Although the existence of a cellular heat shock response is nearly</p><p>universal, its relationship to organismal thermal tolerance is not</p><p>completely understood. Many of the genes involved are known to be</p><p>regulated by the highly conserved heat shock transcription factor-1</p><p>(HSF-1), yet the regulatory network is not fully characterized. Here,</p><p>we investigated the role of HSF-1 in gene expression following</p><p>thermal stress using knockdown of HSF-1 by RNA interference in the</p><p>intertidal copepod Tigriopus californicus. We observed some</p><p>evidence for decreased transcription of heat shock protein genes</p><p>following knockdown, supporting the widely acknowledged role of</p><p>HSF-1 in the heat shock response. However, the majority of</p><p>differentially expressed genes between the control and HSF-1</p><p>knockdown groups were upregulated, suggesting that HSF-1</p><p>normally functions to repress their expression. Differential</p><p>expression observed in genes related to chitin and cuticle formation</p><p>lends support to previous findings that these processes are highly</p><p>regulated following heat stress. We performed a genome scan and</p><p>identified a set of 396 genes associated with canonical heat shock</p><p>elements. RNA-seq data did not find those genes to be more highly</p><p>represented in our HSF-1 knockdown treatment, indicating that</p><p>requirements for binding and interaction of HSF-1 with a given gene</p><p>are not simply predicted by the presence of HSF-1 binding sites.</p><p>Further study of the pathways implicated by these results and future</p><p>comparisons among populations of T. californicus may help us</p><p>understand the role and importance of HSF-1 in the heat shock</p><p>response and, more broadly, in organismal thermal tolerance.
