By Anthony Watts – Re-Blogged From WUWT
Researchers have used gene editing to completely eliminate populations of mosquitoes in the lab.
The team tested their technique on the mosquito Anopheles gambiae, which transmits malaria.
They altered part of a gene called doublesex, which determines whether an individual mosquito develops as a male or as a female.
This allowed the Imperial College London scientists to block reproduction in the female mosquitoes.
They want to see if the technology could one day be used to control mosquito populations in the wild.
Writing in the journal Nature Biotechnology, Prof Andrea Crisanti and colleagues report that caged populations of Anopheles gambiae collapsed within 7-11 generations.
Dr Crisanti said:
“2016 marked the first time in over two decades that malaria cases did not fall year-on-year despite huge efforts and resources, suggesting we need more tools in the fight.”
The approach falls within a category of genetic engineering known as a gene drive. It describes technologies that spread a gene or particular suites of genes through a population.
The researchers used the gene editing technique known as Crispr to modify a part of the doublesex gene that is responsible for female development.
The paper: https://www.nature.com/articles/nbt.4245 (open access)
A CRISPR–Cas9 gene drive targeting doublesex causes complete population suppression in caged Anopheles gambiae mosquitoes
In the human malaria vector Anopheles gambiae, the gene doublesex(Agdsx) encodes two alternatively spliced transcripts, dsx-female(AgdsxF) and dsx-male (AgdsxM), that control differentiation of the two sexes. The female transcript, unlike the male, contains an exon (exon 5) whose sequence is highly conserved in all Anopheles mosquitoes so far analyzed. We found that CRISPR–Cas9-targeted disruption of the intron 4–exon 5 boundary aimed at blocking the formation of functional AgdsxF did not affect male development or fertility, whereas females homozygous for the disrupted allele showed an intersex phenotype and complete sterility. A CRISPR–Cas9 gene drive construct targeting this same sequence spread rapidly in caged mosquitoes, reaching 100% prevalence within 7–11 generations while progressively reducing egg production to the point of total population collapse. Owing to functional constraint of the target sequence, no selection of alleles resistant to the gene drive occurred in these laboratory experiments. Cas9-resistant variants arose in each generation at the target site but did not block the spread of the drive.