Caracterizacion de factores especificos del programa de virulencia en Ustilago maydis
Author
Flor Parra, IgnacioAdvisor
Pérez Martín, JoséEntity
UAM. Departamento de Biología MolecularDate
2007-04-20Subjects
Genética vegetal-Tesis doctorales; Maíz- Genética-Tesis doctorales; Biología y Biomedicina / BiologíaNote
Tesis Doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Ciencias, Departamento de Biología Molecular. Fecha de lectura:20-04-2007Abstract
The dimorphic fungus Ustilago maydis is the causative agent of corn smut
desease. The process of plant invasion involves regulated growth and highly
organized morphological changes. Haploid cells (sporidia) of this fungus are
unicellular, and grow saprophytically by budding. The pathogenic form, the
filamentous dikaryon, is established after fusion of two sporidia that have to
harbor different alleles of the a and b mating type loci of U. maydis. The a locus
controls the cell fusion via a pheromone-receptor based system. Upon
pheromone stimulation cells arrest budding growth and start the formation of
conjugation tubes that are cell cycle arrested in the G2 phase. These mating
filaments are highly polaryzed structures that undergo directed tip growth
towards the pheromone source, followed by cell fusion and the formation of
dikaryotic hyphae. The subsequent steps in filament formation and pathogenic
development are controlled by the multiallelic b-locus that encodes two distinct
homeodomain transcription factors, bE and bW. A heterodimeric complex of the
two proteins is formed when they are derived from different alleles. The
dikaryon formed after the fusion of compatible sporidia is arrested in the G2
phase of the cell cycle. On the plant surface, filaments differentiate appressoria
and penetrate the cuticule. Finally, spores are generated and dispersed by air.
Spores will germinate and upon germination, meiosis takes place and pairs of
compatible haploid cells are generated.
In this work we have identified two new factors involved in pathogenic
development. Pcl7 is a cyclin of Cdk5 implicated in morphogenesis during
pathogenic development. Δpcl7 cells have defects on polarization during the
formation of the conjugative tube and the infective filament. Biz1 (b-dependent
zinc finger protein), is a transcriptional regulator that plays a pivotal role during
the infection process. Δbiz1 cells show a severe reduction in appressoria
formation and plant penetration. In biz1 mutants, when the hypha penetrates, its
pathogenic development is arrested directly after plant penetration. pcl7 is
upregulated by the induction of the amating type locus and both biz1 and pcl7
are induced via the bmating type locus. High levels of biz1 or pcl7 expression
induce highly polarized growth and a G2 cell cycle arrest supporting roles in
morphogenesis and cell cycle regulation.
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