Tributyltin (TBT) is a widespread marine contaminant that affects the development and reproduction of marine invertebrates; however, its molecular impacts on early embryonic development remain poorly understood. In this study, we investigated the effects of environmental concentrations of TBT on the miRNA expression profiles of the marine gastropod Tritia mutabilis during intracapsular embryogenesis. Embryos were exposed for 10 days to low (10−12 M) and high (10−10 M) concentrations of TBT, and the differential expression of miRNAs was assessed by high-throughput sequencing. Obtained results revealed a significant modulation of several miRNAs across treatments, with a set of 11 miRNAs responding to both low and high TBT concentrations, while miR-486-5p and miR-183-5p were specifically modulated under the low TBT concentration, and miR-263b, miR-184, and miR-100-5p were exclusive to the highest concentration. Pathway analyses identified a range of biological processes affected, including nervous system development, cellular functions such as proliferation and cell growth, signal transduction, cellular component assembly and cell-cell interactions. Notably, several pathways were highly enriched (i.e., ≥100 regulated target genes) under both conditions, including focal adhesion, Ras signaling, regulation of actin cytoskeleton, Rap1 signaling, cAMP signaling, calcium signaling, and cGMP-PKG signaling pathways, highlighting the vulnerability of developmental and cellular communication networks, and further supported by the expression analysis of the corresponding miRNA-regulated target genes. These findings demonstrate that TBT contributes to the developmental abnormalities of marine gastropod embryos by modulating miRNA-mediated control of gene transcription. Our results contribute to advancing the understanding of miRNAs' potential utility as biomarkers for environmental monitoring.
miRNome profiling in Tritia mutabilis embryos exposed to tributyltin: insights into developmental toxicity
Cocci, PaoloPrimo
;Mosconi, GilbertoSecondo
;Palermo, Francesco Alessandro
Ultimo
2026-01-01
Abstract
Tributyltin (TBT) is a widespread marine contaminant that affects the development and reproduction of marine invertebrates; however, its molecular impacts on early embryonic development remain poorly understood. In this study, we investigated the effects of environmental concentrations of TBT on the miRNA expression profiles of the marine gastropod Tritia mutabilis during intracapsular embryogenesis. Embryos were exposed for 10 days to low (10−12 M) and high (10−10 M) concentrations of TBT, and the differential expression of miRNAs was assessed by high-throughput sequencing. Obtained results revealed a significant modulation of several miRNAs across treatments, with a set of 11 miRNAs responding to both low and high TBT concentrations, while miR-486-5p and miR-183-5p were specifically modulated under the low TBT concentration, and miR-263b, miR-184, and miR-100-5p were exclusive to the highest concentration. Pathway analyses identified a range of biological processes affected, including nervous system development, cellular functions such as proliferation and cell growth, signal transduction, cellular component assembly and cell-cell interactions. Notably, several pathways were highly enriched (i.e., ≥100 regulated target genes) under both conditions, including focal adhesion, Ras signaling, regulation of actin cytoskeleton, Rap1 signaling, cAMP signaling, calcium signaling, and cGMP-PKG signaling pathways, highlighting the vulnerability of developmental and cellular communication networks, and further supported by the expression analysis of the corresponding miRNA-regulated target genes. These findings demonstrate that TBT contributes to the developmental abnormalities of marine gastropod embryos by modulating miRNA-mediated control of gene transcription. Our results contribute to advancing the understanding of miRNAs' potential utility as biomarkers for environmental monitoring.| File | Dimensione | Formato | |
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2026 Marine Pollution Bulletin.pdf
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