Significant differentially expressed genes (DEG) for midgut tissue from bees maintained for four hours at 35°C or 45°C

Honey bee colonies in the United States have suffered from increased die-off in the last few years with a complex set of interacting stresses playing a key role. With changing climate, an increase in the frequency of severe weather events, such as heat waves, is anticipated. Understanding how these changes may contribute to stress in honey bees is crucial. Individual honey bees appear to have a high capacity to endure thermal stress. One reason for this high-level endurance is likely their robust HSR which contributes to thermotolerance at the cellular level. However, less is known about other mechanisms of thermotolerance, especially those operating at the tissue level. To elucidate other determinants of this resilience in this species, we used thermal stress coupled with RNAseq and identified broad transcriptional remodeling of a number of key signaling pathways in the honey bee, including those pathways known to be involved in digestive tract regeneration in the fruit fly such as the Hippo and JAK/STAT pathways. We also observe cell death and shedding of epithelial cells, which likely leads to induction of this regenerative transcriptional program. We found that thermal stress affects many of these pathways in other tissues, suggesting a shared program of damage response. This study provides important foundational characterization of the tissue damage response program in this key pollinating species. In addition, our data suggest that a robust regeneration program may also be a critical contributor to thermotolerance at the tissue level, a possibility which warrants further exploration in this and other species.

近数年来，美国蜜蜂蜂群的死亡率持续攀升，多种相互作用的复杂胁迫因素在此过程中发挥了关键作用。随着气候变化，热浪等极端天气事件的发生频率预计将进一步升高。阐明此类气候变化如何加剧蜜蜂所受胁迫，具有重要意义。单个蜜蜂似乎具备极强的耐热胁迫能力，这一高耐受性的潜在原因之一，可能是其强大的热休克反应（Heat Shock Response, HSR）——该反应在细胞层面为蜜蜂提供了耐热性。然而，学界对其他耐热机制，尤其是在组织层面发挥作用的耐热机制，仍知之甚少。为阐明该物种耐热性的其他决定因素，本研究通过将热胁迫与RNA测序（RNAseq）相结合，分析发现蜜蜂体内多条关键信号通路发生了广泛的转录重塑；其中包括果蝇中已知参与消化道再生的通路，如Hippo通路与JAK/STAT通路。本研究同时观察到上皮细胞的死亡与脱落现象，这一过程大概率会诱导上述再生相关转录程序的激活。研究还发现，热胁迫在其他组织中也会对多数此类通路产生影响，这表明机体存在一套共享的损伤应答程序。本研究为这一关键传粉物种的组织损伤应答程序提供了重要的基础特征描述。此外，本研究数据表明，一套高效的再生程序或许也是组织层面耐热性的关键促成因素，这一可能性值得在蜜蜂及其他物种中开展进一步研究。

搜集汇总

背景与挑战

背景概述

该数据集包含蜜蜂中肠组织在35°C或45°C热应激四小时后的显著差异表达基因（DEG）数据，通过RNAseq技术揭示了关键信号通路（如Hippo和JAK/STAT）的转录重塑，并观察到细胞死亡和上皮细胞脱落现象，旨在探索组织级耐热性机制，为蜜蜂这一关键传粉物种的损伤响应提供基础性研究。