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Guanyl nucleotide exchange factor Sql2 and Ras2 regulate filamentous growth in Ustilago maydis

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Müller,  Philip
Department of Organismic Interactions, Alumni, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Kahmann,  R.
Emeriti Molecular Phytopathology, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Citation

Müller, P., Katzenberger, J., Loubradou, G., & Kahmann, R. (2003). Guanyl nucleotide exchange factor Sql2 and Ras2 regulate filamentous growth in Ustilago maydis. Eukaryotic Cell, 2(3), 609-617. doi:10.1128/ec.2.3.609-617.2003.


Cite as: https://hdl.handle.net/21.11116/0000-0007-C9F6-1
Abstract
The cyclic AMP (cAMP)-signaling pathway regulates cell morphology and plays a crucial role during pathogenic development of the plant-pathogenic fungus Ustilago maydis. Strains lacking components of this signaling pathway, such as the Galpha-subunit Gpa3 or the adenylyl cyclase Uac1, are nonpathogenic and grow filamentously. On the other hand, strains exhibiting an activated cAMP pathway due to a dominant-active allele of gpa3 display a glossy colony phenotype and are unable to proliferate in plant tumors. Here we present the identification of sql2 as a suppressor of the glossy colony phenotype of a gpa3(Q206L) strain. sql2 encodes a protein with similarity to CDC25-like guanine nucleotide exchange factors, which are known to act on Ras proteins. Overexpression of sql2 leads to filamentous growth that cannot be suppressed by exogenous cAMP, suggesting that Sql2 does not act upstream of Uac1. To gain more insight in signaling processes regulated by Sql2, we isolated two genes encoding Ras proteins. Expression of dominant active alleles of ras1 and ras2 showed that Ras2 induces filamentous growth while Ras1 does not affect cell morphology but elevates pheromone gene expression. These results indicate that Ras1 and Ras2 fulfill different functions in U. maydis. Moreover, observed similarities between the filaments induced by sql2 and ras2 suggest that Sql2 is an activator of Ras2. Interestingly, sql2 deletion mutants are affected in pathogenic development but not in mating, indicating a specific function of sql2 during pathogenesis.