Dataset Information

The puzzling construction of the conidial outer layer of Aspergillus fumigatus

ABSTRACT: The outer layers of the fungal cell wall are the first barrier facing external challenges. In theinvasive morphotype of the airborne pathogen Aspergillus fumigatus, i.e. conidia, the outer cell wall consists of α-(1,3)-glucan, melanin and proteinaceous rodlets made up by the RodA hydrophobin. The hydrophobicity of the RodA rodlets facilitates air dispersal of conidia and progression within lungs. When conidia reach the alveolae, these are phagocytosed by host cells and killed upon germination, which requires melanin and rodlets elimination to occur. The dormant condition of the conidia protects them against activation of the host killing pathways. The outer cell wall of conidia is thus essential for maintaining the viability of the fungus. To study the role of α-(1,3)-glucan, melanin, and RodA rodlets in conidia protection, multiple mutants without two or the three major components of the outer layer were constructed and analyzed. Deletions led to the exposure of new molecules on the conidial surface. Multiple gene deletions did not always lead to logical additivity of the phenotypes. Unexpected compensatory cell wall surface modifications were indeed observed, such as the synthesis of the mycelial virulence factor galactosaminogalactan, the presence of chitin and glycoproteins or specific changes in permeability. In spite of significant modifications, sensitivity to killing by phagocytic host cells of the multiple mutants involving melanin changed little compared to the sensitive parent strain lacking melanin (ΔpksP), further indicating the importance of melanin in protecting conidia against killing by monocytes.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Aspergillus Fumigatus Cea10

DISEASE(S): Fungal Infectious Disease

SUBMITTER: Magalie Duchateau

LAB HEAD: Jean-Paul Latgé

PROVIDER: PXD011734 | Pride | 2019-01-30

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	20161205_Q1_MD_colQ1-31_Mat_Beauvais_A2.raw	Raw
	20161205_Q1_MD_colQ1-31_Mat_Beauvais_AP2.raw	Raw
	20161205_Q1_MD_colQ1-31_Mat_Beauvais_KU2.raw	Raw
	20161205_Q1_MD_colQ1-31_Mat_Beauvais_P2.raw	Raw
	20161205_Q1_MD_colQ1-31_Mat_Beauvais_RodAp.raw	Raw

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The puzzling construction of the conidial outer layer of Aspergillus fumigatus.

Valsecchi Isabel I Dupres Vincent V Michel Jean-Philippe JP Duchateau Magalie M Matondo Mariette M Chamilos Georgios G Saveanu Cosmin C Guijarro J Iñaki JI Aimanianda Vishukumar V Lafont Frank F Latgé Jean-Paul JP Beauvais Anne A

Cellular microbiology 20190118 5

If the mycelium of Aspergillus fumigatus is very short-lived in the laboratory, conidia can survive for years. This survival capacity and extreme resistance to environmental insults is a major biological characteristic of this fungal species. Moreover, conidia, which easily reach the host alveola, are the infective propagules. Earlier studies have shown the role of some molecules of the outer conidial layer in protecting the fungus against the host defense. The outer layer of the conidial cell w ...[more]

PMID: 30552790

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Project description:A. flavus keratitis is one of the predominant fungal infections affecting the tropical parts of the world. Melanin is a virulence factor in numerous pathogenic fungi and the melanin layer maintains the cell wall structure and provides chemical and physical protection to the organism. However, the molecular and biological mechanisms modulating melanin-mediated host-pathogen interaction in A. flavus keratitis are not well understood. This work aimed to compare the morphology, surface proteome profile and virulence of melanized and non-melanized conidia of A. flavus. An environmental isolate and two clinical isolates were included in this study. L-DOPA melanin pathway-specific inhibitor kojic acid (KA) as used to prepare non-melanized conidia. Conidial surface proteins were extracted using 100% formic acid at 0 ºC and the extracted proteins were analyzed using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS PAGE). Formic acid extracts were analyzed in an Orbitrap Velos pro-mass spectrometer. Conidial surface morphology difference was examined using scanning electron microscopy (SEM). Furthermore, lactophenol and calcofluor staining were performed to check the morphology and staining efficiency of melanized conidia (MC) and non-melanized conidia (NMC). A Galleria mellonella insect model was used to examine the virulence efficiency of MC and NMC. Kojic acid treatment inhibited melanin synthesis in A. flavus and the conidial surface protein profile was significantly different in kojic acid-treated non-melanized conidia. Several cell wall-associated proteins and proteins responsible for oxidative stress, carbohydrate, and chitin metabolic pathway were found only in the formic acid extracts of NMC. SEM analysis showed the conidial surface morphology difference between the NMC and MC indicating the role of melanin in the structural integrity of the conidial cell wall. The levels of calcofluor staining efficiency were different, but there was no microscopic morphology difference in lactophenol cotton blue staining of MC and NMC. Evaluation of virulence of MC and NMC in G. mellonella model showed NMC was less virulent compared to MC . Our results showed that the integrity of the conidial surface is controlled by the melanin layer. The alteration in the surface protein profile indicated that many surface proteins are masked by the melanin layer and hence melanin can modulate the host response by preventing the exposure of fungal proteins to the host immune defense system. G. mellonella in vivo virulence assay also confirmed that the non-melanized conidia were susceptible to host defense as in other Aspergillus pathogens.