Abstract:
: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.
journal_name
Mol Microbioljournal_title
Molecular microbiologyauthors
Reyes-Dominguez Y,Bok JW,Berger H,Shwab EK,Basheer A,Gallmetzer A,Scazzocchio C,Keller N,Strauss Jdoi
10.1111/j.1365-2958.2010.07051.xsubject
Has Abstractpub_date
2010-06-01 00:00:00pages
1376-86issue
6eissn
0950-382Xissn
1365-2958pii
MMI7051journal_volume
76pub_type
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