Rebecca’s not really a matchmaker in the lab, but that’s the first thing I thought of when she described her project to us during her chalk talk.
Rebecca’s looking into how certain genes (or lack of) may impact the ability of fruit flies to learn courtship behavior. Specifically, she’s looking at a particular olfactory gene called Or47B, and how knocking this gene out might affect a male fly’s ability to learn courtship cues from other flies. A lot of her lab work seems to consist of raising these knockout flies (and others) and putting each male together with a group of females. Then at specific times she takes each male, puts them alone together in a chamber with one female, and sees whether they’ve picked up on how to pick up a lady from their time interacting with the group.
One thing that struck me during Rebecca’s talk was how this courtship behavior of flies, which I thought was an intrinsically innate instinct, could potentially be “erased”. But then again, what does innate mean? In Rebecca’s case, she’s working with things on a genetic level, literally going down to the DNA that defines a fruit fly, and seeing whether removing/adding components to this molecule changes anything about the whole organism. If we say that any behavior stimulated by characteristics/physiological traits encoded in DNA is innate instinct, then I guess fly courtship behavior still counts. This behavior is apparently learned through things such as olfactory receptors; and when you take away the right olfactory receptors, you block the pathway to learning the behavior. Not only was this project an interesting discussion of what counts as innate and if we can alter innate behavior; it’s also a really interesting example of how behavior and physiology/genetics can be, essentially, directly linked (though I assume that the actual relationship is far more complicated than I just stated!)
Speaking of the link between genetics and behavior, I’ve always been fascinated by how genetics studies often have to utilize both ends of the spectrum in order to gather data. For example, a study like Rebecca’s can start out by deciding what genes they want to leave in or out (resulting a control group and other experimental set-ups). But then, to determine what the presence/absence of this gene signifies, they have to observe the resulting phenotype(s), which includes a physiological and/or behavioral change. Again, this link between what has happened at the molecular level and what is going on in the whole organism fascinates me. I’m sure that elucidating the exact nature of genotype-phenotype relationships is not always (if ever) clear-cut. But it’s still an interesting way to try to learn more about different genes and the roles they play, whether in flies, humans, or across a whole range of Earth’s organisms (we all share some bit of DNA after all!)
Thanks Rebecca for sharing your project with us, and great job to everyone on their awesome chalk talks!
Since choosing a chalk talk to write about was so hard (everyone’s projects are so cool), I decided to go with the topic I found most intellectually intriguing. Martin Acosta’s presentation on ‘Rapid Tryptophan Depletion: Sex-mediated Differences in Rats’ stuck with me because of the parallels between our projects.
Tryptophan is an important amino acid which we obtain through our diets and which is metabolized into serotonin (an important neurotransmitter) in the brain after passing through the blood-brain barrier (BBB). Martin’s project offers an alternative to the social defeat (SD) paradigm to induce depression in rodents since SD is not effective in females and hence cannot be used to study sex-differences in depression. In their protocol, the Kuhn lab feeds rats a mixture of several large neutral amino acids (LNAAs) or a mixture of LNAAs & tryptophan. LNAAs compete with tryptophan molecules to pass through the transport proteins in the BBB. Therefore, rats fed only LNAAs have a higher proportion of them which prevent tryptophan from passing into the brain and being converted into serotonin (serotonin deficiency is associated with depression).
Although preliminary results from Martin’s study (which measures the levels of various metabolites in the rats’ blood and brains) have shown no differences in how male and female rats are affected, this is not the aspect interests me. Tryptophan plays an important role in the gut-brain axis—some bacteria are known to use up tryptophan leaving less to be metabolized by our bodies, while others produce it. Additionally, the kynurenine pathway is another important pathway for tryptophan metabolism. Kynurenine is produced from tryptophan and can be further metabolized in two ways with opposite effects—the end product of one pathway is neuroprotective while the other is neurotoxic. Altogether, tryptophan and its metabolites seem to play an important role in depression and are an important signaling pathway between the gut and brain. This is where my project comes in: I can’t wait to see the bacterial DNA sequencing results from the feces of the SD mice in my project to determine whether the bacterial species which are more/less abundant are implicated in the tryptophan pathway.
P.S. Tryptophan is one of my new favorite sounding words—try saying it, it’s addicting!
When one of my friends first mentioned that he literally did not want to leave his bed sometimes in winter and could have a case of seasonal depression, I was awfully confused.
Seasonal depression? In my mind, depression couldn’t be seasonal; there wasn’t a switch where one could turn “on” or “off” depression.
So, curious, I looked into it, and found that during winter, the change in hours of light can modify one’s biological clock and therefore shift hormone levels of serotonin and melatonin (regulators of mood and sleep, which are correlated with depression) (Lieber). I thought it was fascinating that our own environment could change our bodies and how we feel.
I drew upon this memory when listening to Georgia, a fellow B-SURFer, on her talk Stress and Weather: Environmental Factors Affecting Glucocorticoid (GC) Levels. Her lab studies baboons and how not only their social rank but also their environment in Africa contributes to stress. They extract hormones from baboon fecal samples in order to analyze how the environmental factors recorded correlate to glucocorticoid levels (and therefore stress). Her hypothesis was that GC levels would increase as environmental factors became more extreme, and I completely understood when she referred to the different types of food distributions: scramble and contest. In my senior year of high school, I participated in an international written and oral debate contest on the topic of global food security. Through all the research on global food security and relating topics, I understood the food access, availability, and distribution issues that are quickly rising in the world today. With such different food models dispersed around the world and the advent of climate change, stress levels could vary greatly. I’m very curious as to how exactly these increased stress levels will create side effects that weren’t originally conjectured—perhaps in reproductive stress/hormones? Our levels of health, like seasonal depression? I was very enlightened with Georgia’s work and hope to hear about results or possible new leads soon!