributes to disease if something goes wrong with it. LIKE A MASSIVE DELETION. Got that?

I wasn't implying. I was summarizing. I then linked directly linked to Abby and Ed's blogs encouraging interested parties to read it.

You made some rash assumptions, and have been proven wrong. Suck it up, take it like a man.

ROFL, what is your position on "junkDNA" btw? Let's hear it.

The you seem so enamoured with the term that you cannot resist using it irrespective of it's relevance.

She is flat out wrong if she thinks the gene is responsible for Crohn's disease. She would be right if she implies that insertions and deletions in or near the gene contributes to the development of the disease (which I think was what she wrote, but you did not get that, read YOUR STATEMENT AGAIN AND SEE HOW MISLEADING IT IS).

Is Abby wrong, or is my summary inadequate? Make up your little mind.

If Abby is wrong please do take it up with her. Here's a linky to help you.

If Ed is wrong please do take it up with him. Here's a linky to help you.

If my summary was inadequate, then I apologise to Abby & Ed for my mistakes.

 

[alloytoo]

Kind of weird how you see randomness as an obstacle for FLE(Fairy Loading) when viewed from a FLE (Fairy Loading), randomness can be viewed as a tool for optimization. When you have a system that actively probes random space for innovation (like the immune system), it is bound to reach an optimal solution.

Natural selection results in solutions, they are often not optimal.

Life has all the necessary characteristics to do this.
1)Active mutation induction,
2) An optimal code that is highly optimal for allowing new information and it is highly robust at error minimization, although not perfect to allow for variation and innovation.
3) Controllable repair mechanisms which can bias the outcome of a repair process initiated by induced mutations.
4) Then you have vectors of optimization ... retroviral elements.

So randomness is thus just another tool for FLE (Fairy loading)to optimize future functions with the inevitable emergence of optimal structures and functions.

Now what will happen if an evolutionary algorithm reaches an optimum? Variation (diversity) will become less as it tends to stay close to the optimum (See figure).

B) Fitness landscape with local optima (A, B and D) and a global optima (C). In a memetic algorithm, the initial population of individual are randomly seeded and can be viewed as any of the arrows indicated in the figure.​

So we return to my original question, from long long ago, what distinuishes Fairy loading (as you've just described it) from evolution?

Fairy Loading with grand agency is fantasy. Fairy Loading without grand agency is just plain stupid.

Let's see what we find in humans: Humans have a low genetic diversity when compared to other species.. There are many reasons for speculating why this is so. It makes sense from a FLE (Fairy Loading) perspective.

Low genetic diversity (and it's not unique to humans, Cheatahs, Panda's, American Bison, even Basking Sharks also have low genetic diversity) merely suggests that a species has gone through a genetic bottleneck in the recent past, is an evolutionary event in which a significant percentage of a population or species is killed or otherwise prevented from reproducing.

Makes perfect sense from an evolutionary point of view. No fairy loading(tm) required.

 

[Phronesis]

After reading mamma ERVs "post" about IRGM, I realize she failed to mention the function of IRGM and how it plays a role IFN-gamma induced autophagic processes and how dysregulated autophagic processes play an important part in the development of Crohn's disease.

Do you understand now that a functional IRGM gene and protein plays a crucial regulatory role in autophagic process and that DYSREGULATION of the gene is associated with Crohn's disease?

You might have been unaware of that when posting this:
Alloytoo: A random event restoring a gene to functionality that may actually do more harm than good.

Do you also know a little more about Crohn's disease, IRGM and autophagy ?

 

[Phronesis]

If Abby is wrong please do take it up with her. Here's a linky to help you.

If Ed is wrong please do take it up with him. Here's a linky to help you.

If my summary was inadequate, then I apologise to Abby & Ed for my mistakes.

They are not wrong, they just give half of the information and people like you (who don't even have senior high biology) lap it up to come to wrong conclusions. Heck you did it with ERV's (remember billion year old ERV's ROFL).
Next time ask mama ERV to give you the full heads up on what is what ok .

 

[Phronesis]

Natural selection results in solutions, they are often not optimal.

Natural selection does nothing. Live with it. Fitness is just the outcome of cellular processes. NS does not select for anything. However, the necessary tools and mechanisms to unlock optimal functions are present.

Low genetic diversity (and it's not unique to humans, Cheatahs, Panda's, American Bison, even Basking Sharks also have low genetic diversity) merely suggests that a species has gone through a genetic bottleneck in the recent past, is an evolutionary event in which a significant percentage of a population or species is killed or otherwise prevented from reproducing.

Why does this paper argue this:

The striking fact that human shows the lowest DNA diversity among all species has commonly been explained by the bottleneck hypothesis: most human populations are thought to go extinct at one time in history except one small population that survived to produce the six billion people living today. But this hypothesis is merely an ad hoc tautology. There is no independent evidence of such near extinction event and there is little hope of ever uncovering such evidence. There are also lines of evidence against the bottleneck hypothesis [81, 82].

 

[alloytoo]

After reading mamma ERVs "post" about IRGM, I realize she failed to mention the function of IRGM and how it plays a role IFN-gamma induced autophagic processes and how dysregulated autophagic processes play an important part in the development of Crohn's disease.

Well done, take it up with her.

Do you understand now that a functional IRGM gene and protein plays a crucial regulatory role in autophagic process

In mice.(which have 21 copies vs our paltry 1 hybrid copy)

There seems to be some uncertainty as to the function of the ressurected gene in humans.

Another interesting article:
Some pertinant quotes:

If the resurrected gene notion is right, Eichler said, it raises a host of questions about IRGM. For instance, since IRGM appears to play a critical role in bacterial immunity in mice, it's unclear what led to this gene's obsolescence in the monkey-ape ancestor. And more research is needed to address whether the revitalized form of the gene has the same function as its predecessor or whether it now has additional roles.

For his part, Eichler believes the locus is probably still involved in immunity and possibly auto-immunity. He speculated that another immune mechanism may have evolved around the same time that IRGM became a pseudogene, making it redundant and less crucial.

and that DYSREGULATION of the gene is associated with Crohn's disease?

You might have been unaware of that when posting this:
Alloytoo: A random event restoring a gene to functionality that may actually do more harm than good.

Do you also know a little more about Crohn's disease, IRGM and autophagy ?

Do you know the difference between mice and men?

 

[alloytoo]

They are not wrong,

Nope, I guess you were.

 

[Phronesis]

There seems to be some uncertainty as to the function of the ressurected gene in humans.

READ AGAIN! It plays a role in IFN-gamma mediated autophagy. Without it, autophagy induction through IFN-gamma is abrogated.

Another interesting article:
Some pertinant quotes:

FFS, now you are just quote mining! It is clearly not redundant or less crucial, as explained and evidenced by the association of disease caused by dysregulation of the gene.

Nope, I guess you were.

ROFL, actually you were by misrepresenting them. Your summary was woefully inaccurate and misrepresented what they said (or did not). Glad you apologized for it .