Event Title

Intestinal Gap Junction INX-16 Mediates a Social Foraging Behavior in C. elegans

Presenter Information

Lisa N. Learman, Oberlin College

Location

Science Center A154

Start Date

10-2-2015 3:00 PM

End Date

10-2-2015 4:20 PM

Poster Number

2

Abstract

Social interactions are present in all sorts of organisms, from bacteria forming microfilms to birds navigating a migration. However, the molecular mechanisms determining these behaviors remain poorly understood. We are investigating the role of an intestinal gap junction in a C. elegans social behavior called aggregation, in which worms cluster while foraging. We previously observed aggregation in animals with mutated intestinal gap junction INX-16 and devised a plan to determine the cause of their altered foraging behavior. In wild isolates this behavior is caused by polymorphisms in neuropeptide receptor NPR-1, which suppresses aggregation when active in several neurons. NPR-1 can be activated by FLP-21, a neuropeptide that is released into the body cavity. A second pathway uses DAF-7, a TGF-β homologue, to suppress aggregation. The DAF-7 pathway is independent of NPR-1. Our project aims to determine which aggregation pathway is altered in the inx-16 mutant. Since FLP-21 and INX-16 are both found in the intestine we hypothesize that lack of intestinal FLP-21 secretion in inx-16 mutants leads to insufficient activation of NPR-1 and the resultant aggregation behavior. To test this hypothesis we constructed double mutants daf-7;inx-16 and npr-1;inx-16 and assayed for aggregation. Our results showed that daf-7;inx-16 doubles exhibit increased aggregation compared to either single mutant, which suggests that INX-16 and DAF-7 act independently. npr-1;inx-16 shows no increase in aggregation compared to either single mutant, which suggests that INX-16 and NPR-1 act in the same pathway. Future research will determine whether FLP-21 is properly synthesized, packaged, released, and received in inx-16 mutants.

Notes

Session II, Panel 3 - PATHWAYS: Micro & Macro

Major

Biology; Musical Studies

Project Mentor(s)

Maureen Peters, Biology

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Oct 2nd, 3:00 PM Oct 2nd, 4:20 PM

Intestinal Gap Junction INX-16 Mediates a Social Foraging Behavior in C. elegans

Science Center A154

Social interactions are present in all sorts of organisms, from bacteria forming microfilms to birds navigating a migration. However, the molecular mechanisms determining these behaviors remain poorly understood. We are investigating the role of an intestinal gap junction in a C. elegans social behavior called aggregation, in which worms cluster while foraging. We previously observed aggregation in animals with mutated intestinal gap junction INX-16 and devised a plan to determine the cause of their altered foraging behavior. In wild isolates this behavior is caused by polymorphisms in neuropeptide receptor NPR-1, which suppresses aggregation when active in several neurons. NPR-1 can be activated by FLP-21, a neuropeptide that is released into the body cavity. A second pathway uses DAF-7, a TGF-β homologue, to suppress aggregation. The DAF-7 pathway is independent of NPR-1. Our project aims to determine which aggregation pathway is altered in the inx-16 mutant. Since FLP-21 and INX-16 are both found in the intestine we hypothesize that lack of intestinal FLP-21 secretion in inx-16 mutants leads to insufficient activation of NPR-1 and the resultant aggregation behavior. To test this hypothesis we constructed double mutants daf-7;inx-16 and npr-1;inx-16 and assayed for aggregation. Our results showed that daf-7;inx-16 doubles exhibit increased aggregation compared to either single mutant, which suggests that INX-16 and DAF-7 act independently. npr-1;inx-16 shows no increase in aggregation compared to either single mutant, which suggests that INX-16 and NPR-1 act in the same pathway. Future research will determine whether FLP-21 is properly synthesized, packaged, released, and received in inx-16 mutants.