Submitted to: Mycologia
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 23, 2004
Publication Date: September 1, 2004
Citation: Glenn, A.E., Richardson, E.A., Bacon, C.W. 2004. Genetic and morphological characterization of a Fusarium verticillioides conidiation mutant. Mycologia. 96(5): 968-980. Interpretive Summary: Asexual production of spores (a process called conidiation) by fungi that are pathogenic on plants is critical to their propagation, dispersal, and survival. Conidiation by the corn pathogen Fusarium verticillioides produces abundant, mostly single-celled asexual spores (called conidia) that are in distinctive long chains. These chains of spores are produced from specialized cells called phialides. Since conidia may be critical for establishing infections of corn plants, we have characterized a spontaneous F. verticillioides mutation that is incapable of producing conidia. Instead of the phialides producing conidia, the phialide apex of the mutant strain reinitiated growth. Microscopic examinations found that nuclei were rarely seen in this reinitiated growth, and its wall texture is distinctive from phialide and hyphal walls. The mutant lacked the cellular organization needed to produce conidia. Genetic analyses indicated that a single locus, designated FPH1, was responsible for the mutation. The spontaneous fph1 mutation arises only during certain sexual crosses involving normal conidiating parents. Data are presented clearly detailing how this fungus produces conidia, which will aid future efforts to identify genes involved in specific developmental stages of conidiation. Having such data may provide insight on how to prevent infection of corn by F. verticillioides.
Technical Abstract: Asexual spore production is critical to propagation, dispersal, and survival of most fungi. Enteroblastic phialidic conidiation by the corn pathogen Fusarium verticillioides produces abundant, mostly single-celled microconidia in distinctive long chains. Since conidia may be critical for establishing in planta associations, we have characterized a spontaneous F. verticillioides mutation in which phialides were incapable of producing conidia. Instead of enteroblastic conidiation, the phialide apex reinitiated determinate, convoluted, germ tube-like growth. Nuclei were rarely seen in this reinitiated growth, and its wall texture was distinctive from phialide and hyphal walls. Electron microscopic examinations showed this reinitiated growth to have a thick, rough, highly fibrilar outer wall layer that was continuous with the thinner and smoother outer wall layer of the phialide. The inner wall layer and plasma membrane were also continuous. The apical neck region of mutant phialides lacked both a thickened inner wall layer and a wall building zone, which are critical for conidium initial formation. The mutation did not prevent perithecium development and ascosporogenesis. Genetic analyses indicated that a single locus, designated FPH1, was responsible for the mutation. Sexual recombination data suggested FPH1 was linked (~9 map units) to a second locus (SIG1) controlling ascospore germination phenotypes. The fph1 mutation occurred only during certain sexual crosses involving wild type conidiating parents and then only in some perithecia and not others, all of which suggested the mutation may be meiotically induced, perhaps due to allelic mispairing and deletion events. This work more clearly details conidium ontogeny in this fungus and describes a unique mutation that will aid future efforts to identify genes involved in specific developmental stages of enteroblastic phialidic conidiation.