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Eukaryotic Cell, July 2009, p. 977-989, Vol. 8, No. 7
1535-9778/09/$08.00+0     doi:10.1128/EC.00009-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Ustilago maydis Rho1 and 14-3-3 Homologues Participate in Pathways Controlling Cell Separation and Cell Polarity{triangledown} ,{dagger}

Cau D. Pham,1 Zhanyang Yu,1,{ddagger} Björn Sandrock,2 Michael Bölker,2 Scott E. Gold,3 and Michael H. Perlin1*

Department of Biology, Program on Disease Evolution, University of Louisville, Louisville, Kentucky,1 Department of Biology, Philipps-Universität, Marburg, Germany,2 Department of Plant Pathology, University of Georgia, Athens, Georgia3

Received 6 January 2009/ Accepted 23 April 2009

Proteins of the 14-3-3 and Rho-GTPase families are functionally conserved eukaryotic proteins that participate in many important cellular processes such as signal transduction, cell cycle regulation, malignant transformation, stress response, and apoptosis. However, the exact role(s) of these proteins in these processes is not entirely understood. Using the fungal maize pathogen, Ustilago maydis, we were able to demonstrate a functional connection between Pdc1 and Rho1, the U. maydis homologues of 14-3-3{varepsilon} and Rho1, respectively. Our experiments suggest that Pdc1 regulates viability, cytokinesis, chromosome condensation, and vacuole formation. Similarly, U. maydis Rho1 is also involved in these three essential processes and exerts an additional function during mating and filamentation. Intriguingly, yeast two-hybrid and epistasis experiments suggest that both Pdc1 and Rho1 could be constituents of the same regulatory cascade(s) controlling cell growth and filamentation in U. maydis. Overexpression of rho1 ameliorated the defects of cells depleted for Pdc1. Furthermore, we found that another small G protein, Rac1, was a suppressor of lethality for both Pdc1 and Rho1. In addition, deletion of cla4, encoding a Rac1 effector kinase, could also rescue cells with Pdc1 depleted. Inferring from these data, we propose a model for Rho1 and Pdc1 functions in U. maydis.

* Corresponding author. Mailing address: Department of Biology, Program on Disease Evolution, University of Louisville, Louisville, KY 40292. Phone: (502) 852-5944. Fax: (502) 852-0725. E-mail: mhperl01{at}gwise.louisville.edu

{triangledown} Published ahead of print on 1 May 2009.

{dagger} Supplemental material for this article may be found at http://ec.asm.org/.

{ddagger} Present address: Neuroprotection Research Laboratory, Departments of Neurology and Radiology, Massachusetts General Hospital, and Program in Neuroscience, Harvard Medical School, Boston, Massachusetts.

Eukaryotic Cell, July 2009, p. 977-989, Vol. 8, No. 7
1535-9778/09/$08.00+0     doi:10.1128/EC.00009-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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