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SNARE蛋白同源物Syn8的缺失影响……的生物膜形成

The Lack of SNARE Protein Homolog Syn8 Influences Biofilm Formation of .

作者信息

Chen Xinyue, Iwatani Shun, Kitamoto Toshitaka, Chibana Hiroji, Kajiwara Susumu

机构信息

School of Life Sciences and Technology, Tokyo Institute of Technology, Yokohama, Japan.

School of Materials and Chemical Technology, Tokyo Institute of Technology, Yokohama, Japan.

出版信息

Front Cell Dev Biol. 2021 Feb 12;9:607188. doi: 10.3389/fcell.2021.607188. eCollection 2021.

DOI:10.3389/fcell.2021.607188
PMID:33644045
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7907433/
Abstract

Biofilm formation of species is considered to be a pathogenic factor of host infection. Since biofilm formation of has not been as well studied as that of , we performed genetic screening of , and three candidate genes associated with biofilm formation were identified. (CAGL0H06325g) was selected as the most induced gene in biofilm cells for further research. Our results indicated that the Δ mutant was defective not only in biofilm metabolic activity but also in biofilm morphological structure and biomass. Deletion of seemed to have no effect on extracellular matrix production, but it led to a notable decrease in adhesion ability during biofilm formation, which may be linked to the repression of two adhesin genes, and . Furthermore, hypersensitivity to hygromycin B and various ions in addition to the abnormal vacuolar morphology in the Δ mutant suggested that active vacuolar function is required for biofilm formation of . These findings enhance our understanding of biofilm formation in this fungus and provide information for the development of future clinical treatments.

摘要

某物种的生物膜形成被认为是宿主感染的致病因素。由于该物种生物膜形成的研究不如另一物种深入,我们对该物种进行了基因筛选,并鉴定出三个与生物膜形成相关的候选基因。(CAGL0H06325g)被选为生物膜细胞中诱导程度最高的基因进行进一步研究。我们的结果表明,Δ突变体不仅在生物膜代谢活性方面存在缺陷,而且在生物膜形态结构和生物量方面也存在缺陷。删除该基因似乎对细胞外基质的产生没有影响,但它导致生物膜形成过程中粘附能力显著下降,这可能与两个粘附素基因的抑制有关。此外,Δ突变体对潮霉素B和各种离子的超敏反应以及液泡形态异常表明,活跃的液泡功能是该物种生物膜形成所必需的。这些发现加深了我们对这种真菌生物膜形成的理解,并为未来临床治疗的发展提供了信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/2c10950f1b14/fcell-09-607188-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/b61ade05c474/fcell-09-607188-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/224f69236960/fcell-09-607188-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/5fd0a92da1c0/fcell-09-607188-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/4352a9a9ff93/fcell-09-607188-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/84a1ed94f29f/fcell-09-607188-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/40fbed323923/fcell-09-607188-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/2c10950f1b14/fcell-09-607188-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/b61ade05c474/fcell-09-607188-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/224f69236960/fcell-09-607188-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/5fd0a92da1c0/fcell-09-607188-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/4352a9a9ff93/fcell-09-607188-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/84a1ed94f29f/fcell-09-607188-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/40fbed323923/fcell-09-607188-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c11/7907433/2c10950f1b14/fcell-09-607188-g007.jpg

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