Preadaptations

[Phronesis]

ROFL .

 

[alloytoo]

ROFL .

Please stay on topic.

 

[rwenzori]

Please stay on topic.

Yes, and stop repeating yourself too.
Yes, and stop repeating yourself too.
Yes, and stop repeating yourself too.

 

[Phronesis]

Interesting article:
Dead Gene Comes Back To Life In Humans

ScienceDaily (Mar. 5, 2009) — Researchers have discovered that a long-defunct gene was resurrected during the course of human evolution. This is believed to be the first evidence of a doomed gene – infection-fighting human IRGM – making a comeback in the human/great ape lineage. The study, led by Evan Eichler's genome science laboratory at the University of Washington and the Howard Hughes Medical Institute, is published March 6 in the open-access journal PLoS Genetics.

Just a little bit recombination here and induced but controlled mutation there and old functions (preadaptations) return when needed.

The truncated IRGM gene is one of only two genes of its type remaining in humans. The genes are Immune-Related GTPases, a kind of gene that helps mammals resist germs like tuberculosis and salmonella that try to invade cells. Unlike humans, most other mammals have several genes of this type. Mice, for example, have 21 Immune-Related GTPases. Medical interest in this gene ignited recently, when scientists associated specific IRGM mutations with the risk of Crohn's disease, an inflammatory digestive disorder.

In this latest study, the researchers reconstructed the evolutionary history of the IRGM locus within primates. They found that most of the gene cluster was eliminated by going from multiple copies to a sole copy early in primate evolution, approximately 50 million years ago. Comparisons of Old World and New World monkey species suggest that the remaining copy died in their common ancestor.

The gene remnant continued to be inherited through millions of years of evolution. Then, in the common ancestor of humans and great apes, something unexpected happened. Once again the gene could be read to produce proteins. Evidence suggests that this change coincided with a retrovirus insertion in the ancestral genome.

"The IRGM gene was dead and later resurrected through a complex series of structural events," Eichler said. "These findings tell us that we shouldn't count a gene out until it is completely deleted."

The structural analysis, he added, also suggests a remarkable functional plasticity in genes that experience a variety of evolutionary pressures over time. Such malleability may be especially useful for genes that help in the fight against new or newly resistant infectious agents.

 

[alloytoo]

Interesting article:
Dead Gene Comes Back To Life In Humans

Just a little bit recombination here and induced but controlled mutation there and old functions (preadaptations) return when needed.

Evidence suggests that this change coincided with a retrovirus insertion in the ancestral genome.

Did the Gene become operational in response to the retrovirus which subsequently became part of the human genome?

or

Did the ERV insertion result in circumstances which rendered the gene operational?

 

[Phronesis]

Did the Gene become operational in response to the retrovirus which subsequently became part of the human genome?

or

Did the ERV insertion result in circumstances which rendered the gene operational?

Wow, a surprisingly keen insight there. How are you going to test either scenario? Or do you think you have the answer?

 

[alloytoo]

Wow, a surprisingly keen insight there.

It's the two most obvious questions.

How are you going to test either scenario?

I'd start by asking how common gene ressurection is, especially as it relates to ERV insertions.

Or do you think you have the answer?

Nope, I don't think we have enough data.

 

[rwenzori]

Wow, a surprisingly keen insight there. How are you going to test either scenario? Or do you think you have the answer?

Quite something for a "science cop without senior high biology" ( or should that be martric biology? ) - way ahead of you, clearly.

 

[Phronesis]

I'd start by asking how common gene ressurection is, especially as it relates to ERV insertions.

Very good. And after that? How would you go about (in a lab) to test and verify either one of those. Both of which would make sense from a FLE perspective anyway. Let's do science .

Quite something for a "science cop without senior high biology" ( or should that be martric biology? ) - way ahead of you, clearly.

Heehee, more trash talk. You should give alloytoo a tip regarding the spelling of "ressurection".

 

[rwenzori]

Both of which would make sense from a FLE perspective anyway.

Or not, of course.

 

[alloytoo]

Very good. And after that? How would you go about (in a lab) to test and verify either one of those.

I wouldn't, I would leave it to those who's job it is to do so.

Both of which would make sense from a FLE perspective anyway.

Actually neither support FLE.

Let's do science .

FLE isn't science.

Heehee, more trash talk. You should give alloytoo a tip regarding the spelling of "ressurection".

The irony, it hurts.

 

[alloytoo]

Did the Gene become operational in response to the retrovirus which subsequently became part of the human genome?

or

Did the ERV insertion result in circumstances which rendered the gene operational?

ERV reports

It would seem that the nature of the resurrected gene is significantly changed from it's original location and function rendering my first question moot.

If would seem that the gene resurrected in response to the retrovirus insertion changing the genome.

These sort of events render the whole notion of Front Loaded Evolution (FLE) nonsensical.

 

[alloytoo]

ERV reports

It would seem that the nature of the resurrected gene is significantly changed from it's original location and function rendering my first question moot.

If would seem that the gene resurrected in response to the retrovirus insertion changing the genome.

These sort of events render the whole notion of Front Loaded Evolution (FLE) nonsensical.

Another comment.

It appears that the Retrovirus resurrected the gene by inserting itself at the beginning of the sequence that had been rendered inoperable.

If this is the "Jesus" Gene, then is the ERV "god?"

 

[rwenzori]

It appears that the Retrovirus resurrected the gene by inserting itself at the beginning of the sequence that had been rendered inoperable.

If this is the "Jesus" Gene, then is the ERV "god?"

Maybe they should have named it the "Lazarus" gene, then "Jesus" could be the ERV.

This is certainly very damaging to [-]fairies[/-] theories like FLE, as human genetic makeup is demonstrated to have been altered by a type of virus.

 

[Phronesis]

Mmm, you made two assertions there without backing them up.
Alloytoo:
1) It would seem that the nature of the resurrected gene is significantly changed from it's original location and function rendering my first question moot.
2) If would seem that the gene resurrected in response to the retrovirus insertion changing the genome. These sort of events render the whole notion of Front Loaded Evolution (FLE) nonsensical.

So let's go over this interesting gene:
Immunity-related GTPase family, M (IRGM)
Function (Figure 1):

Figure 1: IGMR plays a role in IFN-gamma mediated induction of autophagy.​

Interferon gamma (IFN-gamma) play a role in immunity and activates cellular pathways that target viral and intracellular bacterial infections. One way in targeting foreign intracellular organisms is through the induction of autophagy. Autophagy is basically a process of sequestered intracellular digestion and degradation of organnelles (and in this case bacteria or viral particles). Now there are several different forms of autophagic processes including chapperone-mediated autophagy, microautophagy and macroautophagy. IFN-gamma induces macroautophagy which is characterized by double-membrane bound vacuoles containing cytosol, organelles and bacterial particles. The exact mechanism of IFN-gamma induced autophagy is currently being investigated, however it is clear that IGRM (the gene of interest here) plays a crucial role in IFN-gamma induced macroautophagy (see Figure 1) [1]. Where exactly it fits in the scheme of things, like I said, remains to be seen. Mice also has this gene (LRG-47 or IGRM1) and it too functions as an inducer of autophagy. So your assertion (or speculation) that it's original functions "seemed" to change is flat-out wrong.



Why would the revival of an old gene through the insertion of ERV9 render FLE nonsensical? I think this is a perfect example of how the notion of junk DNA is... well junk. Genes might become functionless because of lack of use, however copying mechanisms keep these sequences in tact. Now, as you know, the genetic code is optimal for two interesting features:
A) The actual code is far better than other possible codes in minimizing the number of amino acids incorporated until translation is interrupted after a frameshift error occurred.
B) The code is highly optimal for encoding arbitrary additional information, i.e., information other than the amino acid sequence in protein-coding sequences.

Why is this interesting? Well, according to this interesting article, the IGRM gene became non-functional a few million years ago (possibly due to a frame-shift mutation). It did not degrade due to mutations, it was kept in tact by the replication machinery. You will also remember how the immune system makes use of mutations (active mutation induction and subsequent biases repair) to find solutions. From a FLE perspective it would make sense that the replication machinery keeps genetic sequences in tact (especially previously functional genes) just in case they might be reactivated in the future as a result of processes making use of mutations to find solutions (like the immune system does). What makes it even better is that the genetic code is optimal for accepting new information, and in this case ERV9 was the new information. This easy incorporation of this ERV9 resulted in the re-activation of an old gene that plays a crucial role in immunity and autophagic processes.

Thus, this study just aids in uncovering another mechanism in how FLE can be used to unlock future optimal functions (like the function of the IGRM gene) through viral particles. Viral particles from a FLE perspective can thus be seen as vectors of optimization and this study showed it beautifully .


Refs:
1) Singh SB, Davis AS, Taylor GA, Deretic V. Human IRGM induces autophagy to eliminate intracellular mycobacteria. Science. 2006 8;313(5792):1438-41.

 

[rwenzori]

What makes it even better is that the genetic code is optimal for accepting new information, and in this case ERV9 was the new information. This easy incorporation of this ERV9 resulted in the re-activation of an old gene that plays a crucial role in immunity and autophagic processes.

Thus, this study just aids in uncovering another mechanism in how FLE can be used to unlock future optimal functions (like the function of the IGRM gene) through viral particles. Viral particles from a FLE perspective can thus be seen as vectors of optimization and this study showed it beautifully .

LOL! So human genetic makeup, delicately front-loaded by Bebeh Jesus to make the crown of his creation, is reliant on an inherently random event, with a viral remnant blindly and by chance changing a certain gene in a random fashion.

Maybe god does play dice LOL!

 

[Phronesis]

ROFL! So arguments from ignorance and credulity are arguments all of a sudden? Is that really all you have?
Oh, what is the best way to optimize and design?
Check out this study
Optimization of human immunodeficiency virus type 1 envelope glycoproteins with V1/V2 deleted, using virus evolution.

Lol, get out of here until you have anything that is remotely related to science. Oh, and do try and be constructive ROFL...

 

[alloytoo]

Mmm, you made two assertions there without backing them up.
Alloytoo:
1) It would seem that the nature of the resurrected gene is significantly changed from it's original location and function rendering my first question moot.

I'm deferring to ERV's Opinion:

No yay! Cause IRGM isnt the same IRGM that we had 50 million years ago. Its now got an ERV LTR for a promoter, it sits in a different part of the genome, and 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.

So your assertion (or speculation) that it's original functions "seemed" to change is flat-out wrong.

The gene somehow regained its ability to produce a protein, albeit a shortened one.

Perhaps you didn't read their analysis?

Why would the revival of an old gene through the insertion of ERV9 render FLE nonsensical? I think this is a perfect example of how the notion of junk DNA is... well junk. Genes might become functionless because of lack of use, however copying mechanisms keep these sequences in tact.

But the copying mechanisms didn't keep the genes intact.
Ed Yong again:

Most mammals, such as the dog and the mouse, have three copies located one after the other. This trio of genes are "paralogs" - slightly different duplicates of a single ancestor. Two species of lemur - the ring-tailed and mouse lemurs - also share the same three genes, but all monkeys have just the one. This suggests that the IRGM cluster shrank from a trinity into a single gene in the last common ancestor of all apes and monkeys, which lived about 40 million years ago.

If that decline wasn't bad enough, Bekpen found that the remaining IRGM gene of monkeys is actually a dead remnant. It's much shorter than those of other mammals, and it has been so heavily abridged that it has lost the ability to encode a protein. In technical terms, it's a "pseudogene" and to paraphrase the Python boys, it's an ex-gene.

It perfectly demonstrates why FLE is nonsense. A random event restoring a gene to functionality that may actually do more harm than good.

 

[rwenzori]

ROFL! So arguments from ignorance and credulity are arguments all of a sudden? Is that really all you have?

Blather away, throw insults, and try to divert the discussion - doing so is MUCH easier than addressing the points and criticisms that rather blow your FLE out of the water. Maybe Brownian motion diddit!! ROFL!

 

[Phronesis]

I'm deferring to ERV's Opinion:

ERV:
No yay! Cause IRGM isnt the same IRGM that we had 50 million years ago. Its now got an ERV LTR for a promoter, it sits in a different part of the genome, and 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

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.

Perhaps you didn't read their analysis?

Perhaps you are just unaware of the difference between the structure of a gene and the structure of the protein after processing. Perhaps you don't know the difference between an intron and an exon and alternative splicing. The structure of the gene changed, yes. Heck, the ERV9 insertion coincides with the transcription start signal. However after RNA splicing, the protein pretty much does what the IRGM protein does in mice. And dysfunctional IRGM genes (NOT PROTEINS) are associated with Crohn's disease. Got it?

But the copying mechanisms didn't keep the genes intact. Ed Yong again:

The part of the gene coding for the protein was kept in tact. The transcription site was the part that was affected .

It perfectly demonstrates why FLE is nonsense. A random event restoring a gene to functionality that may actually do more harm than good.

The gene works fine. 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 .