Mitochondrial membrane protein-associated neurodegeneration, a subtype of neurodegeneration with brain iron accumulation, is caused by mutations in c19orf12, a gene encoding a small transmembrane protein with largely unknown biological function. While studies in Drosophila have suggested roles for c19orf12 homologs (nazo) in lipid metabolism and antiviral defense, their evolutionary conservation and functional relevance in other species remain unclear. In this study, we identified a homolog of c19orf12 in Pacific white shrimp ( Litopenaeus vannamei ), designated Lvc19orf12. The protein contains a conserved transmembrane domain with a glycine residue characteristic of c19orf12 homologs, and is widely expressed across tissues with enrichment in immune-related tissues. Functional analyses revealed that Lvc19orf12 regulates both metabolism and immunity. Its silencing disrupted multiple metabolic pathways and led to pronounced downregulation of immune-related genes, including antimicrobial peptides, recognition receptors, signaling molecules, and apoptosis regulators. During white spot syndrome virus infection, Lvc19orf12 expression was strongly induced in hemocytes, gills, and the hepatopancreas, while its suppression resulted in enhanced viral replication, increased expression of viral genes, and aggravated tissue damage. These findings identify Lvc19orf12 as a novel antiviral factor in shrimp, extend the functional repertoire of c19orf12 beyond neurodegeneration, and provide new insights into the molecular basis of innate immunity and disease resistance in aquaculture species. • A novel c19orf12 homolog from L. vannamei (Lvc19orf12) was identified. • Lvc19orf12 regulated multiple pathways and immune-related genes. • Lvc19orf12 was involved in antiviral defense against white spot syndrome virus in L. vannamei.
Chen et al. (Sun,) studied this question.