Presenter: Daniel Derrick
Co-Presenters: Jennifer Hampton, Karen Guillemin
Faculty Mentor: Karen Guillemin, Jennifer Hampton
Presentation Type: Poster 56
Primary Research Area: Science
Major: Biology
Funding Source: NIH: National Institute of General Medical Sciences grant, award number P50GM098911, $162,152
Host-microbe interactions are important for normal development of the host, and often, secreted bacterial products play essential roles in these interactions. In zebrafish, the protein BefA is secreted by a subset of resident bacterial species in the gut. Interestingly, BefA is sufficient to induce expansion of pancreatic beta cells during early larval development. Previously, BefA has also been shown to have effects on cultured murine beta cells, suggesting that it may have a direct mechanism of action. This raises an intriguing question: how can a protein secreted by bacteria in the lumen of the gut exert effects on an entirely separate organ? For BefA to act directly on beta cells in vivo, it must somehow travel from the gut to the pancreas. Here, we examined whether a functional hepatopancreatic duct, which connects the pancreas to the gastrointestinal tract, is necessary for BefA-mediated expansion of beta cells. To do so, immunofluorescence labeling and confocal microscopy were used to count pancreatic beta cells in zebrafish that lack an intact hepatopancreatic duct due to a loss-of-function mutation in the sox9b gene. Despite the lack of this duct, sox9b mutants still exhibited a robust response to BefA treatment, which suggests that BefA promotes beta cell expansion independent of the hepatopancreatic duct.