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Heterochromatic marks are associated with the repression of secondary metabolism clusters in Aspergillus nidulans
Author(s) -
ReyesDominguez Yazmid,
Bok Jin Woo,
Berger Harald,
Shwab E. Keats,
Basheer Asjad,
Gallmetzer Andreas,
Scazzocchio Claudio,
Keller Nancy,
Strauss Joseph
Publication year - 2010
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2010.07051.x
Subject(s) - aspergillus nidulans , biology , heterochromatin , histone , chromatin , histone h3 , gene cluster , genetics , psychological repression , secondary metabolism , gene , epigenetics , regulation of gene expression , heterochromatin protein 1 , gene expression , mutant , biosynthesis
Summary Fungal secondary metabolites are important bioactive compounds but the conditions leading to expression of most of the putative secondary metabolism (SM) genes predicted by fungal genomics are unknown. Here we describe a novel mechanism involved in SM‐gene regulation based on the finding that, in Aspergillus nidulans , mutants lacking components involved in heterochromatin formation show de‐repression of genes involved in biosynthesis of sterigmatocystin (ST), penicillin and terrequinone A. During the active growth phase, the silent ST gene cluster is marked by histone H3 lysine 9 trimethylation and contains high levels of the heterochromatin protein‐1 (HepA). Upon growth arrest and activation of SM, HepA and trimethylated H3K9 levels decrease concomitantly with increasing levels of acetylated histone H3. SM‐specific chromatin modifications are restricted to genes located inside the ST cluster, and constitutive heterochromatic marks persist at loci immediately outside the cluster. LaeA, a global activator of SM clusters in fungi, counteracts the establishment of heterochromatic marks. Thus, one level of regulation of the A. nidulans ST cluster employs epigenetic control by H3K9 methylation and HepA binding to establish a repressive chromatin structure and LaeA is involved in reversal of this heterochromatic signature inside the cluster, but not in that of flanking genes.