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Candida albicans Biofilm-Defective Mutants

机译:白色念珠菌生物膜缺陷突变体

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Biofilm formation plays a key role in the life cycles and subsistence of many microorganisms. For the human fungal pathogen Candida albicans, biofilm development is arguably a virulence trait, because medical implants that serve as biofilm substrates are significant risk factors for infection. The development of C. albicans biofilms in vitro proceeds through an early phase, in which yeast cells populate a substrate, an intermediate phase, in which pseudohyphal and hyphal cell types are produced, and a maturation phase, in which continued cell growth is accompanied by accumulation of an extracellular matrix. Here we report the results of a screen for C. albicans biofilm-defective mutants, in which homozygous insertions in NUP85, MDS3, KEM1, and SUV3 were found to block biofilm development. Confocal microscopic examination suggests that nup85, suv3, and mds3 mutations cause early-phase arrest, whereas the kem1 mutation causes intermediate-phase arrest. All of the mutants are defective in hypha production in several media. Analysis of mixed-biofilm development indicates that all of the mutants are defective in the production of hyphae in the context of a biofilm. Because all of the mutants are defective in the retention of cells in the biofilm, we infer that hyphae provide an adherent scaffold that stabilizes the biofilm structure.
机译:生物膜的形成在许多微生物的生命周期和生存中起着关键作用。对于人类真菌病原体 Candida albicans ,生物膜的发展可以说是一种毒性特征,因为充当生物膜底物的医用植入物是感染的重要危险因素。 C的发展。在体外,白色念珠菌的生物膜发生在早期阶段,在该阶段中,酵母细胞构成了底物;在中间阶段,其中产生了假菌丝和菌丝类型的细胞;而在成熟阶段,细胞继续生长并伴随着积累细胞外基质。在这里,我们报告 C屏幕的结果。白色念珠菌生物膜缺陷型突变体,其中 NUP85 MDS3 KEM1 SUV3 被发现阻止生物膜的发育。共聚焦显微镜检查表明, nup85 suv3 mds3 突变引起早期停滞,而 kem1 突变引起中间相停滞。所有突变体在几种培养基中的菌丝产生均存在缺陷。混合生物膜发育的分析表明,在生物膜的情况下,所有突变体在菌丝的产生中都是有缺陷的。由于所有突变体在生物膜中的细胞保留方面均存在缺陷,因此我们推断,菌丝提供了稳定生物膜结构的粘附支架。

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