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Specifically, simultaneous useful lack of Spt3 and Taf1 during stress building was a prerequisite to render the PGK1 promoter Taf1/TFIID-dependent in this stress. Intriguingly, genetic approaches unveiled that an as-yet unidentified trans-acting element reprogrammed the transcriptional mode of the PGK1 promoter from the Taf1/TFIID-independent state into the Taf1/TFIID-dependent state. This factor had been produced into the haploid SPT3 taf1 strain in an Hsp104-depend
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