GstO2 (Drosophila melanogaster) - manual literature review
Manual
GstO2 (Drosophila melanogaster) - manual literature review
No deep-research API provider was available for this session; this file records a manual
literature survey (PubMed search (GstO2 OR GSTO2 OR DmGSTO1 OR CG6673) AND Drosophila, 11 hits,
plus the GOA-cited references). Quotes are from cached publications/PMID_*.md files.
Identity and nomenclature
- FlyBase FBgn0035906, CG6673, GeneID 38974. Omega-class cytosolic GST.
- The gene encodes two alternatively spliced isoforms, A and B, which differ in their N-terminal
first exon including the active-site motif. UniProt Q9VSL5 ("isoform A") has the motif
C31-P-F-S (...SMAFCPFSHR...); Q9VSL4 ("isoform B") has C-P-Y-S, identical to human GSTO2.
- Naming is inconsistent in the literature: Kim et al. 2006/2012 call CG6673 "DmGSTO1" (A and B
isoforms) PMID:22219196; Saisawang et al.
2012 (universal nomenclature) and later papers use GstO2 / DmGSTO2a / DmGSTO2b
PMID:24533905.
Enzymatic activities
- Recombinant CG6673A and CG6673B have thiol transferase and dehydroascorbate (DHA) reductase
activity, low CDNB-conjugating activity, and no pyrimidodiazepine (PDA) synthase activity
PMID:16712527.
- Isoform B has much higher DHAR activity than isoform A PMID:22219196.
- Kinetic parameters for DHA reduction by both isoforms; optimum pH 8.0, 40 C; native ~60 kDa
(dimer) [PMID:24533905 abstract, full text not available].
- The cytosolic GST proteome survey (Saisawang 2012) expressed all fly GSTs and measured
activity with several substrates [PMID:22082028 abstract only].
- Neither GstO2a nor GstO2b alters p38b MAP kinase activity in vitro PMID:25373207.
In vivo roles
- Null allele (imprecise P excision) is viable and fertile; DHAR activity drops to ~5% of wild
type; flies are paraquat sensitive, rescued better by isoform B, which also restores the
ascorbate/DHA ratio PMID:22219196.
- Isoform A (not B, not the C31A active-site mutant) increases glutathionylation of the
mitochondrial F1F0-ATP synthase beta subunit, and does so directly in vitro
PMID:22219196; this restores ATP synthase
activity/assembly and suppresses parkin mutant phenotypes.
- Isoform A expression is reduced in PINK1 mutants and its overexpression suppresses PINK1
phenotypes [PMID:23867819 abstract].
- Overexpression suppresses neurotoxicity in fly models of TDP-43, TAF15 and FUS proteinopathy
[PMID:32674363; PMID:36411469; PMID:35320731]. In the FUS model GstO2 is reported to act by
deglutathionylating FUS Cys447 PMID:35320731 (abstract only).
- A genome-wide in vivo RNAi screen for survival after oral Serratia marcescens infection is the
source of the two HMP immune annotations; GstO2 is not discussed in the main text
PMID:19520911.
Localization
- FlyBase IDA annotations to cytosol and mitochondrion cite PMID:24533905 (full text not cached).
A mitochondrial pool is consistent with the ATP synthase beta target of isoform A.