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FB2026_02
,
released June 18, 2026
Using a larval electroconvulsive seizure recovery assay, it was determined that alleles of the Drosophila gene for exhibit shorter (in the case of higher activity variants) or prolonged (in the case of a null mutation) recovery times. Dmel\for is a member of the protein kinase G family and is orthologous to the human gene PRKG1. Pharmaceuticals known to affect the activity of PRKG1 have been assessed in this system.
The human PRKG1 gene has been transfected into S2 cells, but as not been introduced into flies.
Animals homozygous for amorphic alleles of Dmel\for typically die during the pupal stage. Naturally-occurring for variants with higher levels of activity affect feeding, locomotion, learning and memory, stress, and social behavior phenotypes. A small number of genetic and physical interactions have been described for for; see below and in the for gene report.
[updated Nov. 2019 by FlyBase; FBrf0222196]
PRKG1 is a member of the protein kinase G family, serine/threonine kinases activated by cGMP, and acts as key mediator of the nitric oxide (NO)/cGMP signaling pathway. PRKG1 proteins play a central role in regulating cardiovascular and neuronal functions in addition to relaxing smooth muscle tone, preventing platelet aggregation, and modulating cell growth; numerous protein targets for PRKG1 phosphorylation are implicated in modulating cellular calcium. [Gene Cards, PRKG1; 2019.11.05]
One to one: 1 human to 1 Drosophila (reciprocal best hits); multiple related genes in both species.
High-scoring ortholog of human PRKG1 (reciprocal best hit for PRKG1; multiple related genes in both species). Dmel\for shares 60% identity and 75% similarity with PRKG1.