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The thermoprotective mechanisms of insects remain largely unknown. We reported the  Bombyx mori  contractile ( cot ) behavioral mutant with thermo-sensitive seizures phenotype. At elevated temperatures, the  cot  mutant exhibit seizures associated with strong contractions, rolling, vomiting, and a temporary lack of movement. We narrowed a region containing  cot  to ~268 kb by positional cloning and identified the mutant gene as  Bmsei  which encoded a potassium channel protein. Bmsei was present in both the cell membrane and cytoplasm in wild-type ganglia but faint in  cot . Furthermore, Bmsei was markedly decreased upon high temperature treatment in  cot  mutant. With the RNAi method and injecting potassium channel blockers, the wild type silkworm was induced the  cot  phenotype. These results demonstrated that  Bmsei  was responsible for the  cot  mutant phenotype and played an important role in thermoprotection in silkworm. Meanwhile, comparative proteomic approach was used to investigate the proteomic differences. The results showed that the protein of Hsp-1 and Tn1 were significantly decreased and increased on protein level in  cot  mutant after thermo-stimulus, respectively. Our data provide insights into the mechanism of thermoprotection in insect. As  cot  phenotype closely resembles human epilepsy,  cot  might be a potential model for the mechanism of epilepsy in future.

Functional Loss of Bmsei Causes Thermosensitive Epilepsy in Contractile Mutant Silkworm, Bombyx mori