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Cell Cycle and Morphogenesis Connections During the Formation of the Infective Filament in Ustilago maydis

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Morphogenesis and Pathogenicity in Fungi

Part of the book series: Topics in Current Genetics ((TCG,volume 22))

Abstract

Ustilago maydis is the causal agent of smut disease on corn plants. The infective process depends on the formation of a specific structure called infective filament consisting on a dikaryotic hyphae, which is required to penetrate the plant tissue. The formation of the infective filament in U. maydis is alike to a germination process, although it requires an intermediate mating step that links sexual development and virulence. This way, the induction of the pathogenic program implies strong morphological changes (bud to hypha transition) as well as genetic changes (haploid to dikaryotic transition). As a consequence, an accurate control of the cell cycle as well as morphogenesis is predicted during these transitions: the induction of the infective filament relies on a dual process that involves by one side a specific cell cycle arrest and in other side the specific activation of a hyperpolarization growth. Impairment of any of these processes will have as an outcome the inhibition of the virulence. This review has been framed in three major points: (1) Which transcriptional program is responsible for the induction of the infective filament formation, (2) How polar growth is regulated during the induction of the infective filament, and (3) Which mechanisms are responsible for cell cycle arrest during the infective filament formation.

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Acknowledgements

Our research was financially supported by the SIGNALPATH Marie Curie Research Training Network (MRTN-CT-2005-019277) and by grant BIO2008-04054 from the Spanish Ministerio de Ciencia e Innovación (MICINN).

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Pérez-Martín, J. (2012). Cell Cycle and Morphogenesis Connections During the Formation of the Infective Filament in Ustilago maydis . In: Pérez-Martín, J., Di Pietro, A. (eds) Morphogenesis and Pathogenicity in Fungi. Topics in Current Genetics, vol 22. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-22916-9_6

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