Suppose you are one of many scientists racing to design mosquitoes unable to transmit malaria or other major scourge and you succeed. Now what? You can free the creatures in the real world, but if they are not a unique advantage, they are largely outnumbered by the billions of natural mosquitoes already there.
Now scientists have developed a new genetic trick that might help mosquitoes resistant to diseases spread like wildfire. The system, a so-called gene drive, is published online today in Nature .
The new study is part of an explosion in genetic research mosquitoes is to stop mosquitoes from transmitting malaria-which killed about 800,000 people in 09 and several other diseases. Already, scientists have identified several genes that mosquitoes when tinkered, reduce the ability of mosquitoes to transmit a virus or a parasite; they also gave the insects new genes that do the same thing.
But questions clouding the future of the area was how to "replace" natural populations with these new and improved mosquito. For this, scientists need a system that will help high lab mosquitoes take over wild populations, to ensure that resistance genes become ubiquitous. Scientists are working on several strategies; have many supposedly selfish genes, strange stretches of DNA from natural origin that have the means to spread in populations of almost parasitically. The idea is that these genes could be harnessed to others who mess with the parasite's life cycle and to those who spread as well. But although researchers have had some success in fruit flies, no one was able to get a gene drive system is in mosquitoes.
The new study, conducted by molecular biologists Andrea Crisanti and Austin Burt of Imperial College London, was done in Anopheles gambiae , the mosquito species is by far the support the most important of malaria. The scientists used a gene called homing endonuclease (HEG), a selfish gene found in fungi, plants and bacteria that has the ability to create a second copy of itself in people who have a alone. This ensures that all offspring have the gene as well, and it is one of the fastest genes can spread in nature means, said insect geneticist Jason Rasgon of the Johns Hopkins School of Public Health at Bloomberg Baltimore, Maryland who was not involved in the new study.
To show that they can harness that power, researchers have a high population of Anopheles mosquitoes that glowed in the dark, with a green fluorescent protein. They then released into their cages small numbers of mosquitoes with HEG specifically designed to break the gene of the fluorescent protein in sperm cells and to fit into the same location on the chromosome, thereby ensuring its propagation in the next generation. In this way, the team could simply monitor the spread of the HEG by counting the number of mosquitoes in each generation was lit in green.
As scientific models have predicted, cages quickly grew darker over time. If, for example, only 1% of mosquitoes were HEG early experience, about 60% were 12 generations later. This means that the gene has the ability to turn even large populations in a short period of time, said Crisanti.
The next step, he says, is to not break the HEG gene fluorescent protein but which is crucial to the transmission of malaria. It could be an odor recognition gene that helps the mosquito finds its host, for example, or one that the malaria parasite needs to enter in the salivary glands of the mosquito; the team already 10 to 15 candidates.
Rasgon welcomes the study as the first to show that a gene can drive in mosquitoes, which has long been a critical challenge in the field. "They still have a long way to go," said Rasgon. "But as a proof of principle, it is quite impressive."
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