The mechanism is this: "These scFvs are derived from antibodies specific to a parasite chitinase, the 25 kDa protein and the circumsporozoite protein, respectively."
So you'll spend a ton of money building a fancy CRISPR system in your mosquitoes, release them into the wild, and in a matter of months you will have parasites with on-target mutations in these proteins that will allow them to evade your resistance mechanism. I'd lay $1000 on this without blinking.
You're basically talking about curing malaria in mosquitoes. Why not, instead, just cure malaria in humans?
First, you're confusing wiping out the mosquito species with giving the mosquitos resistance to the malaria parasite. Those are two different things.
Second, there is no reason that a CRISPR-based system is limited to a single target. Will you also lay $1,000 against a system that targets ten species-unique sequences at once?
You're basically talking about curing malaria in mosquitoes.
Neither I nor the article is talking about that. It's a discussion of making the mosquito species itself extinct.
> First, you're confusing wiping out the mosquito species with giving the mosquitos resistance to the malaria parasite. Those are two different things.
You're the one who brought up CRISPR and gene drive. Perhaps you should read the actual paper: http://www.pnas.org/content/112/49/E6736.full; you'll see that the proposal is entirely about giving mosquitoes resistance to the malaria parasite, not about eradication. That is, the goal is to eliminate the parasite in mosquito populations (i.e., cure malaria in mosquitoes), not to kill mosquitoes.
>Second, there is no reason that a CRISPR-based system is limited to a single target. Will you also lay $1,000 against a system that targets ten species-unique sequences at once?
Yes. On-target mutations are trivial to produce, and alleles segregate independently.
"You're the one who brought up CRISPR and gene drive. "
Which can be targeted to eliminate the mosquitos themselves.
"Perhaps you should read the actual paper"
The actual paper? Like there's only one? Hint: there's more than one way to use this technology, and more than one group working with it.
"On-target mutations are trivial to produce, and alleles segregate independently."
I think you're misunderstanding what "independently" means in this context.
If the probability of a mutation that will get around one targeted sequence is (say) 1 in a million, that's almost certainly going to happen, just because there are billions of mosquitos.
However, if you target (say) ten independent sequences, the probability of any one organism having resistance to all of them is going to be 1 in (1 million)^10 = 1 in 10^60 and that is basically not going to happen. It does no good in this case for one organism to be resistant with respect to one target, while another organism is resistant with respect to another target, because all of the targets will have fatal outcomes. The only way for the organism to survive would be for it to be resistant to all of them at the same time, from the beginning.
And there's no reason why you'd have to stop at 10, either.
You should go read about MRSA, which shouldn't exist according to your logic. You also are misunderstanding how independent assortment of alleles work.
Because plasmodium is a eukaryotic species which reproduces sexually, on-target resistance mutations to any number of mechanisms can arise independently in a bunch of different organisms and accumulate through selection + allele segregation. It's also very easy to produce these sorts of mutations, since it is trivial to change an amino acid to disrupt antibody binding/recognition without altering the function of the protein.
>Which can be targeted to eliminate the mosquitos themselves.
This is incorrect; the whole point of a gene drive is that it causes increased propagation of a trait in the mosquito population. What you're describing is a very different strategy, since a trait that kills the mosquito obviously cannot propagate. It can also be achieved much more simply by using sterile males to outcompete fertile males and reduce the population ('sterile insect' technique); however, this technique only works on small populations and almost certainly wouldn't work in Anopheles or some such.
Here is the paper where they talk about the mechanism of resistance being conferred on the mosquito: http://www.pnas.org/content/109/28/E1922.abstract
The mechanism is this: "These scFvs are derived from antibodies specific to a parasite chitinase, the 25 kDa protein and the circumsporozoite protein, respectively."
So you'll spend a ton of money building a fancy CRISPR system in your mosquitoes, release them into the wild, and in a matter of months you will have parasites with on-target mutations in these proteins that will allow them to evade your resistance mechanism. I'd lay $1000 on this without blinking.
You're basically talking about curing malaria in mosquitoes. Why not, instead, just cure malaria in humans?