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Lyssavirus Matrix Protein Stabilizes RGS4 to Suppress Ferroptosis via Incomplete Autophagy and Iron Metabolic Reprogramming [wild type(WT) and RGS4 konckout(RGS4 KO)]

ABSTRACT: This study investigates transcriptomic alterations upon rabies virus CVS strain infection in wild-type and RGS4-knockout mouse Neuro-2A(N2A) neuroblastoma cells. RGS4 is a potential regulator involved in neuronal biological processes, and its functional role during rabies virus(RABV CVS strain) infection remains poorly characterized. Total RNA-seq was applied to profile global gene expression of wild-type N2A and RGS4-knockout N2A cells under RABV-CVS infected conditions. The primary objective is to identify differentially expressed genes and dysregulated signaling pathways triggered by RGS4 deficiency during CVS rabies virus infection, to reveal host molecular networks modulated by RGS4 upon lyssavirus infection in neuronal cells. This RNA-seq dataset provides transcriptomic resources for dissecting the function of RGS4 in host rabies virus interaction.

ORGANISM(S): Mus musculus

PROVIDER: GSE345814 | GEO | 2026/09/13

REPOSITORIES: GEO

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Lyssavirus Matrix Protein Stabilizes RGS4 to Suppress Ferroptosis via Incomplete Autophagy and Iron Metabolic Reprogramming [RABV-infected cells with DGAT activity]

Project description:Rabies virus (RABV), the prototypical lyssavirus, suppresses neuronal ferroptosis through lipid droplet (LD) biogenesis, which is a critical immune evasion strategy we previously identified. However, the mechanistic link between LD formation and ferroptosis regulation during RABV infection remains poorly defined. Here, we report that RABV upregulates Regulator of G Protein Signaling 4 (RGS4), a ferroptosis-associated biomarker, and this induction is strictly dependent on triglyceride synthesis and subsequent LD formation. Functionally, genetic or pharmacological inhibition of RGS4 elevates ferroptosis susceptibility, thereby restricting viral replication. Mechanistically, RGS4 depletion reduces expression of the E3 ubiquitin ligase HERC2, impairing K63-linked ubiquitination of Nuclear Receptor Coactivator 4 (NCOA4) and enhancing NCOA4 stability. Stabilized NCOA4 promotes ferritinophagy, leading to degradation of ferritin heavy chain (FTH) and ultimately inducing ferroptosis. Critically, we identify that the lyssavirus matrix (M) protein directly counteracts this pathway: M protein inhibits RGS4 degradation via the Cys/N-degron system through incomplete autophagy, stabilizing RGS4 to maintain HERC2 expression, promote NCOA4 ubiquitination, and attenuate ferritinophagy. This mechanism reduces ferroptosis susceptibility and enables viral replication. Our findings unveil a novel lyssavirus-specific regulatory axis, RGS4-HERC2-NCOA4-FTH, that modulates ferroptosis, highlighting RGS4 and M protein as promising targets for antiviral therapy.

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