In:
PLOS Genetics, Public Library of Science (PLoS), Vol. 18, No. 4 ( 2022-4-28), p. e1010126-
Abstract:
Two-pore domain potassium channels (K2P) are a large family of “background” channels that allow outward “leak” of potassium ions. The NALCN/UNC80/UNC79 complex is a non-selective channel that allows inward flow of sodium and other cations. It is unclear how K2Ps and NALCN differentially modulate animal behavior. Here, we found that loss of function (lf) in the K2P gene twk-40 suppressed the reduced body curvatures of C . elegans NALCN(lf) mutants. twk-40(lf) caused a deep body curvature and extended backward locomotion, and these phenotypes appeared to be associated with neuron-specific expression of twk-40 and distinct twk-40 transcript isoforms. To survey the functions of other less studied K2P channels, we examined loss-of-function mutants of 13 additional twk genes expressed in the motor circuit and detected defective body curvature and/or locomotion in mutants of twk-2 , twk-17 , twk-30 , twk-48 , unc-58 , and the previously reported twk-7 . We generated presumptive gain-of-function (gf) mutations in twk-40 , twk-2 , twk-7 , and unc-58 and found that they caused paralysis. Further analyses detected variable genetic interactions between twk-40 and other twk genes, an interdependence between twk-40 and twk-2 , and opposite behavioral effects between NALCN and twk-2 , twk-7 , or unc-58 . Finally, we found that the hydrophobicity/hydrophilicity property of TWK-40 residue 159 could affect the channel activity. Together, our study identified twk-40 as a novel modulator of the motor behavior, uncovered potential behavioral effects of five other K2P genes and suggests that NALCN and some K2Ps can oppositely affect C . elegans behavior.
Type of Medium:
Online Resource
ISSN:
1553-7404
DOI:
10.1371/journal.pgen.1010126
DOI:
10.1371/journal.pgen.1010126.g001
DOI:
10.1371/journal.pgen.1010126.g002
DOI:
10.1371/journal.pgen.1010126.g003
DOI:
10.1371/journal.pgen.1010126.g004
DOI:
10.1371/journal.pgen.1010126.g005
DOI:
10.1371/journal.pgen.1010126.g006
DOI:
10.1371/journal.pgen.1010126.t001
DOI:
10.1371/journal.pgen.1010126.t002
DOI:
10.1371/journal.pgen.1010126.s001
DOI:
10.1371/journal.pgen.1010126.s002
DOI:
10.1371/journal.pgen.1010126.s003
DOI:
10.1371/journal.pgen.1010126.s004
DOI:
10.1371/journal.pgen.1010126.s005
DOI:
10.1371/journal.pgen.1010126.s006
DOI:
10.1371/journal.pgen.1010126.s007
DOI:
10.1371/journal.pgen.1010126.s008
DOI:
10.1371/journal.pgen.1010126.s009
DOI:
10.1371/journal.pgen.1010126.s010
DOI:
10.1371/journal.pgen.1010126.s011
DOI:
10.1371/journal.pgen.1010126.s012
DOI:
10.1371/journal.pgen.1010126.s013
DOI:
10.1371/journal.pgen.1010126.s014
DOI:
10.1371/journal.pgen.1010126.s015
DOI:
10.1371/journal.pgen.1010126.s016
DOI:
10.1371/journal.pgen.1010126.s017
DOI:
10.1371/journal.pgen.1010126.s018
DOI:
10.1371/journal.pgen.1010126.s019
DOI:
10.1371/journal.pgen.1010126.s020
DOI:
10.1371/journal.pgen.1010126.s021
DOI:
10.1371/journal.pgen.1010126.s022
DOI:
10.1371/journal.pgen.1010126.s023
DOI:
10.1371/journal.pgen.1010126.s024
DOI:
10.1371/journal.pgen.1010126.s025
DOI:
10.1371/journal.pgen.1010126.s026
DOI:
10.1371/journal.pgen.1010126.s027
DOI:
10.1371/journal.pgen.1010126.s028
DOI:
10.1371/journal.pgen.1010126.s029
DOI:
10.1371/journal.pgen.1010126.s030
DOI:
10.1371/journal.pgen.1010126.s031
DOI:
10.1371/journal.pgen.1010126.s032
DOI:
10.1371/journal.pgen.1010126.s033
DOI:
10.1371/journal.pgen.1010126.s034
DOI:
10.1371/journal.pgen.1010126.s035
DOI:
10.1371/journal.pgen.1010126.s036
DOI:
10.1371/journal.pgen.1010126.s037
DOI:
10.1371/journal.pgen.1010126.s038
DOI:
10.1371/journal.pgen.1010126.s039
DOI:
10.1371/journal.pgen.1010126.s040
DOI:
10.1371/journal.pgen.1010126.s041
DOI:
10.1371/journal.pgen.1010126.s042
DOI:
10.1371/journal.pgen.1010126.s043
DOI:
10.1371/journal.pgen.1010126.s044
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2022
detail.hit.zdb_id:
2186725-2
Permalink