Fig 1.
Modulation of host pH by the phytopathogen Colletotrichum gloeosporioides increases fungal virulence.
C. gloeosporioides infects the tomato fruit in a process initiated upon attachment of the fungal conidia to the plant surface. During the quiescent stage of infection, fruit physiological factors such as nutrient availability, acidic pH, and surface waxes determine the rate of fungal growth and germination. As the fruit ripens, conidia germinate into a specialized structure, named appressorium, which eventually becomes melanized. Melanin alters the permeability of the plant cell wall, creating a hypertonic environment that allows the fungus to penetrate the host epidermis using turgor pressure. This process is accompanied by active metabolism of amino acids, such as glutamate and glutamine, and gradual environmental alkalization. The fungus transitions into the necrotrophic stage, characterized by a dramatic shift in fungal metabolism and activation of pathogenicity factors, such as proteases and lyases, resulting in anthracnose fruit rot.
Fig 2.
Neutralization of the macrophage phagosome by the fungal pathogen C. albicans is essential for host damage.
Upon phagocytosis by the macrophages, C. albicans responds to the presence of amino acids and other alternative carbon sources abundant in the phagosomal milieu. Amino acids (AA) in particular are sensed via the SPS sensor system (orange), leading to activation of the transcription factor Stp2p, which induces the expression of genes encoding for amino acid permeases (green rectangles) and ammonium transporters (purple rectangles). This results in uptake of amino acids into and release of NH4+ from the fungal cell and increase of phagosomal pH. Hyphal growth causes physical damage to the macrophage membranes, leading to leakage of cellular content and death. C. albicans cells defective in utilization of amino acids and/or extrusion of NH4+, such as the stp2Δ mutant, fail to modulate the pH of the phagosome and are readily cleared by the immune cells.