Molecular geneticist Joanna Chiu (Photo by Kathy Keatley Garvey)

If you want to know more about circadian timing and why "circadian timing is everything"--from human beings to fruit flies--don't miss the Science Café session on Wednesday night, March 8 at Davis.

Molecular geneticist Joanna Chiu, vice chair of the UC Davis Department of Entomology and Nematology, will speak on "Circadian Timing Is Everything: From a Good Night's Sleep to Minimizing Insecticide Use" at the Science Café session at 5:30 p.m., Wednesday, March 8 in the G St. Wunderbar, 28 G St., Davis.

Professor Jared Shaw of the UC Davis Division of Math and Physical Science is hosting the informal session. Free and open to all interested persons, it is sponsored by the Capital Science Communicators and the UC Davis Department of Chemistry. Science Café events take place in casual settings and aim to feature an engaging conversation with a scientist about a particular topic.

Chiu, an associate professor who specializes in molecular genetics of animal behavior, joined the UC Davis Department of Entomology faculty in June 2010. She received her doctorate in molecular genetics from the Department of Biology at New York University.

"All living things on our planet, from bacteria to humans, organize their daily activities around the perpetuating 24-hour day-night cycles, the result of earth rotating on its own axis and orbiting around the sun," Chiu says. "In order for organisms to anticipate predictable variations in their environment that naturally occurs over the 24-hour cycle and coordinate their physiology and behavior to perform at their best, they rely on an internal biological clock. At the science cafe presentation, I will discuss how this internal clock, termed the circadian clock, affects many important aspects of our lives, including the timing of when we feel tired and want to go to bed, the time-of-day our immune systems are most susceptible to pathogen attack, and even when medicines should be taken to give you 'the most bang for your buck.'" In addition, I will discuss the consequences of when the circadian clock is 'broken' or 'off-kilter' because of diseases, work-schedule, jetlag, and light pollution."

Back in 2011, Chiu and colleagues from Rutgers University, the State University of New Jersey, published their work on the fruit fly, Drosophila melanogaster, describing how they identified a new mechanism that slows down or speeds up the internal clock of fruit flies. That research, published in the journal Cell, has important implications: it could lead to discoveries on alleviating human sleep disorders.

By mutating one amino acid in a single protein, “we changed the speed of the internal clock and flies now ‘think' it is 16 hours a day instead of 24 hours a day,” Chiu explained in a 2011 interview.  “Our goal, of course, is not to trick flies into thinking the day is shorter or longer, but to dissect this complex phospho-circuit (phosphorylation sites) that controls clock speed in metazoans.”

“Living organisms—plants, animals and even bacteria—have an internal clock or timer that helps them to determine the time of day," she said in that 2011 interview. "This internal clock is vital to their survival since it allows them to synchronize their activity to the natural environment, so that they can perform necessary tasks at biologically advantageous times of day.”

“A functional clock is required to generate proper circadian rhythms of physiology and behavior including the sleep-wake cycle, daily hormonal variations and mating rhythms,” Chiu said.  “Based on genetics, molecular biology and biochemical experiments performed in many different model organisms, we know that the speed of the internal clock is controlled by a core set of circadian proteins."

So if you aren't getting that good night's sleep and you're wondering about that internal clock, be sure to head over to the G St. Wunderbar on March 8. You'll learn the connection between circadian timings and minimizing insecticide use, too.

Researchers in the Walter Leal lab, UC Davis Department of Entomology, are engaging in some exciting research.

They just discovered a "generic insect repellent detector" in the fruit fly (Drosophila melanogaster)--research published today (March 16) in PloS One (Public Library of Science).

What's exciting is that this research may lead to more effective and lower-cost products than DEET, the gold standard of insect repellents.

The five-member team found the sensory organs involved when fruit flies detect and avoid three key insect repellents: DEET, IR3535 and picaridin.  They identified the olfactory receptor neuron (ORN) and characterized its receptor, DmOr42a.

The research team of Leal; primary author and chemical ecologist Zain Syed; chemical ecologist Julien Pelletier; and undergraduate students Eric Flounders and Rodrigo Chitolina, first found that the fruit fly avoids all three well-known repellents, DEET, IR3535 (a compound known as Avon Corporation’s “Skin-So-Soft Bug Guard”) and picaridin (derived from pepper) and then set out to find olfactory  receptor neurons sensitive to those insect repellents. They scanned all olfactory sensilla in the antennae and the mouthpart structure, maxillary palps, using single unit electrophysiological recordings.

The receptor they found “fulfills the requirements for a simplified bioassay for early screening of test insect repellents,” they wrote in the scientific paper.

When you think that it takes about 10 years and $30 million to develop a new repellent--and only one test compound in 20,000 reaches the market--this could really speed up the process.

Zain Syed told us: "In this study, by using established behavioral assays to dissect the mechanism of repulsion in fruit flies, we demonstrated for the first time that Drosophila equally avoid other repellents--picaridin and IR3535. By challenging every type of olfactory sensilla on the antenna and maxillary palps, we identified neurons and then the odorant receptor that detect these repellents."

The UC Davis research, as Syed said, "adds a new dimension in research towards understanding the molecular, cellular and organismal response to repellents."

Chemical ecologist Coby Schal, the Blanton J. Whitmire Distinguished Professor of Entomology at North Carolina State University, praised the research as “an excellent example of translational research that can lead to a streamlined and less expensive path of discovery of new repellents.”

In earlier research, Syed and Leal identified a DEET-sensitive olfactory receptor neuron in the Southern House mosquito. “Going from the neuron to the receptor, however, is like looking for the proverbial needle in a haystack as the mosquito genome has some 181 olfactory receptor genes,” Schal said.

The Leal lab knows DEET. Back in August 2008, Leal and Syed drew international attention when they announced they'd discovered DEET’s mode of action or how it works.  Scientists long surmised that DEET masks the smell of the host, or jams or corrupts the insect’s senses, interfering with its ability to locate a host. The Leal-Syed research showed that mosquitoes actually smell DEET and avoid it because they dislike the smell.

DEET, developed by scientists at the U.S. Department of Agriculture and patented by the U.S. Army in 1946, is the go-to insect repellent. Worldwide, more than 200 million use DEET to ward off vectorborne diseases.