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2. Selective accumulation of matrix proteins inside of peroxisomal subdomains

Author

Ast, Julia, primary, Bäcker, Nils, additional, Martorana, Domenica, additional, Renicke, Christian, additional, Stehlik, Thorsten, additional, Heimerl, Thomas, additional, Taxis, Christof, additional, Bange, Gert, additional, Bölker, Michael, additional, Sandrock, Björn, additional, Schink, Kay Oliver, additional, and Freitag, Johannes, additional

Published
2022
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5. Versatile CRISPR/Cas9 Systems for Genome Editing in

Author

Wege, Sarah-Maria, Gejer, Katharina, Becker, Fabienne, Bölker, Michael, Freitag, Johannes, and Sandrock, Björn

Subjects
lcsh:Biology (General), Ustilago maydis, deletion, point mutation, lcsh:QH301-705.5, CRISPR/Cas9, Article, genetic manipulation
Abstract

The phytopathogenic smut fungus Ustilago maydis is a versatile model organism to study plant pathology, fungal genetics, and molecular cell biology. Here, we report several strategies to manipulate the genome of U. maydis by the CRISPR/Cas9 technology. These include targeted gene deletion via homologous recombination of short double-stranded oligonucleotides, introduction of point mutations, heterologous complementation at the genomic locus, and endogenous N-terminal tagging with the fluorescent protein mCherry. All applications are independent of a permanent selectable marker and only require transient expression of the endonuclease Cas9hf and sgRNA. The techniques presented here are likely to accelerate research in the U. maydis community but can also act as a template for genome editing in other important fungi.

Published
2020

8. Insights from the genome of the biotrophic fungal plant pathogen Ustilago maydis

Author

Kämper, Jörg, Kahmann, Regine, Bölker, Michael, Ma, Li-Jun, Brefort, Thomas, Saville, Barry J., Banuett, Flora, Kronstad, James W., Gold, Scott E., Müller, Olaf, Perlin, Michael H., Wösten, Han A. B., de Vries, Ronald, Ruiz-Herrera, José, Reynaga-Peña, Cristina G., Snetselaar, Karen, McCann, Michael, Pérez-Martín, José, Feldbrügge, Michael, Basse, Christoph W., Steinberg, Gero, Ibeas, Jose I., Holloman, William, Guzman, Plinio, Farman, Mark, Stajich, Jason E., Sentandreu, Rafael, González-Prieto, Juan M., Kennell, John C., Molina, Lazaro, Schirawski, Jan, Mendoza-Mendoza, Artemio, Greilinger, Doris, Münch, Karin, Rössel, Nicole, Scherer, Mario, Vraneš, Miroslav, Ladendorf, Oliver, Vincon, Volker, Fuchs, Uta, Sandrock, Björn, Meng, Shaowu, Ho, Eric C. H., Cahill, Matt J., Boyce, Kylie J., Klose, Jana, Klosterman, Steven J., Deelstra, Heine J., Ortiz-Castellanos, Lucila, Li, Weixi, Sanchez-Alonso, Patricia, Schreier, Peter H., Häuser-Hahn, Isolde, Vaupel, Martin, Koopmann, Edda, Friedrich, Gabi, Voss, Hartmut, Schlüter, Thomas, Margolis, Jonathan, Platt, Darren, Swimmer, Candace, Gnirke, Andreas, Chen, Feng, Vysotskaia, Valentina, Mannhaupt, Gertrud, Güldener, Ulrich, Münsterkötter, Martin, Haase, Dirk, Oesterheld, Matthias, Mewes, Hans-Werner, Mauceli, Evan W., DeCaprio, David, Wade, Claire M., Butler, Jonathan, Young, Sarah, Jaffe, David B., Calvo, Sarah, Nusbaum, Chad, Galagan, James, and Birren, Bruce W.

Published
2006

13. Two Internal Sequence Elements Modulate Transcription From the External Human 7S K RNA Gene Promoter In Vivo

Author

Sandrock, Björn and Benecke, Bernd-Joachim

Subjects
Transcription, Genetic, RNA, Small Nuclear, Genes, Regulator, RNA, Small Cytoplasmic, Humans, RNA Polymerase III, Promoter Regions, Genetic, Article, HeLa Cells
Abstract

Constructs of the external promoter of the human 7S K RNA gene in combination with different reporter elements and varying amounts of 7S K internal sequences were analyzed for efficient transcription by RNA polymerase III (pol III) in vitro and in vivo. In vitro, the 7S K promoter alone (-245 to -1) revealed full activity, compared to the entire wild-type gene. In vivo, however, the activity of the gene-external 7S K promoter, albeit clearly functional by itself, was positively modulated by internal sequence elements. Fusion constructs containing increasing amounts of transcribed 7S K sequences revealed that two elements were responsible for this activation. One element is associated with the initiator region (+1 to +8) of this class III gene. The second sequence comprises the 5' half of a cryptic A-box starting at +10 of the 7S K RNA sequence. In the context of a totally unrelated vector sequence, a GGC element alone was sufficient to functionally replace that cryptic A-box. Thus, it appears that in context of the 7S K RNA gene--and possibly the 7S L and U6 RNA genes as well--structurally divergent A-box-like elements function as internal modulators of these pol III promoters.

Published
2018

19. Insights from the genome of the biotrophic fungal plant pathogen Ustilago maydis

Author

National Human Genome Research Institute (US), Bayer, National Institutes of Health (US), Federal Ministry of Education and Research (Germany), Max Planck Society, Natural Sciences and Engineering Research Council of Canada, Canada Foundation for Innovation, Consejo Nacional de Humanidades, Ciencias y Tecnologías (México), Alexander von Humboldt Foundation, European Commission, Kämper, Jörg, Kahmann, Regine, Bölker, Michael, Ma, Li-Jun, Brefort, Thomas, Saville, Barry J., Banuett, Flora, Kronstad, James W., Gold, Scott E., Müller, Olaf, Perlin, Michael H., Wösten, Han A. B., Vries, Ronald de, Ruiz-Herrera, José, Reynaga-Peña, Cristina G., Snetselaar, Karen, McCann, Michael, Pérez-Martín, José, Feldbrügge, Michael, Basse, Christoph W., Steinberg, Gero, Ibeas, Jose I., Holloman, William K., Guzman, Plinio, Farman, Mark, Stajich, Jason E., Sentandreu, Rafael, González-Prieto, Juan M., Kennell, John C., Molina Delgado, Lázaro, Schirawski, Jan, Mendoza-Mendoza, Artemio, Greilinger, Doris, Münch, Karin, Rössel, Nicole, Scherer, Mario, Vraneš, Miroslav, Ladendorf, Oliver, Vincon, Volker, Fuchs, Uta, Sandrock, Björn, Meng, Shaowu, Ho, Eric C. H., Cahill, Matt J., Boyce, Kylie J., Klose, Jana, Klosterman, Steven J., Deelstra, Heine J., Ortiz-Castellanos, Lucila, Li, Weixi, Sanchez-Alonso, Patricia, Schreier, Peter H., Häuser-Hahn, Isolde, Vaupel, Martin, Koopmann, Edda, Friedrich, Gabi, Voss, Hartmut, Schlüter, Thomas, Margolis, Jonathan, Platt, Darren, Swimmer, Candace, Gnirke, Andreas, Chen, Feng, Vysotskaia, Valentina, Mannhaupt, Gertrud, Güldener, Ulrich, Münsterkötter, Martin, Haase, Dirk, Oesterheld, Matthias, Mewes, Hans-Werner, Mauceli, Evan W., DeCaprio, David, Wade, Claire M., Butler, Jonathan, Young, Sarah, Jaffe, David B., Calvo, Sarah, Nusbaum, Chad, Galagan, James, Birren, Bruce W., National Human Genome Research Institute (US), Bayer, National Institutes of Health (US), Federal Ministry of Education and Research (Germany), Max Planck Society, Natural Sciences and Engineering Research Council of Canada, Canada Foundation for Innovation, Consejo Nacional de Humanidades, Ciencias y Tecnologías (México), Alexander von Humboldt Foundation, European Commission, Kämper, Jörg, Kahmann, Regine, Bölker, Michael, Ma, Li-Jun, Brefort, Thomas, Saville, Barry J., Banuett, Flora, Kronstad, James W., Gold, Scott E., Müller, Olaf, Perlin, Michael H., Wösten, Han A. B., Vries, Ronald de, Ruiz-Herrera, José, Reynaga-Peña, Cristina G., Snetselaar, Karen, McCann, Michael, Pérez-Martín, José, Feldbrügge, Michael, Basse, Christoph W., Steinberg, Gero, Ibeas, Jose I., Holloman, William K., Guzman, Plinio, Farman, Mark, Stajich, Jason E., Sentandreu, Rafael, González-Prieto, Juan M., Kennell, John C., Molina Delgado, Lázaro, Schirawski, Jan, Mendoza-Mendoza, Artemio, Greilinger, Doris, Münch, Karin, Rössel, Nicole, Scherer, Mario, Vraneš, Miroslav, Ladendorf, Oliver, Vincon, Volker, Fuchs, Uta, Sandrock, Björn, Meng, Shaowu, Ho, Eric C. H., Cahill, Matt J., Boyce, Kylie J., Klose, Jana, Klosterman, Steven J., Deelstra, Heine J., Ortiz-Castellanos, Lucila, Li, Weixi, Sanchez-Alonso, Patricia, Schreier, Peter H., Häuser-Hahn, Isolde, Vaupel, Martin, Koopmann, Edda, Friedrich, Gabi, Voss, Hartmut, Schlüter, Thomas, Margolis, Jonathan, Platt, Darren, Swimmer, Candace, Gnirke, Andreas, Chen, Feng, Vysotskaia, Valentina, Mannhaupt, Gertrud, Güldener, Ulrich, Münsterkötter, Martin, Haase, Dirk, Oesterheld, Matthias, Mewes, Hans-Werner, Mauceli, Evan W., DeCaprio, David, Wade, Claire M., Butler, Jonathan, Young, Sarah, Jaffe, David B., Calvo, Sarah, Nusbaum, Chad, Galagan, James, and Birren, Bruce W.

Abstract

Ustilago maydis is a ubiquitous pathogen of maize and a well-established model organism for the study of plant-microbe interactions. This basidiomycete fungus does not use aggressive virulence strategies to kill its host. U. maydis belongs to the group of biotrophic parasites (the smuts) that depend on living tissue for proliferation and development. Here we report the genome sequence for a member of this economically important group of biotrophic fungi. The 20.5-million-base U. maydis genome assembly contains 6,902 predicted protein-encoding genes and lacks pathogenicity signatures found in the genomes of aggressive pathogenic fungi, for example a battery of cell-wall-degrading enzymes. However, we detected unexpected genomic features responsible for the pathogenicity of this organism. Specifically, we found 12 clusters of genes encoding small secreted proteins with unknown function. A significant fraction of these genes exists in small gene families. Expression analysis showed that most of the genes contained in these clusters are regulated together and induced in infected tissue. Deletion of individual clusters altered the virulence of U. maydis in five cases, ranging from a complete lack of symptoms to hypervirulence. Despite years of research into the mechanism of pathogenicity in U. maydis, no 'true' virulence factors had been previously identified. Thus, the discovery of the secreted protein gene clusters and the functional demonstration of their decisive role in the infection process illuminate previously unknown mechanisms of pathogenicity operating in biotrophic fungi. Genomic analysis is, similarly, likely to open up new avenues for the discovery of virulence determinants in other pathogens. ©2006 Nature Publishing Group.

Published
2006

28. Three-Hybrid Screens.

Author

Walker, John M., MacDonald, Paul N., Sandrock, Björn, Tirode, Franck, and Egly, Jean-Marc

Abstract

Recent studies have revealed the existence of several molecular complexes either stable, like the RNA polymerase II holoenzyme, transcription factor TFIID, and mediators, or transient as could be observed in the various steps of the transcription process (e.g., initiation, elongation, and termination). These observations point out the fact that regulation of different cellular mechanisms is orchestrated by interactions between molecular species either to modify proteins or to position one of them within a complex that then will be functional. Several techniques such as affinity precipitation, glycerol gradient sedimentation, and the yeast two-hybrid system are currently used to study protein-protein interactions (1). These various methods, usually investigating the connection between two partners, account for only the strong (and stable) interactions and neglect the weaker ones. Considering the complexes studied so far, it is suspected and sometimes shown that interactions often occur between more than two proteins (e.g., to stabilize the complex). In an effort to understand the various biologic mechanisms—and in our case gene expression regulation—we were interested in developing the yeast three-hybrid (or trihybrid) system. [ABSTRACT FROM AUTHOR]

Published
2001
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30. A Drosophila XPD model links cell cycle coordination with neuro-development and suggests links to cancer

Author

Stettler, Karin, Li, Xiaoming, Sandrock, Björn, Braga-Lagache, Sophie, Heller, Manfred, Dümbgen, Lutz, and Suter, Beat

Abstract

XPD functions in transcription, DNA repair and in cell cycle control. Mutations in human XPD (also known as ERCC2) mainly cause three clinical phenotypes: xeroderma pigmentosum (XP), Cockayne syndrome (XP/CS) and trichothiodystrophy (TTD), and only XP patients have a high predisposition to developing cancer. Hence, we developed a fly model to obtain novel insights into the defects caused by individual hypomorphic alleles identified in human XP-D patients. This model revealed that the mutations that displayed the greatest in vivo UV sensitivity in Drosophila did not correlate with those that led to tumor formation in humans. Immunoprecipitations followed by targeted quantitative MS/MS analysis showed how different xpd mutations affected the formation or stability of different transcription factor IIH (TFIIH) subcomplexes. The XP mutants most clearly linked to high cancer risk, Xpd R683W and R601L, showed a reduced interaction with the core TFIIH and also an abnormal interaction with the Cdk-activating kinase (CAK) complex. Interestingly, these two XP alleles additionally displayed high levels of chromatin loss and free centrosomes during the rapid nuclear division phase of the Drosophila embryo. Finally, the xpd mutations showing defects in the coordination of cell cycle timing during the Drosophila embryonic divisions correlated with those human mutations that cause the neurodevelopmental abnormalities and developmental growth defects observed in XP/CS and TTD patients.

Published
2015
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31. The PAK family kinase Cla4 is required for budding and morphogenesis inUstilago maydis.

Author

a Leveleki, Leonor, Mahlert, Michael, Sandrock, Björn, and Bölker, Michael

Subjects
PROTEIN kinases, USTILAGO maydis, MORPHOGENESIS, CYTOKINESIS, SERINE proteinases, PHYTOPATHOGENIC fungi
Abstract

The phytopathogenic basidiomyceteUstilago maydisdisplays a dimorphic switch between budding growth of haploid cells and filamentous growth of the dikaryon. In a screen for mutants affected in morphogenesis and cytokinesis, we identified the serine/threonine protein kinase Cla4, a member of the family of p21-activated kinases (PAKs). Cells, in whichcla4has been deleted, are viable but they are unable to bud properly. Instead,cla4mutant cells grow as branched septate hyphae and divide by contraction and fission at septal cross walls. Delocalized deposition of chitinous cell wall material along the cell surface is observed incla4mutant cells. Deletion of the Cdc42/Rac1 interaction domain (CRIB) results in a constitutive active Cla4 kinase, whose expression is lethal for the cell.cla4mutant cells are unable to induce pathogenic development in plants and to display filamentous growth in a mating reaction, although they are still able to secrete pheromone and to undergo cell fusion with wild-type cells. We propose that Cla4 is involved in the regulation of cell polarity during budding and filamentation. [ABSTRACT FROM AUTHOR]

Published
2004
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33. Engineering Ustilago maydisfor production of tailor-made mannosylerythritol lipids

Author

Becker, Fabienne, Stehlik, Thorsten, Linne, Uwe, Bölker, Michael, Freitag, Johannes, and Sandrock, Björn

Abstract

Mannosylerythritol lipids (MELs) are surface active glycolipids secreted by various fungi. MELs can be used as biosurfactants and are a biodegradable resource for the production of detergents or pharmaceuticals. Different fungal species synthesize a unique mixture of MELs differing in acetyl- and acyl-groups attached to the sugar moiety. Here, we report the construction of a toolbox for production of glycolipids with predictable fatty acid side chains in the basidiomycete Ustilago maydis. Genes coding for acyl-transferases involved in MEL production (Mac1 and Mac2) from different fungal species were combined to obtain altered MEL variants with distinct physical properties and altered antimicrobial activity. We also demonstrate that a U. maydisparalog of the acyltransferase Mac2 with a different substrate specificity can be employed for the biosynthesis of modified MEL variants. In summary, our data showcase how the fungal repertoire of Mac enzymes can be used to engineer tailor-made MELs according to specific biotechnological or pharmaceutical requirements.

Published
2021
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