| The causative agent of histoplasmosis, the dimorphic fungus Histoplasma capsulatum, is an organism that is endemic to a large part of the United States, as well as other parts of the world, such as Africa and South America. Although it poses no significant concern to healthy individuals, H. capsulatum is a serious health risk to the elderly and immune-compromised populations. Despite an increasing rise in the number of individuals infected with this disease, little is known about the pathogenesis of this organism.;In this study, we will seek insight on the possible roles of H. capsulatum veA (velvet gene). veA is a gene that provides an interesting possible target for a control strategy, as this gene is unique to fungi and is also conserved across many fungal species, particularly Ascomycetes. Previous studies carried out with the model filamentous fungus Aspergillus nidulans indicate that veA is as a global regulator, governing asexual/sexual development and secondary metabolite production. Aspergillus veA deletion mutants are unable to produce fruiting bodies (called cleistothecia), while they hyperconidiate. These mutants are also unable to synthesize numerous natural products. In this study, the similarities of the roles of A. nidulans and H. capsulatum veA homologs were investigated. This was accomplished through complementation of an A. nidulans deletion veA mutant with the H. capsulatum veA homolog. These results show that the H. capsulatum veA gene was able to partially rescue the capacity to produce fruiting bodies in the A. nidulans deletion veA. The H. capsulatum veA homolog was also able to recover the production of the sterigmatocystin toxin in this organism, but only at low levels. This study suggests that although there are certain functional similarities between A. nidulans and H.capsulatum veA homologs, some aspects of their regulatory output are not identical, particularly in the regulation of secondary metabolism. |
