Zhong Xiaobo, Baur Sarah S M, Ongenae Veronique M A, Guerrero Egido Guillermo, Shitut Shraddha, Du Chao, Vijgenboom Erik, van Wezel Gilles P, Carrion Bravo Victor, Briegel Ariane, Bramkamp Marc, Claessen Dennis
Molecular Biotechnology, Institute of Biology, Leiden University, Leiden, The Netherlands.
Institute for General Microbiology, Christian-Albrechts-University of Kiel, Kiel, Germany.
Nat Commun. 2025 Mar 18;16(1):2669. doi: 10.1038/s41467-025-58093-x.
The cell wall represents an essential structure conserved among most bacteria, playing a crucial role in growth and development. While extensively studied model bacteria have provided insights into cell wall synthesis coordination, the mechanism governing polar growth in actinobacteria remains enigmatic. Here we identify the stomatin-like protein StlP as a pivotal factor for orchestrating polar growth in filamentous actinobacteria under hyperosmotic stress. StlP facilitates the establishment of a membrane microdomain with increased membrane fluidity, a process crucial for maintaining proper growth. The absence of StlP leads to branching of filaments, aberrant cell wall synthesis, thinning of the cell wall, and the extrusion of cell wall-deficient cells at hyphal tips. StlP interacts with key components of the apical glycan synthesis machinery, providing protection to filaments during apical growth. Introduction of StlP in actinobacteria lacking this protein enhances polar growth and resilience under hyperosmotic stress, accompanied by the formation of a membrane microdomain. Our findings imply that stomatin-like proteins, exemplified by StlP, confer a competitive advantage to actinobacteria encountering hyperosmotic stress. Given the widespread conservation of StlP in filamentous actinobacteria, our results propose that the mediation of polar growth through membrane microdomain formation is a conserved phenomenon in these bacteria.
细胞壁是大多数细菌共有的一种基本结构，在生长和发育中起着关键作用。虽然广泛研究的模式细菌为细胞壁合成协调提供了见解，但放线菌中控制极性生长的机制仍然不明。在这里，我们确定类stomatin蛋白StlP是在高渗胁迫下协调丝状放线菌极性生长的关键因素。StlP促进了膜流动性增加的膜微区的形成，这一过程对于维持正常生长至关重要。缺乏StlP会导致细丝分支、异常的细胞壁合成、细胞壁变薄以及在菌丝顶端挤出细胞壁缺陷细胞。StlP与顶端聚糖合成机制的关键成分相互作用，在顶端生长期间为细丝提供保护。在缺乏这种蛋白质的放线菌中引入StlP可增强高渗胁迫下的极性生长和恢复力，并伴随着膜微区的形成。我们的研究结果表明，以StlP为代表的类stomatin蛋白赋予了遇到高渗胁迫的放线菌竞争优势。鉴于StlP在丝状放线菌中广泛保守，我们的结果表明通过膜微区形成介导极性生长在这些细菌中是一种保守现象。
