BSC2 induces multidrug resistance via contributing to the formation of biofilm in Saccharomyces cerevisiae

IF 2.6 2区生物学 Q3 CELL BIOLOGY

Cellular Microbiology Pub Date : 2021-09-05 DOI:10.1111/cmi.13391

Zhiwei Huang, Hongsheng Dai, Xiaoyu Zhang, Qiao Wang, Jing Sun, Yunxia Deng, Ping Shi

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引用次数: 1

Abstract

Biofilm plays an important role in fungal multidrug resistance (MDR). Our previous studies showed that BSC2 is involved in resistance to amphotericin B (AMB) through antioxidation in Saccharomyces cerevisiae. In this study, the overexpression of BSC2 and IRC23 induced strong MDR in S. cerevisiae. BSC2-overexpression affected cellular flocculation, cell surface hydrophobicity, biofilm formation and invasive growth. However, it failed to induce caspofungin (CAS) resistance and affect the invasive growth in FLO mutant strains (FLO11Δ, FLO1Δ, FLO8Δ and TUP1Δ). Furthermore, the overexpression of BSC2 compensated for chitin synthesis defects to maintain the cell wall integrity and significantly reduced the cell morphology abnormality induced by CAS. However, it could not repair the cell wall damage caused by CAS in the FLO mutant strains. Although BSC2 overexpression increased the level of mannose in the cell wall, DPM1 overexpression in both BY4741 and bsc2∆ could confer resistance to CAS and AMB. In addition, BSC2 overexpression significantly increased the mRNA expression of FLO11, FLO1, FLO8 and TUP1. BSC2 may function as a regulator of FLO genes and be involved in cell wall integrity in yeast. Taken together, our data demonstrate that BSC2 induces MDR in a FLO pathway-dependent manner via contributing to the formation of biofilms in S. cerevisiae.

Take Aways

Overexpression of BSC2 induced strong MDR in S. cerevisiae.
BSC2 affected cellular flocculation, CSH, biofilm formation and invasive growth.
BSC2 could not repair the cell wall damage caused by CAS in the FLO mutants.
BSC2 may function as a regulator of FLO genes to maintain cell wall integrity.
BSC2 promotes biofilm formation in a FLO pathway-dependent manner to induce MDR.

Abstract Image

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BSC2通过促进酿酒酵母生物膜的形成诱导多药耐药

生物膜在真菌耐多药(MDR)过程中起着重要作用。我们之前的研究表明BSC2通过抗氧化参与酿酒酵母对两性霉素B (AMB)的抗性。在本研究中，BSC2和IRC23的过表达诱导了酿酒葡萄球菌的强耐药。bsc2过表达影响细胞絮凝、细胞表面疏水性、生物膜形成和侵袭性生长。但在FLO突变株(FLO11Δ， FLO1Δ， FLO8Δ和TUP1Δ)中未能诱导caspofungin (CAS)抗性并影响其侵袭性生长。此外，BSC2的过表达弥补了几丁质合成缺陷，维持了细胞壁的完整性，并显著降低了CAS诱导的细胞形态异常。然而，在FLO突变株中，它不能修复CAS引起的细胞壁损伤。虽然BSC2过表达增加了细胞壁中甘露糖的水平，但DPM1过表达在BY4741和BSC2∆中都能赋予对CAS和AMB的抗性。此外，BSC2过表达显著增加了FLO11、FLO1、FLO8和TUP1的mRNA表达。BSC2可能作为FLO基因的调节因子，参与酵母细胞壁的完整性。综上所述，我们的数据表明，BSC2通过促进酿酒葡萄球菌生物膜的形成，以FLO途径依赖的方式诱导MDR。过度表达BSC2可诱导酿酒葡萄球菌产生强耐多药。BSC2影响细胞絮凝、CSH、生物膜形成和侵袭性生长。在FLO突变体中，BSC2不能修复CAS引起的细胞壁损伤。BSC2可能作为FLO基因的调节剂来维持细胞壁的完整性。BSC2以依赖于FLO通路的方式促进生物膜的形成，从而诱导MDR。

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来源期刊

Cellular Microbiology 生物-微生物学

CiteScore

9.70

自引率

0.00%

发文量

审稿时长

3 months

期刊介绍： Cellular Microbiology aims to publish outstanding contributions to the understanding of interactions between microbes, prokaryotes and eukaryotes, and their host in the context of pathogenic or mutualistic relationships, including co-infections and microbiota. We welcome studies on single cells, animals and plants, and encourage the use of model hosts and organoid cultures. Submission on cell and molecular biological aspects of microbes, such as their intracellular organization or the establishment and maintenance of their architecture in relation to virulence and pathogenicity are also encouraged. Contributions must provide mechanistic insights supported by quantitative data obtained through imaging, cellular, biochemical, structural or genetic approaches.