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Reduced Function of the Glutathione S-Transferase S1 Suppresses Behavioral Hyperexcitability in Drosophila Expressing Mutant Voltage-Gated Sodium Channels
Journal article   Open access

Reduced Function of the Glutathione S-Transferase S1 Suppresses Behavioral Hyperexcitability in Drosophila Expressing Mutant Voltage-Gated Sodium Channels

Hung-Lin Chen, Junko Kasuya, Patrick Lansdon, Garrett Kaas, Hanxi Tang, Maggie Sodders and Toshihiro Kitamoto
G3 (Bethesda, Md.), Vol.10(4), pp.1327-1340
04/01/2020
DOI: 10.1534/g3.119.401025
PMCID: PMC7144092
PMID: 32054635
url
https://doi.org/10.1534/g3.119.401025View
Published (Version of record) Open Access

Abstract

Voltage-gated sodium (Na v ) channels play a central role in the generation and propagation of action potentials in excitable cells such as neurons and muscles. To determine how the phenotypes of Na v -channel mutants are affected by other genes, we performed a forward genetic screen for dominant modifiers of the seizure-prone, gain-of-function Dr osophila melanogaster Na v -channel mutant, para Shu . Our analyses using chromosome deficiencies, gene-specific RNA interference, and single-gene mutants revealed that a null allele of glutathione S-transferase S1 ( GstS1 ) dominantly suppresses para Shu phenotypes. Reduced GstS1 function also suppressed phenotypes of other seizure-prone Na v -channel mutants, para GEFS+ and para bss . Notably, para Shu mutants expressed 50% less GstS1 than wild-type flies, further supporting the notion that para Shu and GstS1 interact functionally. Introduction of a loss-of-function GstS1 mutation into a para Shu background led to up- and down-regulation of various genes, with those encoding cytochrome P450 (CYP) enzymes most significantly over-represented in this group. Because GstS1 is a fly ortholog of mammalian hematopoietic prostaglandin D synthase, and in mammals CYPs are involved in the oxygenation of polyunsaturated fatty acids including prostaglandins, our results raise the intriguing possibility that bioactive lipids play a role in GstS1 -mediated suppression of para Shu phenotypes.
epilepsy RNA-sequencing analysis Forward genetic screen genetic modifiers Investigations

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