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Coleoid cephalopods (octopus, squid and cuttlefish) have unusually complex nervous systems. The coleoid nervous system is also the only one currently known to recode the majority of expressed proteins through A-to-I RNA editing. The deamination of adenosine by adenosine deaminase acting on RNA (ADAR) enzymes produces inosine, which is interpreted as guanosine during translation. If this occurs in an open reading frame, which is the case for tens of thousands of editing sites in coleoids, it can recode the encoded protein. Here, we describe recent findings aimed at deciphering the mechanisms underlying high-level recoding and its adaptive potential. We describe the complement of ADAR enzymes in cephalopods, including a recently discovered novel domain in sqADAR1. We further summarize current evidence supporting an adaptive role of high-level RNA recoding in coleoids, and review recent studies showing that a large proportion of recoding sites is temperature-sensitive. Despite these new findings, the mechanisms governing the high level of RNA recoding in coleoid cephalopods remain poorly understood. Recent advances using genome editing in squid may provide useful tools to further study A-to-I RNA editing in these animals.

Cephalopods are known for their large nervous systems, complex behaviors and morphological innovations. To investigate the genomic underpinnings of these features, we assembled the chromosomes of the Boston market squid,Doryteuthis (Loligo) pealeii,and the California two-spot octopus,Octopus bimaculoides, and compared them with those of the Hawaiian bobtail squid,Euprymna scolopes. The genomes of the soft-bodied (coleoid) cephalopods are highly rearranged relative to other extant molluscs, indicating an intense, early burst of genome restructuring. The coleoid genomes feature multi-megabase, tandem arrays of genes associated with brain development and cephalopod-specific innovations. We find that a known coleoid hallmark, extensive A-to-I mRNA editing, displays two fundamentally distinct patterns: one exclusive to the nervous system and concentrated in genic sequences, the other widespread and directed toward repetitive elements. We conclude that coleoid novelty is mediated in part by substantial genome reorganization, gene family expansion, and tissue-dependent mRNA editing.

Freshwater snails of the genusBiomphalariaserve as intermediate hosts for the digenetic trematodeSchistosoma mansoni, the etiological agent for the most widespread form of intestinal schistosomiasis. As neuropeptide signaling in host snails can be altered by trematode infection, a neural transcriptomics approach was undertaken to identify peptide precursors inBiomphalaria glabrata, the major intermediate host forS.mansoniin the Western Hemisphere. Three transcripts that encode peptides belonging to the FMRF‐NH₂‐related peptide (FaRP) family were identified inB.glabrata. One transcript encoded a precursor polypeptide (Bgl‐FaRP1; 292 amino acids) that included eight copies of the tetrapeptide FMRF‐NH₂and single copies of FIRF‐NH₂, FLRF‐NH₂, and pQFYRI‐NH₂. The second transcript encoded a precursor (Bgl‐FaRP2;347amino acids) that comprised 14 copies of the heptapeptide GDPFLRF‐NH₂and 1 copy of SKPYMRF‐NH₂. The precursor encoded by the third transcript (Bgl‐FaRP3; 287 amino acids) recapitulatedBgl‐FaRP2but lacked the full SKPYMRF‐NH₂peptide. The three precursors shared a common signal peptide, suggesting a genomic organization described previously in gastropods. Immunohistochemical studies were performed on the nervous systems ofB.glabrataandB.alexandrina, a major intermediate host forS.mansoniin Egypt. FMRF‐NH₂‐like immunoreactive (FMRF‐NH₂‐li) neurons were located in regions of the central nervous system associated with reproduction, feeding, and cardiorespiration. Antisera raised against non‐FMRF‐NH₂peptides present in the tetrapeptide and heptapeptide precursors labeled independent subsets of the FMRF‐NH₂‐li neurons. This study supports the participation of FMRF‐NH₂‐related neuropeptides in the regulation of vital physiological and behavioral systems that are altered by parasitism inBiomphalaria.