A conserved fungal morphogenetic kinase regulates pathogenic growth in response to carbon source diversity

Adela Martin-Vicente, Ana Camila Oliveira Souza, Xabier Guruceaga, Harrison I. Thorn, Jinhong Xie, Ashley V. Nywening, Wenbo Ge and Jarrod R. Fortwendel ()
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Adela Martin-Vicente: University of Tennessee Health Science Center
Ana Camila Oliveira Souza: St Jude Children’s Research Hospital
Xabier Guruceaga: University of Tennessee Health Science Center
Harrison I. Thorn: University of Tennessee Health Science Center
Jinhong Xie: University of Tennessee Health Science Center
Ashley V. Nywening: University of Tennessee Health Science Center
Wenbo Ge: St Jude Children’s Research Hospital
Jarrod R. Fortwendel: University of Tennessee Health Science Center

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract Fungal pathogens must exhibit strong nutritional plasticity, effectively sensing and utilizing diverse nutrients to support virulence. How the signals generated by nutritional sensing are efficiently translated to the morphogenetic machinery for optimal growth and support of virulence remains incompletely understood. Here, we show that the conserved morphogenesis-related kinase, CotA, imparts isoform-specific control over Aspergillus fumigatus invasive growth in host-mimicking environments and during infection. CotA-mediated invasive growth is responsive to exogenous carbon source quality, with only preferred carbon sources supporting hyphal morphogenesis in a mutant lacking one of two identified protein isoforms. Strikingly, we find that the CotA protein does not regulate, nor is cotA gene expression regulated by, the carbon catabolite repression system. Instead, we show that CotA partially mediates invasive growth in specific carbon sources and virulence through the conserved downstream effector and translational repressor, SsdA. Therefore, A. fumigatus CotA accomplishes its conserved morphogenetic functions to drive pathogenic growth by translating host-relevant carbon source quality signals into morphogenetic outputs for efficient tissue invasive growth.

Date: 2024
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DOI: 10.1038/s41467-024-53358-3

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