Manipulating heat shock factor-1 in Xenopus tadpoles: neuronal tissues are refractory to exogenous expression.

Manipulating heat shock factor-1 in Xenopus tadpoles: neuronal tissues are refractory to exogenous expression.

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BACKGROUND: The aging related decline of heat shock factor-1 (HSF1) signaling may be causally related to protein aggregation diseases.To model pale pink sns such disease, we tried to cripple HSF1 signaling in the Xenopus tadpole.RESULTS: Over-expression of heat shock factor binding protein-1 did not inhibit the heat shock response in Xenopus.RNAi against HSF1 mRNA inhibited the heat shock response by 70% in Xenopus A6 cells, but failed in transgenic tadpoles.

Expression of XHSF380, a dominant-negative HSF1 mutant, was embryonic lethal, which could be circumvented by delaying expression via a tetracycline inducible promoter.HSF1 signaling is thus essential for embryonic Xenopus development.Surprisingly, transgenic expression of the XHSF380 or of full length HSF1, whether driven by a ubiquitous or a neural specific promoter, was not detectable in the larval brain.CONCLUSIONS: Our finding that the majority of neurons, which have little endogenous HSF1, refused to accept short shifter rsx transgene-driven expression of HSF1 or its mutant suggests that HSF1 levels are strictly controlled in neuronal tissue.