Poster Session I
Project Type
Poster
Faculty Mentor’s Full Name
Emily Gagliano
Faculty Mentor’s Department
Division of Biological Sciences
Additional Mentor
Sarah Certel
Abstract / Artist's Statement
Calvin Orser1, Emily Gagliano, Sarah J Certel2
Research on the gut-brain axis is a major focus in biology because the gastrointestinal tract and central nervous system communicate continuously. This bidirectional signaling helps organisms maintain homeostasis by relaying information from the gut to the brain and shaping innate behaviors such as feeding and reproduction. The adrenergic, “fight or flight”, system has emerged as a key component of this signaling. Adrenergic receptors are expressed in multiple gut epithelial cell types, including enteroendocrine cells (EEs), the main secretory cells of the gut, which synthesize and release the neuropeptides that can communicate with the brain. For these reasons, it is essential to define how adrenergic receptor signaling in the gut epithelium regulates enteroendocrine neuropeptide release and, in turn, reshapes gut brain communication to impact behavior.
Octopamine (OA) is the invertebrate analog of the adrenergic neurotransmitter norepinephrine. OA receptors are categorized based on their structural and pharmacological similarities to mammalian adrenergic receptors. Recent work in mammals indicates that β2 adrenergic receptors in the intestinal epithelium can act as nutrient sensors, linking luminal sugars to rapid changes in glucose uptake and broader gut signaling. Because reproductive output is tightly coupled to nutritional state, these findings motivate the hypothesis that OAβ2R activity in enteroendocrine cells (EEs) helps translate gut derived cues into hormone signals that support reproductive success and healthy offspring. Here, we investigate the role of the adrenergic receptors in EEs and how their activity in the gut epithelium affects reproductive behavior using the model organism Drosophila melanogaster. Here, we investigate the role of the OAβ2R receptor in EEs and how their activity in the gut epithelium affects reproductive behavior using the model organism Drosophila melanogaster. To test this, we used the Gal4/UAS system to knock down OAβ2R in a subset of EEs and measured embryo production.
Our preliminary data suggests that this knockdown results in a decrease in fecundity. The most likely reason for this is a decrease in stimulatory OAβ2R-mediated neuropeptide release from EEs, which are known to affect embryo production. Another explanation could be the sugar sensing aspect of OAβ2R which, when knocked down, could alter nutrient status in gut cells and change the subsequent relay of this information to the brain. Upon completion of this project, we hope by gaining an understanding of the behavioral impacts of knocking down OAβ2R in EEs, we then can delve into the biomechanics behind OAβ2R signaling.
Category
Life Sciences
Defining how adrenergic receptors may translate gut nutrient signals into starvation resistance and fecundity
UC South Ballroom
Calvin Orser1, Emily Gagliano, Sarah J Certel2
Research on the gut-brain axis is a major focus in biology because the gastrointestinal tract and central nervous system communicate continuously. This bidirectional signaling helps organisms maintain homeostasis by relaying information from the gut to the brain and shaping innate behaviors such as feeding and reproduction. The adrenergic, “fight or flight”, system has emerged as a key component of this signaling. Adrenergic receptors are expressed in multiple gut epithelial cell types, including enteroendocrine cells (EEs), the main secretory cells of the gut, which synthesize and release the neuropeptides that can communicate with the brain. For these reasons, it is essential to define how adrenergic receptor signaling in the gut epithelium regulates enteroendocrine neuropeptide release and, in turn, reshapes gut brain communication to impact behavior.
Octopamine (OA) is the invertebrate analog of the adrenergic neurotransmitter norepinephrine. OA receptors are categorized based on their structural and pharmacological similarities to mammalian adrenergic receptors. Recent work in mammals indicates that β2 adrenergic receptors in the intestinal epithelium can act as nutrient sensors, linking luminal sugars to rapid changes in glucose uptake and broader gut signaling. Because reproductive output is tightly coupled to nutritional state, these findings motivate the hypothesis that OAβ2R activity in enteroendocrine cells (EEs) helps translate gut derived cues into hormone signals that support reproductive success and healthy offspring. Here, we investigate the role of the adrenergic receptors in EEs and how their activity in the gut epithelium affects reproductive behavior using the model organism Drosophila melanogaster. Here, we investigate the role of the OAβ2R receptor in EEs and how their activity in the gut epithelium affects reproductive behavior using the model organism Drosophila melanogaster. To test this, we used the Gal4/UAS system to knock down OAβ2R in a subset of EEs and measured embryo production.
Our preliminary data suggests that this knockdown results in a decrease in fecundity. The most likely reason for this is a decrease in stimulatory OAβ2R-mediated neuropeptide release from EEs, which are known to affect embryo production. Another explanation could be the sugar sensing aspect of OAβ2R which, when knocked down, could alter nutrient status in gut cells and change the subsequent relay of this information to the brain. Upon completion of this project, we hope by gaining an understanding of the behavioral impacts of knocking down OAβ2R in EEs, we then can delve into the biomechanics behind OAβ2R signaling.