Transcriptional and translational mechanisms of starvation priming in Staphylococcus aureus increase tolerance to oxidative and electrophile stress (C08)

金黄色葡萄球菌饥饿引发的转录和翻译机制增加对氧化和亲电子应激的耐受性 (C08)

• 批准号: 358467443
• 金额: --
• 依托单位: Arbeitsgruppe Strukturbiochemie
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2017
• 资助国家: 德国
• 起止时间: 2016-12-31 至 2020-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/358467443?language=en
• 关键词: Transcriptional; translational; mechanisms; starvation; priming

Staphylococcus aureus acquires non-specific tolerance to redox-active compounds and antibiotics during entry into stationary phase (“starvation priming”). We will study the stressor-specific transcriptional mechanisms (AldA, MerA, MhqR) and the role of non-specific stationary phase factors, such as (p)ppGpp and σB, in starvation priming. The role of transcription regulation in starvation priming will be investigated via functional and structural studies of RNA polymerase with interacting factors (e.g. DNA helicase HelD/HelIV and regulators of ribosomal RNA synthesis). We will elucidate the mechanisms, which promote redox stress and antibiotics tolerance of starved S. aureus.

金黄色葡萄球菌在进入稳定期期间获得对氧化还原活性化合物和抗生素的非特异性耐受性（“饥饿引发”）。我们将研究胁迫特异性转录机制（AldA、MerA、MhqR）和非特异性稳定期因子（如（p）ppGpp和σB）在饥饿引发中的作用。转录调控在饥饿引发中的作用将通过RNA聚合酶与相互作用因子（例如DNA解旋酶HelD/HelIV和核糖体RNA合成的调节剂）的功能和结构研究来研究。我们将阐明饥饿促进氧化还原应激和抗生素耐受的机制。金黄色。