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ABSTRACTPenicillium marneffeiis an emerging human-pathogenic fungus endemic to Southeast Asia. Like a number of other fungal pathogens, P. marneffeiexhibits temperature-dependent dimorphic growth and grows in two distinct cellular morphologies, hyphae at 25°C and yeast cells at 37°C. Hyphae can differentiate to produce the infectious agents, asexual spores (conidia), which are inhaled into the host lung, where they are phagocytosed by pulmonary alveolar macrophages. Within macrophages, conidia germinate into unicellular yeast cells, which divide by fission. This minireview focuses on the current understanding of the genes required for the morphogenetic control of conidial germination, hyphal growth, asexual development, and yeast morphogenesis in P. marneffei.

Cytokinesis is essential for proliferative growth but also plays equally important roles during morphogenesis and development. The human pathogen Penicillium marneffei is capable of dimorphic switching in response to temperature, growing in a multicellular filamentous hyphal form at 25°C and in a unicellular yeast form at 37°C. P. marneffei also undergoes asexual development at 25°C to produce multicellular differentiated conidiophores. Thus, P. marneffei exhibits cell division with and without cytokinesis and division by budding and fission, depending on the cell type. The type II myosin gene, myoB, from P. marneffei plays important roles in the morphogenesis of these cell types. Deletion of myoB leads to chitin deposition defects at sites of cell division without perturbing actin localization. In addition to aberrant hyphal cells, distinct conidiophore cell types are lacking due to malformed septa and nuclear division defects. At 37°C, deletion of myoB prevents uninucleate yeast cell formation, instead producing long filaments resembling hyphae at 25°C. The ΔmyoB cells also often lyse due to defects in cell wall biogenesis. Thus, MyoB is essential for correct morphogenesis of all cell types regardless of division mode (budding or fission) and defines differences between the different types of growth.

ABSTRACTThe maize pathogen Ustilago maydisswitches from budding to filamentous, dikaryotic growth in response to environmental signals including nutrient status, growth in the host, and the presence of mating pheromones. The filamentous dikaryon is capable of proliferating within host tissue to cause disease symptoms including tumors. The transition from yeast cells to hyphal filaments is regulated by a mitogen-activated protein kinase cascade and a cyclic-AMP-protein kinase A (PKA) pathway. Serial analysis of gene expression with PKA mutants identified orthologs of components of the PHO phosphate acquisition pathway as transcriptional targets of the PKA pathway, and these included genes for Pho84, an acid phosphatase, and the vacuolar transport chaperones Vtc1 and Vtc4. In Saccharomyces cerevisiae, Vtc4p is required during the fusion of inorganic-phosphate-containing vesicles to the vacuolar membrane and the consequent accumulation of phosphate stored as polyphosphate (polyP) in the vacuole. We found that deletion of vtc4in U. maydisalso reduced polyP stored in vacuoles. Intriguingly, ?vtc4mutants possessed a filamentous cellular morphology, in contrast to the budding, yeast-like growth of the wild-type parent. The ?vtc4mutants also displayed decreased symptom development and reduced proliferation in planta. The interaction with PKA signaling was further investigated by the generation of ?vtc4 ubc1double mutants. Deletion of vtc4completely suppressed the multiple-budded phenotype of a ?ubc1mutant, indicating that polyP stores are essential for this PKA-induced trait. Overall, this study reveals a novel role for PKA-regulated polyP accumulation in the control of fungal morphogenesis and virulence.

ABSTRACTDuring maize infection, the fungal pathogen Ustilago maydisundergoes a dimorphic transition from budding, yeast-like cells to a filamentous dikaryon that proliferates in the host. This transition is regulated by mating and environmental signals. Septation is likely to be important in the growth of the infectious dikaryon because of the need to maintain specific cellular compartments during dikaryotic growth. Recently, we found that the transcript level for a septin gene was influenced by the conserved cyclic AMP (cAMP)/protein kinase A signaling pathway that participates in regulating dimorphism in U. maydis. In this study, we describe the detailed analysis of the function of this septin gene, designated sep3, in the growth, development, and pathogenesis of U. maydis. We show that sep3is required for normal cellular morphology and the division of budding haploid cells. The gene is also required for lipid-induced filamentous growth in culture but not during the formation of mating filaments on agar medium or in planta. Strains with a deletion in sep3have a reduction in symptom development in maize, with filamentous cells in planta displaying morphological defects. In addition, sep3influences the differentiation of hyphae into teliospores and the germination of these teliospores to produce the meiotic haploid progeny that complete the disease life cycle. Finally, the deletion of sep3was found to influence the multiple budding phenotype of a mutant with a defect in the regulatory subunit of protein kinase A. This result is consistent with a link between sep3and the control of morphogenesis by cAMP signaling. Overall, this study highlights the importance of regulating septation and changes in morphology during phytopathogenesis.