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In vertebrates, Snails are evolutionarily conserved and consist of 4–6 Cys2-His2 (C2H2)-Zinc finger domains. The key role of the Snails is well illustrated in cancer, but its role in immunity is limited. Two Snail2 genes, named Snail2α and Snail2β , containing 5 C2H2 at C-terminus, were identified in Procambarus clarkii. Snail2α was highly expressed in heart, gills and intestine, and Snail2β in gills, stomach and intestine. Decreased expression of Snail2α and Snail2β in gills and intestine at 6 h after White spot syndrome virus (WSSV) infection. Early WSSV replication levels are inhibited in dsSnail2α or dsSnail2β-injected crayfish compared to dsGFP-injected crayfish. The early WSSV replication levels are increased in rSnail2α or rSnail2β-injection crayfish. Further studies revealed that both Snail2α and Snail2β regulate the nuclear translocation of Relish. Relish entry into the nucleus promotes the expression of the WSSV immediate-early genes ie1 and ie15. WSSV abducts the host Snail2α and Snail2β in an unknown manner, facilitating the nuclear translocation of Relish and inducing ie1 and ie15 transcription. Crayfish responds to this escape mechanism of WSSV by reducing the expression of Snail2α and Snail2β at early stage of WSSV infection. This study provides new insights in immune response of crayfish to WSSV escape. • Snail2α and Snail2β promote the early replication of WSSV. • Snail2α and Snail2β assist the nuclear translocation of Relish. • Snail2α and Snail2β regulate the transcription of the immediate-early gene ie1 and ie15. [ABSTRACT FROM AUTHOR]

Temperature is one of the most prevalent environmental factors that affects the growth and development of organisms. The survival of aquatic animals is closely related to the changes in temperature, low temperature could cause physiological damage even death. In this study, we revealed the regulatory mechanisms of low-temperature stimulation from the transcriptomics in the hepatopancreas of the red swamp crayfish, Procambarus clarkii. Transcriptome sequencing revealed that lipid metabolism pathways were significantly enriched at low temperature. Crayfish improved their cold tolerance by increasing expression levels of thermogenic gene prdm16 and uncoupling protein genes ucp4 and ucp5. Furthermore, lipid and triglyceride content increased significantly in cold-sensitive crayfish, which in turn increased the expression levels of proinflammatory factors (cox2 and tgfβr) and the amount of hepatopancreas bacteria. In addition, low-temperature stimulation could cause more severe damage to cold-sensitive crayfish spermatophores, accompanied by downregulated of spermatozoa viability-related genes such as alp and ldh. Estradiol 17β-dehydrogenase 8-like (17βde8) may contain a critical SNP site at exon 544, the bases of this site were "G" in cold-tolerant crayfish and "A" in cold-sensitive crayfish. Above all, our results reveal that lipid metabolism is the main factor affecting cold tolerance in crayfish and reveal the key loci for cold tolerance, providing a reference for cold tolerance breeding. • 17βde8 contains a SNP site and may be critical for cold tolerance in crayfish. • The crayfish improved cold tolerance by regulating the expression levels of prdm16 , ucp4 and ucp5. • Cold-sensitive crayfish has a high lipid content. [ABSTRACT FROM AUTHOR]

Pathogen infection does not directly cause host death. Secondary infection is the main factor that leads to severe damage. Nuclear respiratory factor 1 (NRF1) is a nuclear transcription factor that regulate mitochondrial biogenesis. However, the function of NRF1 in antiviral immunity, especially its role in the process of co-infection is largely unknown. NRF1 inhibited virus infection by mediating apoptosis in arthropod, Procambarus clarkii. Notably, NRF1 expression was significantly induced in the early stage of white spot syndrome virus (WSSV) infection and reduced during the later stage of infection. NRF1 mediated apoptosis, phagocytosis, and reactive oxygen species (ROS) production 24 h after WSSV infection. The number of culturable bacteria was significantly increased and induced hypoxia in vivo 72 h after WSSV infection. Hypoxia exposure resulted in a decrease in NRF1 expression led to a decrease in body immunity and a vicious cycle until the crayfish died. This study demonstrated that secondary infections may be a major cause of biological mortality in crustaceans. • NRF1 inhibited virus infection by mediating apoptosis. • WSSV infection induces the increase in bacteria, leading to hypoxia in hemolymph. • The hypoxia in hemolymph suppress the immune response of crayfish. [ABSTRACT FROM AUTHOR]