Rozner Marlena, Nukarinen Ella, Wolfinger Michael T, Amman Fabian, Weckwerth Wolfram, Bläsi Udo, Sonnleitner Elisabeth
Department of Microbiology, Immunobiology and Genetics, Max Perutz Labs, Vienna Biocenter (VBC), University of Vienna, Vienna, Austria.
Molecular Systems Biology, Department of Functional and Evolutionary Ecology, Faculty of Life Sciences, University of Vienna, Vienna, Austria.
Front Microbiol. 2022 Jun 23;13:919539. doi: 10.3389/fmicb.2022.919539. eCollection 2022.
In , the RNA chaperone Hfq and the catabolite repression protein Crc act in concert to regulate numerous genes during carbon catabolite repression (CCR). After alleviation of CCR, the RNA CrcZ sequesters Hfq/Crc, which leads to a rewiring of gene expression to ensure the consumption of less preferred carbon and nitrogen sources. Here, we performed a multiomics approach by assessing the transcriptome, translatome, and proteome in parallel in strain O1 during and after relief of CCR. As Hfq function is impeded by the RNA CrcZ upon relief of CCR, and Hfq is known to impact antibiotic susceptibility in , emphasis was laid on links between CCR and antibiotic susceptibility. To this end, we show that the operon encoding an efflux pump for the antibiotic norfloxacin and the virulence factor 5-Methyl-phenazine is upregulated after alleviation of CCR, resulting in a decreased susceptibility to the antibiotic norfloxacin. A model for indirect regulation of the operon by Hfq is presented.
在[具体情况未提及处]，RNA伴侣蛋白Hfq和分解代谢物阻遏蛋白Crc协同作用，在碳分解代谢物阻遏（CCR）过程中调控众多基因。CCR解除后，RNA CrcZ隔离Hfq/Crc，这导致基因表达重新布线，以确保消耗较不偏好的碳源和氮源。在此，我们通过在CCR解除期间和之后并行评估菌株O1的转录组、翻译组和蛋白质组，采用了多组学方法。由于CCR解除后RNA CrcZ会阻碍Hfq的功能，且已知Hfq会影响[具体情况未提及处]的抗生素敏感性，因此重点关注CCR与抗生素敏感性之间的联系。为此，我们表明，编码抗生素诺氟沙星外排泵和毒力因子5-甲基吩嗪的[具体操纵子未提及处]操纵子在CCR解除后上调，导致对抗生素诺氟沙星的敏感性降低。我们提出了一个Hfq对[具体操纵子未提及处]操纵子进行间接调控的模型。
