State Key Laboratory of Crop Biology, College of Life Sciences, Shandong Agricultural University, Taian, Shandong 271018, PR China.
Statistics Department, University of Auckland, 38 Princes Street, Auckland, New Zealand.
Sci Total Environ. 2020 May 10;716:137036. doi: 10.1016/j.scitotenv.2020.137036. Epub 2020 Feb 5.
There is clear evidence of severe honeybee declines in recent years, and parallel declines of plant community and crop productivity that rely on them. Different stresses, including heat stress, are among the primary drivers of this decline. However, the mechanisms by which honeybees respond to heat stress are elusive. Though heat shock proteins (Hsps) play important roles in heat stress response, the function of DnaJs (a subfamily of Hsps) is unclear. Here, we aimed to determine the underlying regulatory mechanism of honeybees to heat stress mediated by DnaJs. We found that several DnaJ genes, including DnaJA1, DnaJB12 and DnaJC8, are key for honeybee heat tolerance. DnaJA1 and DnaJB12 are cytoplasmic proteins, and DnaJC8 is a nuclear protein. The expression of DnaJA1, DnaJB12 and DnaJC8 was induced at different levels under short-term and long-term heat stress. Phenotypic analysis indicated that DnaJA1, DnaJB12 and DnaJC8 knockdown attenuated honeybee heat resistance. In addition, DnaJA1 participated in the heat stress response by upregulating many heat-inducible genes at the transcriptome-wide level, especially LOC108002668 and LOC107995148. Importantly, the upregulation of LOC108002668 and LOC107995148 was significantly repressed under heat stress when DnaJA1 was knocked down. We also found that knockdown of DnaJA1, DnaJB12 and DnaJC8 decreased antioxidant defense ability and increased the degree of oxidative damage in the honeybee. Taken together, our results indicate that DnaJ genes play important roles under heat stress in the honeybee. Overexpression of DnaJ genes may protect honeybees from heat stress-induced injuries and increase their survival rate.
近年来，明显有大量证据表明蜜蜂数量严重减少，而依赖于蜜蜂的植物群落和作物生产力也在平行减少。其中包括热应激在内的不同压力是导致这种下降的主要驱动因素之一。然而，蜜蜂对热应激的反应机制尚不清楚。虽然热休克蛋白（Hsps）在热应激反应中发挥着重要作用，但 DnaJs（Hsps 的一个亚家族）的功能尚不清楚。在这里，我们旨在确定 DnaJs 介导的蜜蜂对热应激的潜在调节机制。我们发现，包括 DnaJA1、DnaJB12 和 DnaJC8 在内的几个 DnaJ 基因是蜜蜂耐热的关键。DnaJA1 和 DnaJB12 是细胞质蛋白，而 DnaJC8 是核蛋白。在短期和长期热应激下，DnaJA1、DnaJB12 和 DnaJC8 的表达水平不同程度地被诱导。表型分析表明，DnaJA1、DnaJB12 和 DnaJC8 的敲低减弱了蜜蜂的耐热性。此外，DnaJA1 通过上调许多热诱导基因在转录组水平上参与热应激反应，特别是 LOC108002668 和 LOC107995148。重要的是，当 DnaJA1 被敲低时，LOC108002668 和 LOC107995148 的上调在热应激下受到显著抑制。我们还发现，DnaJA1、DnaJB12 和 DnaJC8 的敲低降低了蜜蜂的抗氧化防御能力并增加了氧化损伤的程度。综上所述，我们的结果表明 DnaJ 基因在蜜蜂的热应激中发挥着重要作用。DnaJ 基因的过表达可能会保护蜜蜂免受热应激诱导的损伤，提高其存活率。
