Neurexin drives Caenorhabditis elegans avoidance behavior independently of its post-synaptic binding partner neuroligin

Author:

Muirhead Caroline S1,Reddy Kirthi C2,Guerra Sophia1,Rieger Michael2,Hart Michael P3,Srinivasan Jagan1ORCID,Chalasani Sreekanth H2ORCID

Affiliation:

1. Department of Biology and Biotechnology, Worcester Polytechnic Institute , Worcester, MA 01605 , USA

2. Molecular Neurobiology Laboratory, The Salk Institute for Biological Studies , La Jolla, CA 92037 , USA

3. Department of Genetics, University of Pennsylvania , Philadelphia, PA 19104 , USA

Abstract

Abstract Neurexins and their canonical binding partners, neuroligins, are localized to neuronal pre-, and post-synapses, respectively, but less is known about their role in driving behaviors. Here, we use the nematode C. elegans to show that neurexin, but not neuroligin, is required for avoiding specific chemorepellents. We find that adults with knockouts of the entire neurexin locus exhibit a strong avoidance deficit in response to glycerol and a weaker defect in response to copper. Notably, the C. elegans neurexin (nrx-1) locus, like its mammalian homologs, encodes multiple isoforms, α and γ. Using isoform-specific mutations, we find that the γ isoform is selectively required for glycerol avoidance. Next, we used transgenic rescue experiments to show that this isoform functions at least partially in the nervous system. We also confirm that the transgenes are expressed in the neurons and observe protein accumulation in neurites. Furthermore, we tested whether these mutants affect the behavioral responses of juveniles. We find that juveniles (4th larval stages) of mutants knocking out the entire locus or the α-isoforms, but not γ-isoform, are defective in avoiding glycerol. These results suggest that the different neurexin isoforms affect chemosensory avoidance behavior in juveniles and adults, providing a general principle of how isoforms of this conserved gene affect behavior across species.

Funder

NIH

Nippert Foundation

Caenorhabditis Genetics Center

NIH Office of Research Infrastructure Programs

Publisher

Oxford University Press (OUP)

Reference40 articles.

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