Decoding cadmium toxicity in spiders: F-actin and Hippo pathway insights

Heavy metals have notable effects on arthropods, but their regulatory mechanisms remain unclear. This study reveals the potential regulatory roles and mechanisms of F-actin and Hippo signaling pathway in response to cadmium (Cd) toxicity of spider. The actin gene encoding G-actin (F-actin subunit) in Pardosa pseudoannulata (P. pseudoannulata) was cloned and found to be up-regulated in Cd-exposed spiders, particularly in the 3rd and 5th instars. RNA interference (RNAi) of this gene led to increased Cd levels and suppressed physiological traits, affecting antioxidant, detoxification, immune enzyme levels, digestive activities, and damaging venom gland cell structures. F-actin depletion suppressed the expression of core Hippo pathway genes and proteins including Cpa, Cpb and Yki, and altered transcripts related to cytoskeleton, epidermis, antioxidation and metabolism. Rescue assays confirmed F-actin overexpression markedly elevates Yki transcription and protein abundance under Cd exposure. Deficient F-actin may activate Hippo signaling to inhibit Yki transcriptional activity, disrupting cytoskeletal integrity, weakening Cd detoxification, and repressing growth, anti-apoptotic and antioxidant genes, which modulates spider responses to Cd stress. This study elucidates Cd toxic mechanisms in arthropods, a potential regulatory pathway involved between F-actin and the key Hippo pathway factor Yki upon heavy metal stress, and validates spiders as promising environmental pollution biomarkers.