TY - JOUR
T1 - Trpm channels mediate learned pathogen avoidance following intestinal distention
AU - Filipowicz, Adam
AU - Lalsiamthara, Jonathan
AU - Aballay, Alejandro
N1 - Funding Information:
We thank Danielle A Garsin (McGovern Medical School) for providing the E. faecalis OG1RF DfsrB and GFP strains. Some strains used in this study were provided by the Caenorhabditis Genetics Center (CGC), which is funded by the NIH Office of Research Infrastructure Programs (P40OD01044). Images were created using Microsoft PowerPoint and BioRender.com.
Funding Information:
We thank Danielle A Garsin (McGovern Medical School) for providing the E. faecalis OG1RF ?fsrB and GFP strains. Some strains used in this study were provided by the Caenorhabditis Genetics Center (CGC), which is funded by the NIH Office of Research Infrastructure Programs (P40OD01044). Images were created using Microsoft PowerPoint and BioRender.com. National Institutes of Health GM070977 Alejandro Aballay National Institutes of Health AI156900 Alejandro Aballay.
Publisher Copyright:
© Filipowicz et al.
PY - 2021/5
Y1 - 2021/5
N2 - Upon exposure to harmful microorganisms, hosts engage in protective molecular and behavioral immune responses, both of which are ultimately regulated by the nervous system. Using the nematode Caenorhabditis elegans, we show that ingestion of Enterococcus faecalis leads to a fast pathogen avoidance behavior that results in aversive learning. We have identified multiple sensory mechanisms involved in the regulation of avoidance of E. faecalis. The G-protein coupled receptor NPR-1-dependent oxygen-sensing pathway opposes this avoidance behavior, while an ASE neuron-dependent pathway and an AWB and AWC neuron-dependent pathway are directly required for avoidance. Colonization of the anterior part of the intestine by E. faecalis leads to AWB and AWC mediated olfactory aversive learning. Finally, two transient receptor potential melastatin (TRPM) channels, GON-2 and GTL-2, mediate this newly described rapid pathogen avoidance. These results suggest a mechanism by which TRPM channels may sense the intestinal distension caused by bacterial colonization to elicit pathogen avoidance and aversive learning by detecting changes in host physiology.
AB - Upon exposure to harmful microorganisms, hosts engage in protective molecular and behavioral immune responses, both of which are ultimately regulated by the nervous system. Using the nematode Caenorhabditis elegans, we show that ingestion of Enterococcus faecalis leads to a fast pathogen avoidance behavior that results in aversive learning. We have identified multiple sensory mechanisms involved in the regulation of avoidance of E. faecalis. The G-protein coupled receptor NPR-1-dependent oxygen-sensing pathway opposes this avoidance behavior, while an ASE neuron-dependent pathway and an AWB and AWC neuron-dependent pathway are directly required for avoidance. Colonization of the anterior part of the intestine by E. faecalis leads to AWB and AWC mediated olfactory aversive learning. Finally, two transient receptor potential melastatin (TRPM) channels, GON-2 and GTL-2, mediate this newly described rapid pathogen avoidance. These results suggest a mechanism by which TRPM channels may sense the intestinal distension caused by bacterial colonization to elicit pathogen avoidance and aversive learning by detecting changes in host physiology.
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U2 - 10.7554/eLife.65935
DO - 10.7554/eLife.65935
M3 - Article
C2 - 34032213
AN - SCOPUS:85107714069
SN - 2050-084X
VL - 10
JO - eLife
JF - eLife
M1 - e65935
ER -