Elongation factor TFIIS (transcription factor IIS) is structurally and biochemically probably the best characterized elongation cofactor of RNA polymerase II. However, little is known about TFIIS regulation or its roles during stress responses. Here, we show that, although TFIIS seems unnecessary under optimal conditions in Arabidopsis, its absence renders plants supersensitive to heat; tfIIs mutants die even when exposed to sublethal high temperature. TFIIS activity is required for thermal adaptation throughout the whole life cycle of plants, ensuring both survival and reproductive success. By employing a transcriptome analysis, we unravel that the absence of TFIIS makes transcriptional reprogramming sluggish, and affects expression and alternative splicing pattern of hundreds of heat-regulated transcripts. Transcriptome changes indirectly cause proteotoxic stress and deterioration of cellular pathways, including photosynthesis, which finally leads to lethality. Contrary to expectations of being constantly present to support transcription, we show that TFIIS is dynamically regulated. TFIIS accumulation during heat occurs in evolutionary distant species, including the unicellular alga Chlamydomonas reinhardtii, dicot Brassica napus and monocot Hordeum vulgare, suggesting that the vital role of TFIIS in stress adaptation of plants is conserved.

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Heat shock factors (HSFs) are at the core of heat stress (HS) response in plants. However, the contribution of HSFs governing the inherent thermotolerance mechanism in tomato from sub-tropical hot climates is poorly understood. With the above aim, comparative expression profiles of the HSF family in a HS tolerant (CLN1621L) and a sensitive cultivar (CA4) of tomato under HS revealed cultivar-biased regulation of an activator (HSFA7a) and repressor (HSFB4a) class HSF. Functional characterization of HSFA7a that was strongly up-regulated in the tolerant cultivar by VIGS-based silencing and overexpression established it as a positive regulator of HS-tolerance. While knock-down and overexpression analyses of HSFB4a that was down-regulated in CLN1621L in HS, showed it as a negative regulator of thermotolerance. Promoter:GUS reporter assays and promoter sequence analyses suggest heat-mediated transcriptional control of both the HSF genes in the contrasting cultivars. Moreover, we show HSFB4a is also regulated post-transcriptionally by microRNA Sly-miR4200 using degradome, short-tandem-target-mimic of Sly-miR4200 and transient in-planta Sly-miR4200-effector:HSFB4a-reporter assays. This miRNA is induced several folds upon HS in the tolerant variety thereby reducing HSFB4a levels. We thus propose that the alleviation of HSFB4a repressor governs thermotolerance in the tolerant cultivar by regulating downstream heat stress responsive genes.