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A yeast catabolic enzyme controls transcriptional memory.

Zacharioudakis I, Gligoris T, Tzamarias D.

Institute of Molecular Biology & Biotechnology-Foundation of Research and Technology, 71110 Heraklion, Crete, Greece.

It has been postulated that chromatin modifications can persist through mitosis and meiosis, thereby securing memory of transcriptional states. Whether these chromatin marks can self-propagate in progeny independently of relevant trans-acting factors is an important question in phenomena related to epigenesis. "Adaptive cellular memory" displayed by yeast cells offers a convenient system to address this question. The yeast GAL genes are slowly activated by Gal4 when cells are first exposed to galactose, but their progeny, grown in glucose media, exhibit a fast activation mode upon re-exposure to this sugar. This "galactose memory" persists for several generations and was recently proposed to involve chromatin modifications and perinuclear topology of the GAL genes cluster. Here, we perform a heterokaryon assay demonstrating that this memory does not have a chromatin basis but is maintained by cytoplasmic factor(s) produced upon previous galactose induction. We show that Gal3, the cytoplasmic rate-limiting factor that releases the Gal4 activator, is dispensable for preserving galactose memory. Instead, the important memory determinant is a close Gal3 homolog, the highly expressed Gal1 galactokinase, the residual activity of which preserves memory in progeny cells by rapidly turning on the Gal4 activator upon cells' re-exposure to galactose.

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PMID: 17997309 [PubMed - indexed for MEDLINE]