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Joseph Strauss

Researcher at University of Natural Resources and Life Sciences, Vienna

Publications -  113
Citations -  6146

Joseph Strauss is an academic researcher from University of Natural Resources and Life Sciences, Vienna. The author has contributed to research in topics: Aspergillus nidulans & Gene. The author has an hindex of 42, co-authored 106 publications receiving 5314 citations. Previous affiliations of Joseph Strauss include University of Vienna & University of Veterinary Medicine Vienna.

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Chromatin-level regulation of biosynthetic gene clusters

TL;DR: Loss-of-function Aspergillus nidulans CclA, a Bre2 ortholog involved in histone H3 lysine 4 methylation, activated the expression of cryptic secondary metabolite clusters in A. niduans, which generated monodictyphenone, emodin and emod in derivatives and encoded two anti-osteoporosis polyketides.
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Bacteria-induced natural product formation in the fungus Aspergillus nidulans requires Saga/Ada-mediated histone acetylation.

TL;DR: It is reported that the streptomycete triggers modification of fungal histones, providing previously undescribed evidence of Saga/Ada dependent histone acetylation triggered by prokaryotes.
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The effect of resource quantity and resource stoichiometry on microbial carbon-use-efficiency.

TL;DR: The results suggest that the links between biomass stoichiometry, resource demand and CUE may provide a mechanism for commonly observed temporal and spatial patterns in microbial community structure and function in natural habitats.
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Crel, the carbon catabolite repressor protein from Trichoderma reesei

TL;DR: It is concluded that T. reesei Cre1 is the functional homologue of Aspergillus CreA and that it binds to its target sequence probably as a protein complex.
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Heterochromatic marks are associated with the repression of secondary metabolism clusters in Aspergillus nidulans

TL;DR: 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.