Brave new world of genetic editing for reptiles-

[MarkL1561]

The topic is snakes not farming!

Sorry my bad


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[Alter-Echo]

If they start adding plant genes to snakes, then this thread WILL be about farming!

[Ax01]

If they start adding plant genes to snakes, then this thread WILL be about farming!

that's a good idea! maybe we can finally get some green BP morphs.

Edit: or some veggies that taste like snakes and reptiles.

[MarkL1561]

If they start adding plant genes to snakes, then this thread WILL be about farming!

Maybe we can get actual vine snakes.....?


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[bcr229]

How about a snake that can turn sunlight into food through photosynthesis?

[MarkL1561]

How about a snake that can turn sunlight into food through photosynthesis?

You’d have to incorporate chloroplasts within every cell of the animal which likely is impossible. It would be awesome if it was possible though!


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[Ax01]

ok, update!

looks like there is reportedly shorter lives for CRISPR gene-edited human babies. not sure about those CRISPR Albino lizards tho.

story: https://www.sciencedaily.com/release...0603124709.htm

CRISPR baby mutation significantly increases mortality
Two copies of mutated CCR5 gene associated with lower survivability

A genetic mutation that a Chinese scientist attempted to create in twin babies born last year, ostensibly to help them fend off HIV infection, is also associated with a 21% increase in mortality in later life, according to an analysis by University of California, Berkeley, scientists.

The researchers scanned more than 400,000 genomes and associated health records contained in a British database, UK Biobank, and found that people who had two mutated copies of the gene had a significantly higher death rate between ages 41 and 78 than those with one or no copies.

Previous studies have associated two mutated copies of the gene, CCR5, with a fourfold increase in the death rate after influenza infection, and the higher overall mortality rate may reflect this greater susceptibility to death from the flu. But the researchers say there could be any number of explanations, since the protein that CCR5 codes for, and which no longer works in those having the mutation in both copies of the gene, is involved in many body functions.

"Beyond the many ethical issues involved with the CRISPR babies, the fact is that, right now, with current knowledge, it is still very dangerous to try to introduce mutations without knowing the full effect of what those mutations do," said Rasmus Nielsen, a UC Berkeley professor of integrative biology. "In this case, it is probably not a mutation that most people would want to have. You are actually, on average, worse off having it."

"Because one gene could affect multiple traits, and because, depending on the environment, the effects of a mutation could be quite different, I think there can be many uncertainties and unknown effects in any germline editing," said postdoctoral fellow Xinzhu "April" Wei.

Wei is first author and Nielsen is senior author of a paper describing the research that will appear online on Monday, June 3, in the journal Nature Medicine.

Mutation prevents HIV infection
The gene CCR5 codes for a protein that, among other things, sits on the surface of immune cells and helps some strains of HIV, including the most common ones, to enter and infect them. Jiankui He, the Chinese scientist who last November shocked the world by announcing he had experimented with CCR5 on at least two babies, said he wanted to introduce a mutation in the gene that would prevent this. Naturally-occurring mutations that disable the protein are rare in Asians, but a mutation found in about 11% of Northern Europeans protects them against HIV infection.

The genetic mutation, ∆32 (Delta 32), refers to a missing 32-base-pair segment in the CCR5 gene. This mutation interferes with the localization on the cell surface of the protein for which CCR5 codes, thwarting HIV binding and infection. He was unable to duplicate the natural mutation, but appears to have generated a similar deletion that would also inactivate the protein. One of the twin babies reportedly had one copy of CCR5 modified by CRISPR-Cas9 gene editing, while the other baby had both copies edited.

But inactivating a protein found in all humans and most animals is likely to have negative effects, Nielsen said, especially when done to both copies of the gene -- a so-called homozygous mutation.

"Here is a functional protein that we know has an effect in the organism, and it is well-conserved among many different species, so it is likely that a mutation that destroys the protein is, on average, not good for you," he said. "Otherwise, evolutionary mechanisms would have destroyed that protein a long time ago."

After He's experiment became public, Nielsen and Wei, who study current genetic variation to understand the origin of human, animal and plant traits, decided to investigate the effect of the CCR5-∆32 mutation using data from UK Biobank. The database houses genomic information on a half million U.K. citizens that is linked to their medical records. The genomic information is much like that acquired by Ancestry.com and 23andMe: details on nearly a million individual variations in the genetic sequence, so-called single nucleotide polymorphisms (SNPs).

Two independent measures indicated a higher mortality rate for those with two mutated genes. Fewer people than expected with two mutations enrolled in the database, indicating that they had died at a higher rate than the general population. And fewer than expected survived from ages 40 to 78.

"Both the proportions before enrollment and the survivorship after enrollment tell the same story, which is that you have lower survivability or higher mortality if you have two copies of the mutation," Nielsen said. "There is simply a deficiency of individuals with two copies."

Because the ∆32 mutation is relatively common in Northern Europeans, it must have been favored by natural selection at some point, Nielsen said, though probably not to protect against HIV, since the virus has circulated among humans only since the 1980s.

Wei said that some evidence links the mutation to increased survival after stroke and protection against smallpox and flaviviruses, a group that includes the dengue, Zika and West Nile viruses.

Despite these possible benefits, the potential unintended effects of creating genetic mutations, in both adult somatic cells and in embryonic, germline cells, argue for caution, the researchers said.

"I think there are a lot of things that are unknown at the current stage about genes' functions," Wei said. "The CRISPR technology is far too dangerous to use right now for germline editing."

and here: https://www.theatlantic.com/science/...babies/590815/

A Mutation That Resists HIV Has Other Harmful Consequences

He Jiankui chose a famous mutation to edit into human embryos. Scientists are still trying to figure out everything it does.

In the 1990s, virologists in New York learned of a genetic mutation that would become one of the most famous ever discovered. They found it in a man who could not be infected with HIV. He turned out to be missing just 32 letters in a gene called CCR5, and remarkably, it was enough to make him resistant to the virus killing so many others. About 1 percent of people of European descent carry two copies of this mutation, now known as CCR5-Δ32.

In 2018, a Chinese scientist named He Jiankui made the mutation infamous when he attempted to use CRISPR to edit CCR5-Δ32 (pronounced “CCR5-delta-32”) into human embryos. He chose this mutation, he said, because the babies’ father was HIV-positive, and he wanted to make the resulting twin girls resistant to the virus. CCR5-Δ32 is also, after all, one of the most studied mutations.

He’s work immediately provoked outrage among scientists, who knew enough to know how much they did not know about the risks of altering CCR5. And now a new study suggests that CCR5-Δ32 is indeed harmful overall.

The girls’ CCR5 genes were altered, according to data He presented, but they do not exactly match the 32-letter deletion; it’s unclear whether either of them is actually resistant to HIV. Even if they were unable to get HIV, a body of research already suggested that CCR5-Δ32 made people more vulnerable to the flu and West Nile virus. A “good” mutation in the context of HIV can be “bad” in another context. No one knew, exactly, the net effect of a CCR5-Δ32 mutation.

However, the new study, by Rasmus Nielsen and Xinzhu “April” Wei of UC Berkeley, shows that people with two copies of the mutation are 21 percent more likely to die at the age of 76, with a mortality rate of 16.5 percent, compared with 13.6 percent for those who have only one or zero copies. Only recently, Nielsen told me, have genetic databases even become big enough for these effects on mortality to be apparent.

The effect of CCR5-Δ32 on mortality is ultimately subtle, but it follows from what’s already known about this gene. CCR5 usually codes for a receptor on the surface of white blood cells, and it plays a role in normal immune responses. HIV co-opts CCR5 as a way to get into white blood cells. So to block HIV is, ironically, also to eliminate a small piece of the normal immune system.

“If you think about what these people are with Δ32, they’re like human knockouts for a fairly important gene in immune response,” says Bill Paxton, a microbiologist at the University of Liverpool who helped discover the role of CCR5 in HIV. “It’s not wholly surprising you [would] read a paper like this, and the finding is there.”

After HIV researchers made CCR5-Δ32 famous, scientists in other fields got interested in the mutation, too. Flu researchers who studied it found that it predisposes people to fatal outcomes with flu. West Nile virus researchers found the same with that disease. Neurobiologists have found evidence that CCR5-Δ32 actually enhances recovery from stroke. But this process of understanding the full scope of CCR5 has been piecemeal, essentially limited by what scientists think to look for.

Geneticists have proposed more systematic ways to understand all the effects of a single gene. Instead of picking a disease and looking for associated genes among a large group of people, geneticists can pick a gene of interest and look for associated traits. This is called PheWAS, or phenome-wide association study, where phenome refers to the set of observable traits. The idea is to look for links “that we just never knew to look for before,” says Marylyn Ritchie, a geneticist at the University of Pennsylvania who uses PheWAS in her research. Crucially, PheWAS requires not just DNA from volunteers but rich and detailed health data from those same volunteers—everything that could be conceivably linked to a gene, from height to brain volume to white-blood-cell count. PheWAS studies are necessarily limited by what health data have been collected.

Nielsen and Wei told me that they also tried to see whether CCR5-Δ32 was linked to other traits in the U.K. Biobank, and they found a few additional expected associations, such as white-blood-cell count. But their results are restricted by the health data scientists thought to begin collecting back in 2006, when the U.K. Biobank project began.

And despite its size, the U.K. Biobank is not representative of all people in all situations. In a population with more non-British ancestry and in a part of the world where certain viruses are more prevalent than others, CCR5-Δ32 could be more harmful or less beneficial. It depends on the environment, and the environment could also change in the future. A new epidemic could emerge, and so could new treatments.

That is ultimately what makes the proposition of editing genes like CCR5 so tricky. It can be hard to predict what the net effect will be, in a future we do not yet know, and harder still when all of the trade-offs today have not even been fully studied. In May, scientists launched an international commission on gene editing that will discuss these concerns, including how to balance the benefits and harm to not just a gene-edited child but also “subsequent generations.”

tons of stories breaking on this:
https://www.newscientist.com/article...ene-mutations/
https://www.technologyreview.com/s/6...earlier-death/
https://www.engadget.com/2019/06/03/...fe-expectancy/

[Bogertophis]

You’d have to incorporate chloroplasts within every cell of the animal which likely is impossible. It would be awesome if it was possible though!


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"Spoil-sport", lol...

[dr del]

Woah!! this is not known by the general public in the uk!

[4stringed]

Finally a post on here that I can contribute to. My background is in biochemistry and my higher level courses were all on synthetic biology and genetic engineering (mostly from a microbiology standpoint).

So the funny thing that someone mentioned about glow in the dark snakes is dead on. One of the most common genes that's added to an organism for proof of concept is a flourescent gene from jellyfish. They've put in in everything from bacteria to cats and they glow under plack light. So glowing snakes are very possible and would probably be one of the first ones we see.

Because these changes are genetic the offspring will cary the trait so once a gene is added it can be bred into other animals. The potential of this is that if you could isolate a gene from another species like a green tree python involved in green pigmentation you could splice that into a ball and get green ball pythons.

Could this have adverse effects? Yes, but there are genes that breeders work with now that have detrimental effects on animals, such as any of the wobble genes and I guarentee that scientists would not add an animal with anything as much as a wobble to the breeding pool and multiple generations would likely be studied before they were available to the public. Now if the spider gene was isolated and found to be linked to a gene that causes the wobble issues, the spider gene could be isolated, copied and spliced into another animal and we could have spiders without wobble.