Multiomics profiling reveals the adaptive responses of largemouth bass to high temperature stress.

BACKGROUND

Largemouth bass (Micropterus salmoides) is among the most economically important freshwater fish species. High temperature is a major abiotic stressor, leading to increased mortality and significant economic losses. However, research on the regulatory mechanisms of heat stress response in largemouth bass is limited. This study aims to elucidate the mechanisms of adaptability in largemouth bass during heat stress and subsequent recovery.

RESULTS

The morphobiochemical alterations and adaptive mechanisms induced by high water temperature in the gill, brain and liver tissues of largemouth bass are investigated through biochemical blood analysis, haematoxylin and eosin staining, transmission electron microscopy and transcriptomic and proteomic profiles. The results reveal that heat stress-induced oxidative stress causes severe damage to the gill, brain and liver tissues, as well as to the mitochondria, endoplasmic reticulum and Golgi apparatus of these tissues. Such damage is alleviated during the recovery stage, which is closely associated with the PPAR signalling pathway, focal adhesion, ErbB signalling pathway, retinoid metabolism, and cytochrome P450 pathways. These pathways contribute to damage repair, functional recovery, and maintenance of homeostasis after heat stress. Furthermore, experimental validation reveals the pivotal role of Hspa9 in the heat stress response.

CONCLUSIONS

These findings reveal that oxidative stress induced by heat stress can severely damage critical tissues in largemouth bass, but the tissues are heterogeneous and have complex and flexible heat stress response regulatory mechanisms. Furthermore, Hspa9 plays an important protective role in the process of heat stress.