Mokpo National University

The innate immune system of teleost fish depends on antimicrobial peptides (AMPs) to combat diverse pathogens. Pleurocidins, cationic α-helical AMPs of the piscidin family, are conserved in flatfish and other teleosts, with amphipathic structures evolved for antimicrobial defense. These peptides exhibit potent activity against bacteria, viruses, and fungi, making them promising candidates for aquaculture disease control and therapeutic applications. Their structural conservation reflects adaptations to diverse aquatic environments, enhancing host defense against microbial threats. The starry flounder (Platichthys stellatus), a commercially valuable demersal species resilient to low temperatures and salinity, relies on AMPs to maintain robust disease resistance, supporting its growing role in aquaculture. In this study, we identified a novel pleurocidin gene (SF1) in starry flounder using liver transcriptome data. The SF1 gene encodes a 68-amino-acid prepro-pleurocidin, yielding a 22-amino-acid mature peptide. Phylogenetic analysis confirmed the SF1 mature peptide's close relation to flatfish pleurocidins. Moreover, quantitative RT-PCR revealed elevated SF1 mRNA expression in immune organs, significantly upregulated by lipopolysaccharide (LPS) stimulation, indicating a key role in innate immune responses. Structural modeling demonstrated an amphipathic α-helical conformation in the SF1 mature peptide, with optimized hydrophobicity and charge driving its potent antimicrobial activity against Gram-positive and -negative bacteria. Finally, scanning electron microscopy evidenced marked membrane disruption, corroborating its mechanism of action. These findings establish SF1 as a critical component of starry flounder's innate immunity, suggesting the potential of the SF1 mature peptide as a sustainable antibiotic alternative for aquaculture and therapeutic applications.

Autism spectrum disorder (ASD) is characterized by impaired social interaction and repetitive stereotyped behavior, and effective interventions for the core autistic symptoms are currently limited. This study examines the protective role of L-tyrosine in alleviating ASD-like behavioral disorders in a valproic acid (VPA)-induced ASD mouse model and explores the underlying mechanisms via integrated multi-omics. We first investigated the potential of dietary L-tyrosine in mitigating autistic behavior. Subsequently, 16S rRNA sequencing, hippocampal transcriptomics, and neurotransmitter metabolome were employed to elucidate the underlying mechanism. Further, we conducted transplantation of the L-tyrosine-regulated microbiota in VPA-induced ASD mice. The results showed that L-tyrosine supplementation significantly mitigates ASD-like behavioral disorders, alleviates social communication deficits, and reduces repetitive behavior in autistic mice. L-tyrosine also attenuates the neuronal loss caused by VPA treatment in the DG and CA1 hippocampal regions in mice. The hippocampi of the L-tyrosine-treated mouse model for ASD displays modified gene expression profiles and different neurotransmitter levels. L-tyrosine also mitigates colonic barrier damage and amends the gut microbial composition and function. The integrative transcriptomic, metabolomic, and microbiome analysis shows strong connections between the hippocampal genes, neurotransmitters, and gut microbiota affected by L-tyrosine. The transplantation of microbiota from L-tyrosine-treated mice to VPA-induced ASD mice recipients recapitulated the preventive and protective effects of L-tyrosine on autistic behavior disorders. These findings suggest that dietary L-tyrosine may represent a viable, effective treatment option for managing the physiological and behavioral deficits associated with ASD.