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Eukaryotic Cell, December 2003, p. 1187-1199, Vol. 2, No. 6
1535-9778/03/$08.00+0 DOI: 10.1128/EC.2.6.1187-1199.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Andreas Brachmann,
Michael Feldbrügge, and Regine Kahmann*
Max Planck Institute for Terrestrial Microbiology, D-35043 Marburg, and Institute of Genetics and Microbiology, Ludwig-Maxilians-Universität-München, D-80638 Munich, Germany
Received 11 April 2003/ Accepted 16 September 2003
In the phytopathogenic fungus Ustilago maydis, pheromone-mediated cell fusion is a prerequisite for the generation of the infectious dikaryon. The pheromone signal elevates transcription of the pheromone genes and elicits formation of conjugation hyphae. Cyclic AMP and mitogen-activated protein kinase (MAPK) signaling are involved in this process. The MAPK cascade is presumed to be composed of Ubc4 (MAPK kinase kinase), Fuz7 (MAPK kinase), and Ubc3/Kpp2 (MAPK). We isolated the kpp4 gene and found it to be allelic to ubc4. Epistasis analyses with constitutively active alleles of kpp4 and fuz7 substantiate that Kpp4, Fuz7, and Kpp2/Ubc3 are components of the same module. Moreover, we demonstrate that Fuz7 activates Kpp2 and shows interactions in vitro. Signaling via this cascade regulates expression of pheromone-responsive genes, presumably through acting on the transcription factor Prf1. Interestingly, the same cascade is needed for conjugation tube formation, and this process does not involve Prf1. In addition, fuz7 as well as kpp4 deletion strains are nonpathogenic, while kpp2 deletion mutants are only attenuated in pathogenesis. Here we show that strains expressing the unphosphorylatable allele kpp2T182A/Y184F are severely affected in tumor induction and display defects in early infection-related differentiation.
Present address: Vossius & Partner, D-81675 Munich, Germany.
Present address: NIH, NIDDK, LBG, Bethesda, MD 20892.
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