In this report, we explored if G protein coupled receptor kinases (GRKs) can help modulate the heat stress responses of Caenorhabditis (C.) elegans. Loss of function grk-2 C. elegans mutants were more tolerant to increases in heat and display an ability for heat stress-associated hormesis at a longer exposure time unlike the wild type N2 animals and the loss of function grk-1 C. elegans mutants. The loss of function grk-1 mutants recovered more from acute heat stress compared to the wild type N2 animals. Animals with low Ce-GRK2 protein expression showed increased DAF-16 nuclear localization during the early stages of heat stress exposure compared to the other RNAi-treated animals, demonstrating altered insulin/insulin-like growth factor signaling (IIS) pathway activity in response to the stress. pdk-1 and akt-1 may play key roles in conjunction with Ce-GRK2 in the heat stress response. Collectively, these findings demonstrate that GRKs influence C. elegans heat stress behaviors.

在这份报告中，我们探讨了G蛋白偶联受体激酶（GRKs）是否可以帮助调节秀丽隐杆线虫的热应激反应。功能丧失GRK-2线虫突变体更耐受在热的增加和显示热应激相关兴奋效应在不同于野生型N2动物更长的曝光时间的能力和功能的丧失GRK-1线虫突变体。与野生型N2动物相比，功能丧失的grk-1突变体可从急性热应激中恢复更多。Ce-GRK2低的动物与其他RNAi处理的动物相比，蛋白表达显示在热应激暴露的早期阶段，DAF-16核的定位增加，表明响应于应激，胰岛素/胰岛素样生长因子信号转导（IIS）途径活性发生了改变。pdk-1和akt-1可能与Ce-GRK2一起在热应激反应中起关键作用。总的来说，这些发现表明GRKs影响线虫的热应激行为。