SUV3 (Suppressor of Var1 3-like 1) is a nuclear-encoded mitochondrial helicase critical for:
Mitochondrial RNA Turnover: SUV3 partners with polynucleotide phosphorylase (PNPase) to form the mitochondrial degradosome, which processes and degrades mitochondrial RNA .
Mitochondrial DNA (mtDNA) Stability: SUV3 maintains mtDNA integrity by resolving R-loops and preventing toxic RNA-DNA hybrids, thereby ensuring replication fidelity .
Energy Metabolism: SUV3 modulates poly(A) tail lengths of mitochondrial mRNAs in response to cellular energy changes, influencing translation efficiency .
Apoptosis Regulation: Depletion of SUV3 triggers mitochondrial dysfunction, reactive oxygen species (ROS) accumulation, and cell death .
Key studies utilizing SUV3 antibodies have revealed:
mtDNA Replication Dependency: ATPase-deficient SUV3 mutants (K245A) fail to support mtDNA replication, linking helicase activity to genome stability .
Mitochondrial Morphology: SUV3 knockdown causes mitochondrial fragmentation and reduced mtDNA copy number, correlating with OXPHOS complex deficiencies .
Poly(A) Tail Modulation: SUV3 bridges PNPase and mitochondrial poly(A) polymerase (mtPAP) to dynamically adjust RNA poly(A) tail lengths under varying phosphate levels .
Tumor Suppression: Heterozygous SUPV3L1 mice exhibit accelerated aging and tumorigenesis, underscoring SUV3’s role in preventing genomic instability .
SUV3 antibodies are pivotal for: