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The promoter-poised Rpd3 HDAC complex orchestrates global chromatin reprogramming upon nutrient transition.

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    Histone deacetylase Rpd3 reprograms chromatin during nutrient shifts in yeast, balancing gene expression. This ensures proper metabolic adaptation by controlling gene activity and maintaining cellular function.

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    Area of Science:

    • Molecular Biology
    • Yeast Genetics
    • Chromatin Biology

    Background:

    • Metabolic flexibility in *Saccharomyces cerevisiae* relies on adaptive transcriptional rewiring.
    • Histone deacetylases (HDACs) play a role in regulating gene expression, but their precise function during metabolic transitions remains unclear.
    • The paradox of HDAC enrichment at active promoters needs resolution.

    Purpose of the Study:

    • To investigate the role of the histone deacetylase Rpd3 in mediating nutrient-dependent chromatin reprogramming.
    • To understand how Rpd3 coordinates transcriptional shutdown and global acetylation balance during metabolic transitions.
    • To elucidate the mechanism by which HDACs act as metabolic gatekeepers.

    Main Methods:

    • Genome-wide analyses of chromatin immunoprecipitation and gene expression.
    • Studies involving yeast mutants lacking Rpd3 or its subunit Pho23.
    • Assessment of histone acetylation levels (H3K9ac) and activity of acetyltransferase Gcn5.

    Main Results:

    • Rpd3 complexes mediate rapid, reversible histone deacetylation at gene promoters and bodies, fine-tuning transcription.
    • Rpd3, particularly the Rpd3L complex, localizes at active gene promoters enriched in H3K9ac and Gcn5.
    • Nutrient shifts cause Gcn5 disengagement and Rpd3-mediated deacetylation, enforcing gene repression.
    • Loss of Rpd3 or Pho23 leads to persistent growth gene expression during starvation and impaired respiratory gene activation with glucose.

    Conclusions:

    • Rpd3 acts as a crucial mediator of nutrient-dependent chromatin reprogramming in yeast.
    • HDACs function as metabolic gatekeepers, coupling nutrient availability to transcriptional control.
    • This mechanism ensures transcriptional fidelity during metabolic transitions, resolving the HDAC enrichment paradox.