Abstract: In yeast, environmental stresses provoke sudden and dramatic increases in gene expression at stress inducible loci. Stress gene transcription is accompanied by the transient eviction of histones from the promoter and the transcribed regions of these genes. We found that mutants defective in subunits of the INO80 complex as well as in several histone chaperone systems exhibit extended expression windows that can be correlated with a distinct delay in histone re-deposition during adaptation. Surprisingly, Ino80 became associated with the open reading frames of stress genes in a stress specific way suggesting a direct function in the repression during adaptation. This recruitment required elongation by RNA Pol II, but none of the histone modifications that are usually associated with active transcription such as H3 K4/K36 methylation. A mutant lacking the Asf1 associated H3K56 acetyltransferase Rtt109 or Asf1 itself also showed enhanced stress induced transcript levels. Genetic data, however, suggest that Asf1 and Rtt109 function in parallel with INO80 to restore histone homeostasis whereas Spt6 seems to have an overlapping function with the chromatin remodeler. Thus, chromatin remodeling by INO80 in cooperation with Spt6 determines the shape of the expression profile during acute stress conditions possibly by an elongation dependent mechanism.