HRPU-2, a Homolog of Mammalian hnRNP U, Regulates Synaptic Transmission by Controlling the Expression of SLO-2 Potassium Channel in Caenorhabditis elegans

Evoked transmitter release is abnormal at the larval neuromuscular junctions of two Drosophila mutants. Following a single nerve impulse, the increased calcium conductance at the nerve terminal, which lasts for 1 ms in normal larvae, lasts for at least 60 ms in one mutant and several seconds in the other. Both mutations appear to affect the same gene on the X-chromosome. Normal larvae treated with 4-aminopyridine, a potassium channel blocking agent, mimic the abnormal synaptic transmission of one mutant. Normal larvae treated with tetraethylammonium, another potassium channel blocking agent, mimic the abnormal synaptic transmission of the other mutant. From these and other experiments, we suggest that the abnormal neuromuscular transmission in these mutants may be caused by defective potassium channels in the nerve terminal membrane.

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A genetic selection for Caenorhabditis elegans synaptic transmission mutants.

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.93.22.12593 ◽

1996 ◽

Vol 93 (22) ◽

pp. 12593-12598 ◽

Cited By ~ 272

Author(s):

K. G. Miller ◽

A. Alfonso ◽

M. Nguyen ◽

J. A. Crowell ◽

C. D. Johnson ◽

...

Keyword(s):

Caenorhabditis Elegans ◽

Synaptic Transmission ◽

Genetic Selection ◽

Selection For

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Repression of a Potassium Channel by Nuclear Hormone Receptor and TGF-β Signaling Modulates Insulin Signaling in Caenorhabditis elegans

PLoS Genetics ◽

10.1371/journal.pgen.1002519 ◽

2012 ◽

Vol 8 (2) ◽

pp. e1002519 ◽

Cited By ~ 9

Author(s):

Donha Park ◽

Karen L. Jones ◽

Hyojin Lee ◽

Terrance P. Snutch ◽

Stefan Taubert ◽

...

Keyword(s):

Caenorhabditis Elegans ◽

Potassium Channel ◽

Insulin Signaling ◽

Hormone Receptor ◽

Nuclear Hormone Receptor

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High-Throughput All-Optical Analysis of Synaptic Transmission and Synaptic Vesicle Recycling in Caenorhabditis elegans

PLoS ONE ◽

10.1371/journal.pone.0135584 ◽

2015 ◽

Vol 10 (8) ◽

pp. e0135584 ◽

Cited By ~ 9

Author(s):

Sebastian Wabnig ◽

Jana Fiona Liewald ◽

Szi-chieh Yu ◽

Alexander Gottschalk

Keyword(s):

Caenorhabditis Elegans ◽

Synaptic Transmission ◽

Synaptic Vesicle ◽

High Throughput ◽

Optical Analysis ◽

Synaptic Vesicle Recycling ◽

Vesicle Recycling ◽

All Optical

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Caenorhabditis elegans mutants defective in the functioning of the motor neurons responsible for egg laying.

Genetics ◽

10.1093/genetics/121.4.703 ◽

1989 ◽

Vol 121 (4) ◽

pp. 703-721 ◽

Cited By ~ 8

Author(s):

C Desai ◽

H R Horvitz

Keyword(s):

Caenorhabditis Elegans ◽

Synaptic Transmission ◽

Motor Neurons ◽

Egg Laying ◽

The Other ◽

Single Type ◽

Sensitive Period ◽

Temperature Sensitive ◽

Sensitive Allele

Abstract We have isolated and characterized 45 Caenorhabditis elegans mutants presumed to be defective in the functioning of the hermaphrodite-specific neurons (HSNs). Like hermaphrodites that lack the HSN motor neurons, these mutants are egg-laying defective and do not lay eggs in response to exogenous imipramine but do lay eggs in response to exogenous serotonin. Twenty of the 45 mutations define 10 new egl genes; the other 25 mutations are alleles of five previously defined genes, four of which are known to affect the HSNs. Seven mutations in three genes cause the HSNs to die in hermaphrodites, as they normally do in males. These genes appear to be involved in the determination of the sexual phenotype of the HSNs, and one of them (egl-41) is a newly identified gene that may function generally in sex determination. Five of the 15 genes are defined only by mutations that have dominant effects on egg laying. One gene egl(n1108), is defined by a temperature-sensitive allele that has a temperature-sensitive period after HSN development is complete, suggesting that egl(n1108) may be involved in HSN synaptic transmission. Four of the genes are defined by single alleles, which suggests that other such genes remain to be discovered. Mutations in no more than 4 of the 15 genes specifically affect the HSNs, indicating that there are few genes with functions needed only in this single type of nerve cell.

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