Anoxic stress and rapid cold hardening enhance cold tolerance of the migratory locust.

Anoxia and rapid cold hardening (RCH) can increase the cold tolerance of many animals. However, mechanisms underlying these two kinds of stresses remain unclear. In this study, we aimed to explore the relationship of acclimation to cold stress with acclimation to anoxic stress in the migratory locust, Locusta migratoria. RCH at 0°C for 3h promoted the survival of cold stress-exposed locusts. Anoxic hypercapnia (CO2 anoxic treatment) for 40 min exerted an effect similar to that of RCH. Anoxic hypercapnia within 1h can all promote the cold hardiness of locusts. We investigated the transcript levels of six heat shock protein (Hsp) genes, namely, Hsp20.5, Hsp20.6, Hsp20.7, Hsp40, Hsp70, and Hsp90. Four genes, namely, Hsp90, Hsp40, Hsp20.5, and Hsp20.7, showed differential responses to RCH and anoxic hypercapnia treatments. Under cold stress, locusts exposed to the two regimens showed different responses for Hsp90, Hsp20.5, and Hsp20.7. However, the varied responses disappeared after recovery from cold stress. Compared with the control group, the transcript levels of six Hsp genes were generally downregulated in locusts subjected to anoxic hypercapnia or/and RCH. These results indicate that anoxic stress and RCH have different mechanisms of regulating the transcription of Hsp family members even if the two treatments exerted similar effects on cold tolerance of the migratory locust. However, Hsps may not play a major role in the promotion of cold hardiness by the two treatments.