Is The "chickenosaurus" Project Actually Possible?

[Mediospirifer]

So many genes are linked in so many unknown ways that the only way to know what else will happen is to try it and see.

Truth!

[Carcharodontosaurus]

If Horner is really desperate to use teeth, he will have to use genes from other animals, such as crocodilians. Or he could try predicting the functional enamelin gene sequence from the last common ancestor of birds and crocodilians as was done with a rhodopsin protein in 2002. Of course, he would have to choose from several evolutionary models to do this, and he wouldn't be able to predict the ancestral regulatory DNA sequences.

[Mediospirifer]

If Horner is really desperate to use teeth, he will have to use genes from other animals, such as crocodilians. Or he could try predicting the functional enamelin gene sequence from the last common ancestor of birds and crocodilians as was done with a rhodopsin protein in 2002. Of course, he would have to choose from several evolutionary models to do this, and he wouldn't be able to predict the ancestral regulatory DNA sequences.

From what I've read so far, it's more complicated than that. Yes, he will likely need to get a new, functional enamelin gene. He'll also have to figure out how to regulate the gene expression within the chick jaw without altering the rest of the body.

The paper I read about chicken tooth development described the difference between the ta² mutants and normal chicks in detail. There are two tissue types involved (mesenchyme and epithelium), and a differentiation zone or horizon (I may be misremembering the terminology, I don't have the paper on this computer and can't get it from here) dividing the oral region from the aboral region. In teeth, the crown is the oral surface, while the root is the aboral surface. Tooth buds form when the embryo has interactions between epithelium and mesenchyme within the differentiation zone. In normal chicks, that zone is separated from the mesenchyme/epithelium boundary; ta² mutants (and alligators) have the tissue interactions within the differentiation zone.

Did I phrase that in a way that makes sense? What it boils down to is that a functional enamelin gene in an otherwise normal chick will simply not have the opportunity to be expressed, and the currently-known examples of gene regulation that could cause it to be expressed are lethal. I don't know if it's possible to alter gene expression in one part of a developing body without affecting the rest of that body.

There's another paper on the ta² mutant that I want to look up (I can access it from my job on Monday, until then it's behind a paywall) that discusses ta² limb morphology. The abstract mentions polydactyl wings developing. It might be that this mutation has the potential to make the kind of clawed wing-fingers that Horner wants, too! If he can only mitigate the other effects.

I haven't yet found a description of why the mutaton is lethal, beyond the brief mention that it affects multiple organ systems. I'll have to spend some time with Google scholar to see what I can find out.

This is a very interesting topic to research!

[Carcharodontosaurus]

From what I've read so far, it's more complicated than that. Yes, he will likely need to get a new, functional enamelin gene. He'll also have to figure out how to regulate the gene expression within the chick jaw without altering the rest of the body.

The paper I read about chicken tooth development described the difference between the ta² mutants and normal chicks in detail. There are two tissue types involved (mesenchyme and epithelium), and a differentiation zone or horizon (I may be misremembering the terminology, I don't have the paper on this computer and can't get it from here) dividing the oral region from the aboral region. In teeth, the crown is the oral surface, while the root is the aboral surface. Tooth buds form when the embryo has interactions between epithelium and mesenchyme within the differentiation zone. In normal chicks, that zone is separated from the mesenchyme/epithelium boundary; ta² mutants (and alligators) have the tissue interactions within the differentiation zone.

Did I phrase that in a way that makes sense? What it boils down to is that a functional enamelin gene in an otherwise normal chick will simply not have the opportunity to be expressed, and the currently-known examples of gene regulation that could cause it to be expressed are lethal. I don't know if it's possible to alter gene expression in one part of a developing body without affecting the rest of that body.

There's another paper on the ta² mutant that I want to look up (I can access it from my job on Monday, until then it's behind a paywall) that discusses ta² limb morphology. The abstract mentions polydactyl wings developing. It might be that this mutation has the potential to make the kind of clawed wing-fingers that Horner wants, too! If he can only mitigate the other effects.

I haven't yet found a description of why the mutaton is lethal, beyond the brief mention that it affects multiple organ systems. I'll have to spend some time with Google scholar to see what I can find out.

This is a very interesting topic to research!

Has there ever been a case in any organism or animal where scientists have been able to allow one effect of a mutation to happen while cancelling other effects?

[Auspex]

Has there ever been a case in any organism or animal where scientists have been able to allow one effect of a mutation to happen while cancelling other effects?

Science has yet to understand the "other effects"; the genetic chemistry of self-replication is so complicated and intertwined that they hardly know what will happen until they do it.

[Scylla]

Has there ever been a case in any organism or animal where scientists have been able to allow one effect of a mutation to happen while cancelling other effects?

Yes, there are systems that can mitigate where a gene is expressed by using a tissue specific promoter region to regulate the gene. So if you want a gene to be expressed in one organ that would be lethal if expressed in other organs, you can design your genetic construct to only turn on in the target organ (if a tissue specific regulatory system is known for that organ or tissue).

Also when a gene is expressed can be controlled by using promoters that are conditional in nature. That basically means the scientist controls when the gene is expressed by adding a specific molecule that triggers the specified gene to be expressed (Tetracycline is one common example). Other triggers can be used, even some temperature sensitive ones. This is one way scientists can study the function of gene changes that are lethal during embryogenesis.

[Carcharodontosaurus]

I found a picture of a normal chick (left) compared to a talpid2 chick (right): http://i.livescience.com/images/i/000/005/868/i02/060222_mutant_mouth_02.jpg?1296085683

From what I can see, the mutation allows stubby teeth to grow, but also deforms the skull.

[xonenine]

Development of teeth in chick embryos after mouse

neural crest transplantations

Thimios A. Mitsiadis, Yvonnick Cheraud, Paul Sharpe, and Josiane Fontaine-Perus

The Development of Archosaurian

First-Generation Teeth

in a Chicken Mutant

Matthew P. Harris,

Sean M. Hasso, Mark W.J. Ferguson,

and John F. Fallon

here are two of the pertinent PDFs

[Carcharodontosaurus]

Yes, there are systems that can mitigate where a gene is expressed by using a tissue specific promoter region to regulate the gene. So if you want a gene to be expressed in one organ that would be lethal if expressed in other organs, you can design your genetic construct to only turn on in the target organ (if a tissue specific regulatory system is known for that organ or tissue).

Also when a gene is expressed can be controlled by using promoters that are conditional in nature. That basically means the scientist controls when the gene is expressed by adding a specific molecule that triggers the specified gene to be expressed (Tetracycline is one common example). Other triggers can be used, even some temperature sensitive ones. This is one way scientists can study the function of gene changes that are lethal during embryogenesis.

So, are tissue-specific regulatory systems known for the jaws? Or do you mean a regulatory system found in the talpid2 mutation?

[Mediospirifer]

If someone wanted to use talpid² to grow teeth, they'd have to suppress the gene expression in the body, and only allow it to express in the jaws.

I read in one paper a mention that in normal development, the appearance of the embryo is consistent and predictable throughout incubation. With a mutation like ta², that isn't true. Someone growing mutant chicks will find that every chick they grew would be deformed in a different way.

I'm currently reading a paper titled "Talpid² Mutant Chick Limb Has Anteroposterior Polarity and Altered Patterns of Programmed Cell Death", published in The Anatomical Record 231: 251-260 (1991). That has some photos of the difference in bone structure of ta² wings and legs compared to normal development. The wings and feet both looks like stubby, wide hands with distorted arm bones. Something like a ping-pong paddle overall! The authors also mention that bone ossification begins several days later in ta² mutants. The oldest embyros they had lived to 21 days, and had incomplete ossification.

They also mention a talpid¹ mutant (extinct) and a talpid³ mutant (available for study in the UK, and extensively described in the literature).

Interesting reading, although it's very technical. I'm interested in the subject, but I'm not a geneticist!

[Scylla]

So, are tissue-specific regulatory systems known for the jaws? Or do you mean a regulatory system found in the talpid2 mutation?

I was not specifically referring to teeth, or talpid2 mutants. I was answering the more general question posed if scientists were able to allow a mutation in some areas and suppress its effects in others. The short answer is yes. Here is some hunting grounds for mandible specific genetic control, happy reading!

[Carcharodontosaurus]

I am now wondering whether it would be possible to make chickens quadrupedal with this method, and whether you could eventually make a sauropod-like animal with this method. It would take a lot of genetic modification though.

[mck0101]

So here's an idea: why not take the genes responsible for, say, a snow goose's beak and splicing them into the chicken's genome? A lot of geese have beaks which already vaguely resemble snouts and come complete with pseudo-teeth. I know somebody already mentioned that it's unlikely that the scientists engineering these animals would take to the idea of modifying them with another species' genetic material, but if push came to shove at least they're both birds and the end result would look more like a non-avian dinosaur.

[Auspex]

Why not just start with a goose, then?

[Mediospirifer]

Why not just start with a goose, then?

Maybe because the chicken genome is better understood, due to their status as the standard lab-experiment bird? I'm largely guessing here.

[Scylla]

I say start with an Ostrich, and work on re-creating moas at the same time!

[Mediospirifer]

I say start with an Ostrich, and work on re-creating moas at the same time!

An emu might be genetically closer to a moa. Hey, we might actually get some moa DNA from bones to work with!

[Scylla]

Yes, I was joking. By the way, we have lots of Moa DNA already.

For Example:http://www.sciencedaily.com/releases/2009/06/090630215938.htm

Edited April 17, 2014 by Scylla

[Mediospirifer]

Very cool!

If we can reliably get DNA from multiple-thousand-year old feathers, that does increase the potential for the project trying to recreate the passenger pigeon...

[PFOOLEY]

Why not just start with a goose, then?

Nooooooooooooooooooo!!!!

[Auspex]

The lamellae in a duck's bill are part of the bill sheath, not the jaws. They are a filter-feeding adaptation among the dabblers, and fish-grippers among the mergansers. One could not turn them into "teeth", and they would be gone with it when you engineered the bill away.

[Carcharodontosaurus]

Yes, I was joking. By the way, we have lots of Moa DNA already.

For Example:http://www.sciencedaily.com/releases/2009/06/090630215938.htm

I've seen moa DNA sequences on GenBank. It seems to be just mitochondrial DNA, which is useless for any de-extinction attempts. We need the nuclear DNA.

[Scylla]

I've seen moa DNA sequences on GenBank. It seems to be just mitochondrial DNA, which is useless for any de-extinction attempts. We need the nuclear DNA.

Here, try this:

http://www.nature.com/nature/journal/v425/n6954/full/nature01838.html

[PA Fossil Finder]

The lamellae in a duck's bill are part of the bill sheath, not the jaws. They are a filter-feeding adaptation among the dabblers, and fish-grippers among the mergansers. One could not turn them into "teeth", and they would be gone with it when you engineered the bill away.

So mergansers don't actually have teeth? Huh. Does that mean it would be more of a serrated duck bill than teeth and jaws?

[Auspex]

So mergansers don't actually have teeth? Huh. Does that mean it would be more of a serrated duck bill than teeth and jaws?

That is correct.