The transcription factor heat shock factor-1 (HSF-1) regulates the heat shock response (HSR), a cytoprotective response induced by proteotoxic stresses. Data from model organisms has shown that HSF-1 also has non-stress biological roles, including roles in the regulation of development and longevity. To better study HSF-1 function, we created a C. elegans strain containing HSF-1 tagged with GFP at its endogenous locus utilizing CRISPR/Cas9-guided transgenesis. We show that the HSF-1::GFP CRISPR worm strain behaves similarly to wildtype worms in response to heat and other stresses, and in other physiological processes. HSF-1 was expressed in all tissues assayed. Immediately following the initiation of reproduction, HSF-1 formed nuclear stress bodies, a hallmark of activation, throughout the germline. Upon the transition to adulthood, of HSF-1 nuclear stress bodies appeared in most somatic cells. Genetic loss of the germline suppressed nuclear stress body formation with age, suggesting that the germline influences HSF-1 activity. Interestingly, we found that various neurons did not form nuclear stress bodies after transitioning to adulthood. Therefore, the formation of HSF-1 nuclear stress bodies upon the transition to adulthood does not occur in a synchronous manner in all cell types. In sum, these studies enhance our knowledge of the expression and activity of the aging and proteostasis factor HSF-1 in a tissue-specific manner with age.

转录因子热休克因子-1 (HSF-1) 调节热休克反应 (HSR)，这是一种由蛋白毒性应激诱导的细胞保护反应。来自模式生物的数据表明，HSF-1 还具有非应激生物学作用，包括调节发育和寿命的作用。为了更好地研究 HSF-1 功能，我们利用 CRISPR/Cas9 引导的转基因技术，创建了一种线虫菌株，其内源基因座上含有 GFP 标记的 HSF-1。我们表明，HSF-1::GFP CRISPR 蠕虫菌株在响应热和其他应激以及其他生理过程方面的行为与野生型蠕虫相似。 HSF-1 在所有测定的组织中都有表达。繁殖开始后，HSF-1 立即在整个种系中形成核应激体，这是激活的标志。过渡到成年后，大多数体细胞中出现了 HSF-1 核应激体。随着年龄的增长，种系遗传损失抑制了核应激体的形成，表明种系影响 HSF-1 活性。有趣的是，我们发现各种神经元在过渡到成年后并没有形成核应激体。因此，在过渡到成年期时HSF-1核应激体的形成并非在所有细胞类型中以同步方式发生。总之，这些研究增强了我们对衰老和蛋白稳态因子 HSF-1 随着年龄的组织特异性表达和活性的了解。