Evolution of the pathogenic mold on high copper levels identifies novel resistance genes.

is the leading cause of severe mold infections in immunocompromised patients. This common fungus possesses innate attributes that allow it to evade the immune system, including its ability to survive the high copper (Cu) levels in phagosomes. Our previous work has revealed that under high Cu levels, the transcription factor AceA is activated, inducing the expression of the copper exporter CrpA to expel excess Cu.

Cytosolic pH Controls Fungal MAPK Signaling and Pathogenicity.

Mitogen-activated protein kinases (MAPKs) regulate a variety of cellular processes in eukaryotes. In fungal pathogens, conserved MAPK pathways control key virulence functions such as infection-related development, invasive hyphal growth, or cell wall remodeling. Recent findings suggest that ambient pH acts as a key regulator of MAPK-mediated pathogenicity, but the underlying molecular events are unknown.

Casein Kinase 1, a Negative Regulator of the Plasma Membrane H-ATPase Pma1, Is Required for Development and Pathogenicity.

Like many hemibiotrophic plant pathogens, the root-infecting vascular wilt fungus induces an increase in the pH of the surrounding host tissue. How alkalinization promotes fungal infection is not fully understood, but recent studies point towards the role of cytosolic pH (pH) and mitogen-activated protein kinase (MAPK) signaling. In fungi, pH is mainly controlled by the essential plasma membrane H-ATPase Pma1.