ECE1 and fungal infectious disease: To determine whether processing of Ece1p at Arg61 and Arg93 was required for successful fungal infection in vivo, we challenged immunosuppressed WT mice with positive-control strains (WT and ece1Δ/Δ+ECE1), negative-control strains (ece1Δ/Δ), and selected alanine substitution mutants (R61A + R93A and ALL KA) and quantified fungal burdens in tongue tissue after 24 or 48 h.