{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE329nnn/GSE329009/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Aquarana catesbeiana"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE329009"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Systemic oxidative stress and paradoxical upregulation of melanogenic genes in albino American bullfrogs: insights from multi‑tissue transcriptomics and UVB challenge","description":"Albinism results from defects in melanin synthesis and is associated with increased sensitivity to ultraviolet (UV) radiation. While the genetic basis of albinism is well studied, the systemic physiological consequences of melanin deficiency remain poorly understood, particularly in amphibians where the skin serves additional respiratory and osmoregulatory functions. Here we investigated the morphological, physiological and transcriptomic basis of the albino phenotype in the American bullfrog (Rana catesbeiana), a species that naturally experiences variable UVB exposure in its aquatic habitats. We compared albino and wild‑type bullfrogs using histology, a time‑course UVB irradiation experiment (1000 μW cm⁻² for 4 h with five recovery time points), and multi‑tissue transcriptomics of dorsal skin, liver and eyeball. Albino bullfrogs completely lacked melanin in skin and retina. Under basal conditions, they had markedly lower total antioxidant capacity (T‑AOC) and catalase (CAT) activity in skin and liver, and showed elevated protein carbonyl content, indicating chronic oxidative stress. After UVB exposure, wild‑type bullfrogs mounted a dynamic antioxidant response, whereas albino individuals failed to recover. Transcriptomic analysis identified 520, 1074 and 1355 differentially expressed genes in skin, liver and eye, respectively, with 51 genes shared across all three tissues. Unexpectedly, key melanogenic genes (TYR, TYRP1, MLANA, SLC24A5, OCA2) were significantly upregulated in albino skin and eye–a paradoxical finding given the absence of pigment. Pathway enrichment revealed direct photoxidative damage in the two light‑exposed organs (skin: downregulation of glutathione metabolism; eye: downregulation of cell cycle, p53 and DNA replication pathways) and secondary metabolic stress in the liver (downregulation of PPAR and glutathione pathways). qRT‑PCR validation of four representative genes (TYR, CHAC1, GADD45A, ARL5C) confirmed the RNA‑seq trends (Pearson’s R² = 0.91). These results demonstrate that albinism in the bullfrog is not merely a local pigmentation defect but a systemic condition involving direct photoxidative injury to skin and eye, secondary oxidative burden on the liver, and a paradoxical transcriptional activation of the melanogenic machinery. Our findings provide a multi‑tissue resource for understanding the physiological consequences of pigmentation loss in vertebrates and highlight the vulnerability of albino individuals to environmental UVB exposure.","dates":{"publication":"2026/04/30"},"accession":"GSE329009","cross_references":{"GSM":["GSM9695759","GSM9695748","GSM9695758","GSM9695749","GSM9695755","GSM9695754","GSM9695765","GSM9695757","GSM9695756","GSM9695762","GSM9695751","GSM9695761","GSM9695750","GSM9695764","GSM9695753","GSM9695763","GSM9695752","GSM9695760"],"GPL":["36857"],"GSE":["329009"],"taxon":["Aquarana catesbeiana"]}}