ArticleMarine biotechnology (New York, N.Y.)2026
IP3K Knockdown Induces Oxidative Stress and Apoptosis in Sinonovacula constricta Under Low-Salinity.
Article in Marine biotechnology (New York, N.Y.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Inositol 1,4,5-trisphosphate kinase (IP3K) is a key regulatory enzyme within the phosphatidylinositol signaling pathway, modulating downstream signal transduction via the phosphorylation of inositol trisphosphate (IP3). Our previous comparative transcriptomic analysis of the razor clam (Sinonovacula constricta) under low salinity stress revealed significant enrichment of the phosphatidylinositol pathway. In this study, we characterized the IP3K gene and employed RNA interference (RNAi) to investigate its regulatory role by assessing downstream signaling, oxidative stress, and apoptosis under low-salinity (5 ppt) in S. constricta. The results showed that IP3K has a ubiquitous expression pattern along with significant increases in its expression in the gill under low-salinity stress. IP3K knockdown led to significant decreases in phosphatidylinositol (PI) and IP3 levels, altered Ca2+ level, and also triggered accumulation of reactive oxygen species (ROS). Concurrently, inhibition of IP3K significantly reduced the activities of superoxide dismutase (SOD) and catalase (CAT), while significantly increasing the content of malondialdehyde (MDA) (P < 0.01). TUNEL staining confirmed that IP3K suppression exacerbated apoptosis in gill tissues, leading to a marked decline in cell viability. Overall, these findings demonstrate that IP3K plays an essential role in regulating oxidative stress and maintaining cellular homeostasis under low salinity conditions, providing a potential target for improving salinity tolerance in shellfish.
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