Author
TSAI, H - NIH | |
CHANG, Y - NIH | |
WASHBURN, R - WAKE FOREST UNIVERSITY | |
Wheeler, Michael - Mike | |
KWON-CHUNG, K - WAKE FOREST UNIVERSITY |
Submitted to: American Society for Microbiology
Publication Type: Abstract Only Publication Acceptance Date: 5/17/1998 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: Aspergillus fumigatus, an important opportunistic pathogen commonly affecting neutropenic patients, produces conidia with bluish-green pigment synthesized via the dihydroxynaphthalene (DHN)-melanin pathway. The fungus propagates by conidia which are the initial structures encountered by the human host. We have previously reported that the conidial pigmentation process in A. fumigatus might influence complement deposition on conidial surfaces. Deposition of complement components on conidia is believed to be a pivotal step for opsonophagocytosis. Here, we identified a gene, alb 1, which is required for conidial pigmentation. The alb 1 gene encodes a putative polyketide synthase and disruption of alb 1 results in an albino conidial phenotype. Expression of alb 1 is developmentally regulated and the 7 kb transcript is only detected during the conidiation stage. Scanning electron microscopy studies showed that the alb 1 disruptant exhibits a smooth conidial surface whereas complementation of the alb 1 deletion restored the echinulate wild-type surface. Furthermore, the alb 1 disruptant had a statistically significant loss in virulence compared to both the wild-type and alb 1 complemented strains in a murine model. These results suggest that disruption of alb 1 causes pleiotropic effects on conidial morphology, and that the conidial pigmentation process is likely to be an important virulence determinant for A. fumigatus. |