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

**Authors:** Wenzhi Guan, Yongqing Yu, Jinpeng Zhang, Jieliang Jian, Baolong Niu, Bao Lou, Dayan Hu, Xiaojun Xu

PMC · DOI: 10.1186/s13059-026-03964-9 · Genome Biology · 2026-01-22

## TL;DR

This study explores how largemouth bass respond to high temperatures, revealing tissue damage and recovery mechanisms linked to specific biological pathways.

## Contribution

The study identifies novel regulatory pathways and the role of Hspa9 in largemouth bass during heat stress recovery.

## Key findings

- Heat stress causes oxidative damage to gill, brain, and liver tissues in largemouth bass.
- Recovery involves PPAR, focal adhesion, ErbB, retinoid metabolism, and cytochrome P450 pathways.
- Hspa9 is shown to play a pivotal protective role during heat stress.

## Abstract

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.

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.

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.

The online version contains supplementary material available at 10.1186/s13059-026-03964-9.

## Linked entities

- **Genes:** HSPA9 (heat shock protein family A (Hsp70) member 9) [NCBI Gene 3313]
- **Species:** Micropterus salmoides (taxon 27706)

## Full-text entities

- **Chemicals:** retinoid (MESH:D012176), haematoxylin (MESH:D006416)
- **Species:** Micropterus salmoides (largemouth bass, species) [taxon 27706]

## Full text

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## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12911189/full.md

## References

5 references — full list in the complete paper: https://tomesphere.com/paper/PMC12911189/full.md

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Source: https://tomesphere.com/paper/PMC12911189