Nature reports on a lifesaving use for diet drugs:
Female Aedes aegypti, like other mosquito species, feed on blood to get the protein they need to produce their eggs, and spread diseases such as dengue in the process. But once the mosquitoes have had their blood fix, they stop biting until they’ve laid their eggs several days later.
Leslie Vosshall, a neurobiologist at the Rockefeller University in New York City, wondered whether she could hijack this biological process to switch off a mosquito’s appetite.
Previous research had suggested that a mosquito’s desire to feed is controlled by neuropeptides, molecules used by the nervous system to communicate. Vosshall and her team suspected that neuropeptide Y (NPY) receptors might be particularly important, because they form part of the molecular pathway involved in food-seeking behaviour for many animals — including humans.
Some human appetite-suppressant drugs already target the NPY receptors, so Vosshall decided to take a “completely zany” approach: feed these drugs to mosquitoes and see what happens.
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They cultivated 49 different mosquito proteins in tissue culture and examined which ones responded to the drug. One stood out: NPY-like receptor 7 (NPYLR7).
The team then used CRISPR gene-editing to create mosquitoes that had a mutation in the NPYLR7 gene that prevented it from functioning properly. When they fed the drug to these modified mosquitoes, it no longer had an effect, suggesting that NPYLR7 gene was the key to regulating the insects’ appetites.
Vosshall says that a project that started “as kind of a lark” gained momentum after a representive from the philanthropic Bill & Melinda Gates Foundation in Seattle, Washington — which funds research on diseases transmitted by mosquitoes such as dengue and malaria — expressed enthusiasm at early results presented at a conference. “That encouraged me,” she says. “If the major funder of public health worldwide felt like it wasn’t science fiction — we were going to do it.”