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In order to colonize the host and cause disease,Candida albicans must avoid being killed by host defense peptides. Previously, we determined that the regulatory protein Ssd1 governs antimicrobial peptide resistance inC. albicans . Here, we sought to identify additional genes whose products govern susceptibility to antimicrobial peptides. We discovered that abcr1 Δ/Δ mutant, like thessd1 Δ/Δ mutant, had increased susceptibility to the antimicrobial peptides, protamine, RP-1, and human β defensin-2. Homozygous deletion ofBCR1 in thessd1 Δ/Δ mutant did not result in a further increase in antimicrobial peptide susceptibility. Exposure of thebcr1 Δ/Δ andssd1 Δ/Δ mutants to RP-1 induced greater loss of mitochondrial membrane potential and increased plasma membrane permeability than with the control strains. Therefore, Bcr1 and Ssd1 govern antimicrobial peptide susceptibility and likely function in the same pathway. Furthermore,BCR1 mRNA expression was downregulated in thessd1 Δ/Δ mutant, and the forced expression ofBCR1 in thessd1 Δ/Δ mutant partially restored antimicrobial peptide resistance. These results suggest that Bcr1 functions downstream of Ssd1. Interestingly, overexpression of 11 known Bcr1 target genes in thebcr1 Δ/Δ mutant failed to restore antimicrobial peptide resistance, suggesting that other Bcr1 target genes are likely responsible for antimicrobial peptide resistance. Collectively, these results demonstrate that Bcr1 functions downstream of Ssd1 to govern antimicrobial peptide resistance by maintaining mitochondrial energetics and reducing membrane permeabilization.

Bcr1 Functions Downstream of Ssd1 To Mediate Antimicrobial Peptide Resistance in Candida albicans