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初次宿主寄生后超小外共生菌TM7x和宿主细菌的转录活性。

Ultrasmall epibiont strain TM7x and host bacteria transcriptional activity after initial host parasitism.

作者信息

Hendrickson Erik L, Bor Batbileg, Kerns Kristopher A, Cen Lujia, Shi Wenyuan, He Xuesong, McLean Jeffrey S

机构信息

Department of Periodontics, University of Washington, Seattle, WA, USA.

Department of Microbiology, The Forsyth Institute, Cambridge, MA, USA.

出版信息

J Oral Microbiol. 2023 Nov 30;16(1):2287349. doi: 10.1080/20002297.2023.2287349. eCollection 2024.

DOI:10.1080/20002297.2023.2287349
PMID:38188073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10768705/
Abstract

BACKGROUND

Oral Saccharibacteria strain TM7× lives as an ultrasmall epibiont on the surface of its host, strain XH001. Establishing this interaction is a poorly understood multi-step process. The recovery phase marks a shift in the TM7×/host interaction, switching from the early killing phase, with extensive host cell death, to a stable symbiosis phase where the host and epibiont can grow together.

RESULTS

Transcriptomes of TM7× and host, XH001, were captured during the recovery phase and compared to uninfected host and the early host/epibiont interaction (initial encounter). XH001 showed increased expression for rhamnose cell wall components and for the precursor to peptidoglycan while TM7× showed increases in the peptidoglycan pathway. Transporter expression was generally increased for both organisms during recovery compared to the initial encounter, though, XH001 showed lower amino acid transporter expression. Consistent with host parasitism, XH001 showed increased expression of various stress-related genes during recovery while TM7× showed reduced stress. TM7× displayed higher expression of type IV pili, consistent with increased attachment to new hosts.

CONCLUSION

As TM7× is a member of the broadly distributed Candidate Phyla Radiation with small genomes lacking numerous biosynthetic pathways, this study provides further insights into how these epibionts interact and modulate their host bacteria.

摘要

背景

口腔糖菌属菌株TM7×作为一种超小的体表共生菌生活在其宿主XH001菌株的表面。建立这种相互作用是一个尚不清楚的多步骤过程。恢复期标志着TM7×/宿主相互作用的转变,从早期导致大量宿主细胞死亡的杀伤阶段,转变为宿主和体表共生菌可以共同生长的稳定共生阶段。

结果

在恢复期获取了TM7×和宿主XH001的转录组,并与未感染的宿主以及宿主/体表共生菌的早期相互作用(初次相遇)进行了比较。XH001的鼠李糖细胞壁成分和肽聚糖前体的表达增加,而TM7×的肽聚糖途径表达增加。与初次相遇相比,恢复期两种生物体的转运蛋白表达普遍增加,不过,XH001的氨基酸转运蛋白表达较低。与宿主寄生现象一致,XH001在恢复期各种应激相关基因的表达增加,而TM7×的应激反应降低。TM7×的IV型菌毛表达较高,这与对新宿主的附着增加一致。

结论

由于TM7×是广泛分布的候选门辐射成员,基因组较小,缺乏许多生物合成途径,本研究进一步深入了解了这些体表共生菌如何与宿主细菌相互作用并对其进行调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/10768705/cfeac062f37e/ZJOM_A_2287349_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/10768705/124f8ffdaa82/ZJOM_A_2287349_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/10768705/1743765681a6/ZJOM_A_2287349_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/10768705/8383efcd261f/ZJOM_A_2287349_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/10768705/29c7beaf2198/ZJOM_A_2287349_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/10768705/65885e9c6286/ZJOM_A_2287349_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/10768705/cfeac062f37e/ZJOM_A_2287349_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/10768705/124f8ffdaa82/ZJOM_A_2287349_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/10768705/1743765681a6/ZJOM_A_2287349_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/10768705/8383efcd261f/ZJOM_A_2287349_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/10768705/29c7beaf2198/ZJOM_A_2287349_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/10768705/65885e9c6286/ZJOM_A_2287349_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/10768705/cfeac062f37e/ZJOM_A_2287349_F0006_OC.jpg

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