The transcription factor Heat Shock Factor-1 (HSF-1) regulates the Heat Shock Response (HSR), a cytoprotective response induced by various proteotoxic stresses. Recent data from model organisms also suggests that HSF-1 is involved in non-stress roles including the regulation of development and longevity. In order to better study HSF-1 function in a whole organism model, we have created a C. elegans strain containing HSF-1 tagged with GFP at its endogenous locus utilizing CRISPR/Cas9-guided transgenesis. Previous C. elegans models with tagged HSF-1 have relied on rescuing a mutant variant of HSF-1 in an exogenous locus, but it has been noted that mutant variants of HSF-1 can still retain some regulatory function in C. elegans and other organisms. This may lead to non-representational data of HSF-1 regulation collected in existing C. elegans models. Our endogenously tagged HSF-1 model should therefore provide more accurate data on HSF-1 function. We show here that our HSF-1::GFP is functional, as our worm strain behaves similarly to wild-type worms as well as to a previously described HSF-1::GFP model in response to heat stress, sodium azide, osmotic stress, and acute cadmium exposure. Upon further characterization of our HSF-1::GFP strain, we observe robust HSF-1 expression in the oocytes of C. elegans, which previously has not been reported, as well as a more complex response to oxidative damage than previously described. Further studies are planned with our model to investigate these and other potential new roles for HSF-1 in organismal biology. This model thus is unique in that it is the only endogenously-tagged HSF-1 whole-organism model currently available, and represents a novel experimental platform to study HSF-1 function within and outside of the HSR.