Nucleobase-Ascorbate Transporter (NAT) family includes ascorbic acid, nucleobases, and uric acid transporters: With broad evolutionary distribution. In vertebrates, four members have been previously recognized, the ascorbate transporters Slc23a1 and Slc3a2, the nucleobase transporter Slc23a4 and an orphan transporter Slc23a3. Using phylogenetic and synteny analysis, we identify a fifth member of the vertebrate slc23 complement (slc23a5), present in neopterygians (gars and teleosts) and amphibians, and clarify the evolutionary relationships between the novel gene and known slc23 genes. Further comparative analysis puts forward uric acid as the preferred substrate for Slc23a5. Gene expression quantification, using available transcriptomic data, suggests kidney and testis as major expression sites in Xenopus tropicalis (western clawed frog) and Danio rerio (zebrafish). Additional expression in brain was detected in D. rerio, while in the Neoteleostei Oryzias latipes (medaka) slc23a5 expression is restricted to the brain. The biological relevance of the retention of an extra transporter in fish and amphibians is discussed.

To preserve homeostasis in the face of continual chemical insult, animals evolved dedicated molecular systems that detect, detoxify, and eliminate foreign compounds. Collectively, these enzymes, transporters, and regulatory pathways constitute the chemical defensome. In cetaceans, the loss of two key nuclear receptors (NR1I2/PXR and NR1I3/CAR) suggests a profound rearrangement of the chemical defense systems. Therefore, we investigated the gene inventory of the chemical defensome in Cetacea and two other major marine mammal lineages (Pinnipedia and Sirenia), using their closest terrestrial relatives to understand the extent and patterns of chemical defensome remodelling. We demonstrate large-scale gene loss in chemical defensome genes of cetaceans, as well as smaller scale gene loss in the other two marine mammal lineages, indicating possible convergent evolution. Gene loss occurred predominantly in phase I and phase II biotransformation enzymes, including CYPs, FMOs, SULTs, and GSTs. Many of the lost genes in cetaceans are known to be regulated by PXR and/or CAR, while genes lost in multiple marine mammal lineages are often not regulated by these transcription factors. We hypothesize that the transition to aquatic environments, often accompanied by corresponding changes in feeding habits, led to convergent loss of chemical defensome genes, and loss of PXR and CAR in cetaceans accelerated these losses. These findings reveal systematic erosion of chemical defense capabilities across marine mammal lineages, suggesting that adaptation to marine life involves trade-offs in detoxification capacity that may have significant implications for these species’ responses to increasing chemical pollution in present-day ocean environments.

Nucleobase-Ascorbate Transporter (NAT) family includes ascorbic acid, nucleobases and uric acid transporters, with a broad evolutionary distribution. In vertebrates, four members have been previously recognized, the ascorbate transporters Slc23a1 and Slc3a2, the nucleobase transporter Slc23a4 and an orphan transporter SLC23A3. Here we identify a fifth member of the vertebrate slc23 complement ( slc23a5 ), expressed in neopterygians (gars and teleosts) and amphibians, and clarify the evolutionary relationships between the novel gene and known slc23 genes. Further comparative analysis puts forward uric acid as the preferred substrate for Slc23a5. Gene expression quantification suggests kidney and testis as major expression sites in Xenopus tropicalis (western clawed frog) and Danio rerio (zebrafish). Additional expression in brain was detected in D. rerio , while in the Neoteleostei Oryzias latipes (medaka) slc23a5 expression is restricted to brain. The biological relevance of the retention of an extra transporter in fish and amphibians is examined: with respect to the (1) antioxidant role of uric and ascorbic acid in seminal fluid and brain, (2) the ability to endogenously synthesize ascorbic acid and (3) the morphological adaptations of the male urogenital system.

Background: The reproductive cycle of Octopus mimus is regulated by environmental and hormonal factors, with photoperiod playing a key role in spawning induction and reproductive maturation. Understanding its underlying molecular mechanisms is essential for developing strategies to enhance controlled reproduction in aquaculture. Methods: We analyzed the expression of genes involved in the photoperiod-activated spawning induction cascade in the optic lobe and its downstream effects on the oviducal gland by performing transcriptomic analyses on females exposed to continuous light (24:0), which inhibits reproductive development, and a natural photoperiod, which induces spawning. The mRNA sequencing (RNA-Seq), quality control, gene annotation, and differential expression analyses were conducted using edgeR. Results: Spawning was completely inhibited under constant light, while 80% of control females spawned. Expression profiling revealed 89 downregulated and 34 upregulated genes in the optic lobe, and 178 downregulated and 237 upregulated genes in the oviducal gland (FDR < 0.05, |log2FC| ≥ 2), including key orthologs such as FMRFamide and myomodulin. Conclusions: These results show that the optic lobe integrates photoperiodic cues that modulate reproductive activation via a neuroendocrine cascade and coordinates spawning regulation through the oviducal gland, providing insights for improving reproductive control in aquaculture systems.