Ever wonder why male mosquitoes don’t bite?
“They don’t have to make eggs,” explained Immo Hansen, associate professor of biology at New Mexico State University in the College of Arts and Sciences. “But, the females need nutrient proteins, so they take up our blood.”
It’s through this process that vector, or disease-causing, mosquitoes transmit malaria, dengue fever, chikungunya, yellow fever viruses and other illnesses.
Fortunately, as these mosquitoes continue to develop resistance to common insecticides, researchers in the biology department at NMSU, in collaboration with the Department of Physiology and Biophysics at Rosalind Franklin University, may have identified a new way to stop this cycle at its earliest stages.
Specifically, the team has discovered a new type of amino acid transport in the yellow fever mosquito that may lead to the development of safer and more effective insecticides that target the mosquito’s ability to produce eggs. The findings were published last month in “Nature Communications,” in a paper titled “Substrate specificity and transport mechanism of amino-acid transceptor Slimfast from Aedes aegypti.”
“In the process of producing eggs, mosquitoes convert the blood meal into nutrients and into the components of the eggs,” said Hitoshi Tsujimoto, paper co-author and postdoctoral researcher in NMSU’s Molecular Vector Physiology Lab. “Those are mostly proteins, and are digested into smaller pieces, which are amino acids.”
These amino acids, which are large and cannot cross cell membranes, are distributed throughout the body of the mosquito using specific transport proteins that allow them to pass through the cell membranes, he explained. These transport proteins allow mosquitoes to distribute the nutrients necessary for reproduction within their bodies.
“If we could inhibit the transporter,” Tsujimoto said, “the mosquito cannot develop eggs, so they can’t reproduce — that way we can stop the cycle.”
Tsujimoto and collaborators focused their study on an amino acid transporter called Slimfast, which they found to have different modes of action depending on the concentration of amino acids in the mosquito’s body during reproduction.
The first mode, they said, is the mode of action the mosquito uses when it hasn’t yet received blood meal.
“That means there are very little amino acids to go around,” said Hansen, also involved in the study. “So, in order to get the amino acids in the cell, you have to be really efficient; this is what we call the high-affinity mode of action.”
However, when Slimfast is exposed to high levels of amino acids after a blood meal, the transporter behaves very differently.
“It opens up just like a pore and lets everything through — fast,” Hansen said. “ We call this low affinity.”
“This is unprecedented,” he continued. “Nobody has ever shown an amino acid transporter that does anything like that. This explains how a mosquito can switch from high affinity transport to low affinity blood transport within seconds, without changing the complement of amino acid transporters in its membranes.”
While this discovery alone is a novel contribution to mosquito physiology research, Hansen and
Tsujimoto said inhibiting this transport system through a new insecticide could also present a relatively safe form of pest control.
“These transporters are quite mosquito specific,” Hansen said. “So, an insecticide that attacks this one will most likely have no effect on humans because we don’t have these transporters.”
The full “Nature Communications” article can be viewed at nature.com/ncomms/2015/151009/ncomms9546/full/ncomms9546.html.
For more information on the Molecular Vector Physicology Lab in NMSU’s College of Arts and Sciences, visit biology-web.nmsu.edu/~hansen/.