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The two-component sensor kinase TcsC and its role in stress resistance of the human-pathogenic mold Aspergillus fumigatus.

McCormick A, Jacobsen ID, Broniszewska M, Beck J, Heesemann J, Ebel F - PLoS ONE (2012)

Bottom Line: Both hyperosmotic stress and treatment with fludioxonil result in a TcsC-dependent phosphorylation of SakA, the final MAP kinase in the high osmolarity glycerol (HOG) pathway, confirming a role for TcsC in this signaling pathway.Several types of stress, such as hypoxia, exposure to farnesol or elevated concentrations of certain divalent cations, trigger a differentiation in A. fumigatus toward a "fluffy" growth phenotype resulting in white, dome-shaped colonies.Although TcsC plays a role in the adaptation of A. fumigatus to hypoxia, it seems to be dispensable for virulence.

View Article: PubMed Central - PubMed

Affiliation: Max-von-Pettenkofer-Institut, Ludwig-Maximilians-University, Munich, Germany.

ABSTRACT
Two-component signaling systems are widespread in bacteria, but also found in fungi. In this study, we have characterized TcsC, the only Group III two-component sensor kinase of Aspergillus fumigatus. TcsC is required for growth under hyperosmotic stress, but dispensable for normal growth, sporulation and conidial viability. A characteristic feature of the ΔtcsC mutant is its resistance to certain fungicides, like fludioxonil. Both hyperosmotic stress and treatment with fludioxonil result in a TcsC-dependent phosphorylation of SakA, the final MAP kinase in the high osmolarity glycerol (HOG) pathway, confirming a role for TcsC in this signaling pathway. In wild type cells fludioxonil induces a TcsC-dependent swelling and a complete, but reversible block of growth and cytokinesis. Several types of stress, such as hypoxia, exposure to farnesol or elevated concentrations of certain divalent cations, trigger a differentiation in A. fumigatus toward a "fluffy" growth phenotype resulting in white, dome-shaped colonies. The ΔtcsC mutant is clearly more susceptible to these morphogenetic changes suggesting that TcsC normally antagonizes this process. Although TcsC plays a role in the adaptation of A. fumigatus to hypoxia, it seems to be dispensable for virulence.

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Infection of immuno-compromized mice.Intranasal infection of cortisone-acetate treated mice infected with 1×106 conidia of the ΔtcsC mutant (n = 20), the parental strain AfS35 (n = 20) and the complemented strain (n = 20). Controls received PBS only. Survival of mice is shown over time.
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pone-0038262-g007: Infection of immuno-compromized mice.Intranasal infection of cortisone-acetate treated mice infected with 1×106 conidia of the ΔtcsC mutant (n = 20), the parental strain AfS35 (n = 20) and the complemented strain (n = 20). Controls received PBS only. Survival of mice is shown over time.

Mentions: The ability to respond to certain kinds of stress is clearly impaired in the ΔtcsC mutant. In order to investigate whether this negatively affects its virulence potential, cortisone-acetate treated mice were infected via the intra-nasal route. Survival of mice infected with the ΔtcsC mutant was comparable to those infected with the control strains (Figure 7) and the histological analysis of samples from the lungs of mice that succumbed to infection also revealed no apparent differences (data not shown). A normal virulence was furthermore observed in a alternative infection model using embryonated eggs [24](data not shown).


The two-component sensor kinase TcsC and its role in stress resistance of the human-pathogenic mold Aspergillus fumigatus.

McCormick A, Jacobsen ID, Broniszewska M, Beck J, Heesemann J, Ebel F - PLoS ONE (2012)

Infection of immuno-compromized mice.Intranasal infection of cortisone-acetate treated mice infected with 1×106 conidia of the ΔtcsC mutant (n = 20), the parental strain AfS35 (n = 20) and the complemented strain (n = 20). Controls received PBS only. Survival of mice is shown over time.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3366943&req=5

pone-0038262-g007: Infection of immuno-compromized mice.Intranasal infection of cortisone-acetate treated mice infected with 1×106 conidia of the ΔtcsC mutant (n = 20), the parental strain AfS35 (n = 20) and the complemented strain (n = 20). Controls received PBS only. Survival of mice is shown over time.
Mentions: The ability to respond to certain kinds of stress is clearly impaired in the ΔtcsC mutant. In order to investigate whether this negatively affects its virulence potential, cortisone-acetate treated mice were infected via the intra-nasal route. Survival of mice infected with the ΔtcsC mutant was comparable to those infected with the control strains (Figure 7) and the histological analysis of samples from the lungs of mice that succumbed to infection also revealed no apparent differences (data not shown). A normal virulence was furthermore observed in a alternative infection model using embryonated eggs [24](data not shown).

Bottom Line: Both hyperosmotic stress and treatment with fludioxonil result in a TcsC-dependent phosphorylation of SakA, the final MAP kinase in the high osmolarity glycerol (HOG) pathway, confirming a role for TcsC in this signaling pathway.Several types of stress, such as hypoxia, exposure to farnesol or elevated concentrations of certain divalent cations, trigger a differentiation in A. fumigatus toward a "fluffy" growth phenotype resulting in white, dome-shaped colonies.Although TcsC plays a role in the adaptation of A. fumigatus to hypoxia, it seems to be dispensable for virulence.

View Article: PubMed Central - PubMed

Affiliation: Max-von-Pettenkofer-Institut, Ludwig-Maximilians-University, Munich, Germany.

ABSTRACT
Two-component signaling systems are widespread in bacteria, but also found in fungi. In this study, we have characterized TcsC, the only Group III two-component sensor kinase of Aspergillus fumigatus. TcsC is required for growth under hyperosmotic stress, but dispensable for normal growth, sporulation and conidial viability. A characteristic feature of the ΔtcsC mutant is its resistance to certain fungicides, like fludioxonil. Both hyperosmotic stress and treatment with fludioxonil result in a TcsC-dependent phosphorylation of SakA, the final MAP kinase in the high osmolarity glycerol (HOG) pathway, confirming a role for TcsC in this signaling pathway. In wild type cells fludioxonil induces a TcsC-dependent swelling and a complete, but reversible block of growth and cytokinesis. Several types of stress, such as hypoxia, exposure to farnesol or elevated concentrations of certain divalent cations, trigger a differentiation in A. fumigatus toward a "fluffy" growth phenotype resulting in white, dome-shaped colonies. The ΔtcsC mutant is clearly more susceptible to these morphogenetic changes suggesting that TcsC normally antagonizes this process. Although TcsC plays a role in the adaptation of A. fumigatus to hypoxia, it seems to be dispensable for virulence.

Show MeSH
Related in: MedlinePlus