Deletion of CDR1 reveals redox regulation of pleiotropic drug resistance in Candida glabrata.

摘要: Abstract Microbial cells sense the presence of xenobiotics and, in response, upregulate genes involved pleiotropic drug resistance (PDR). In yeast, PDR activation to a major extent relies on transcription factor Pdr1. addition, many induce oxidative stress, which may independently Pdr1 activity. Mitochondria are important sources reactive oxygen species under stressful conditions. To evaluate relevance this redox pathway, we studied yeast Candida glabrata, treated with mitochondrially targeted antioxidant plastoquinonyl-decyl-triphenylphosphonium and dodecyltriphenylphosphonium (C12TPP) as control. We found that both compounds induced decreased intracellular concentration transporter substrate Nile red. Interestingly, deletion gene CDR1 inhibited decrease red accumulation by but not C12TPP. Moreover, alpha-tocopherol C12TPP-mediated Δcdr1 wild-type strain. Furthermore, pre-incubation low concentrations hydrogen peroxide Δpdr1 well control cells. Deletion PDR1 C12TPP-induced FLR1, is redox-regulated gene. It appears disruption PDR1/CDR1 regulatory circuit makes auxiliary regulation mechanisms crucial. Our data suggest dispensable because redundancy pathways, manifested upon CDR1.