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Objective: The impact of various environmental stresses on native Apis cerana cerana fitness has attracted intense attention in China. However, the defence responses of A. cerana cerana to different stressors are poorly understood. Here, we aimed to elucidate the regulatory mechanism mediated by the tumorous imaginal discs (Tid) protein of A. cerana cerana (AccTid) in response to stressors. Methods: We used some bioinformatics softwares to analyse the characterisation of Tid. Then, qRT-PCR, RNA interference and heat resistance detection assays were used to explore the function of Tid in stress response in A. cerana cerana. Results: AccTid is a homologous gene of human Tid1 and Drosophila Tid56, contains a conserved J domain and belongs to the heat shock protein DnaJA subfamily. The level of AccTid induced expression was increased under temperature increases from 40°C to 43°C and 46°C, and AccTid knockdown decreased the heat resistance of A. cerana cerana, indicating that the upregulation of AccTid plays an important role when A. cerana cerana is exposed to heat stress. Interestingly, contrary to the results of heat stress treatment, the transcriptional level of AccTid was inhibited by cold, H2O2 and some agrochemical stresses and showed no significant change under ultraviolet ray and sodium arsenite stress. These results suggested that the requirement of A. cerana cerana for Tid differs markedly under different stress conditions. In addition, knockdown of AccTid increased the mRNA levels of some Hsps and antioxidant genes. The upregulation of these Hsps and antioxidant genes may be a functional complement of AccTid knockdown. Conclusion: AccTid plays a crucial role in A. cerana cerana stress responses and may mediate oxidative damage caused by various stresses. Our findings will offer fundamental knowledge for further investigations of the defence mechanism of A. cerana cerana against environmental stresses. [ABSTRACT FROM AUTHOR]

• Ngb protected rat CGNs against arsenic-induced ROS generation. • Ngb protected rat CGNs against arsenic-induced apoptosis. • Serum Ngb level is negatively correlated with As exposure through drinking water. People who drink water contaminated with arsenic for a long time develop neuritis, cerebellar symptoms, and deficits in memory and intellectual function. Arsenic induces oxidative stress and promotes apoptosis through multiple signalling pathways in nerve cells. Neuroglobin (Ngb), as a key mediator, is considered to be protective against oxidative stress. In this study, we aimed to study the effects of Ngb knockdown in arsenite-treated rat neurons on levels of apoptosis markers and reactive oxygen species and serum Ngb levels of subjects from arsenic-endemic regions in China. We discovered that arsenic-induced apoptosis and reactive oxygen species production were enhanced in Ngb -knocked-down rat neurons. Silencing of Ngb aggravated the arsenic-induced decrease in the rate of Bcl-2/Bax and the levels of Bcl-2 protein following arsenite treatment. The results also showed that serum Ngb levels were independently negatively correlated with arsenic concentration in drinking water. Furthermore, the serum Ngb levels of four groups (245 individuals) according to different degree exposure to arsenic were 815.18 ± 89.52, 1247.97 ± 117.18, 774.79 ± 91.55, and 482.72 ± 49.30 pg/mL, respectively. Taken together, it can be deduced that Ngb has protective effects against arsenic-induced apoptosis by eliminating reactive oxygen species. [ABSTRACT FROM AUTHOR]