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链霉菌 ylmE 突变体的孢子形成特异性细胞分裂缺陷可通过额外缺失 ylmD 来挽救。

Sporulation-specific cell division defects in ylmE mutants of Streptomyces coelicolor are rescued by additional deletion of ylmD.

机构信息

Molecular Biotechnology, Institute of Biology, Leiden University, Sylviusweg 72, 2333 BE, Leiden, The Netherlands.

Strathclyde Institute of Pharmacy and Biomedical Science, University of Strathclyde, 161 Cathedral Street, Glasgow, G4 0RE, United Kingdom.

出版信息

Sci Rep. 2018 May 9;8(1):7328. doi: 10.1038/s41598-018-25782-1.

DOI:10.1038/s41598-018-25782-1
PMID:29743540
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5943314/
Abstract

Cell division during the reproductive phase of the Streptomyces life-cycle requires tight coordination between synchronous formation of multiple septa and DNA segregation. One remarkable difference with most other bacterial systems is that cell division in Streptomyces is positively controlled by the recruitment of FtsZ by SsgB. Here we show that deletion of ylmD (SCO2081) or ylmE (SCO2080), which lie in operon with ftsZ in the dcw cluster of actinomycetes, has major consequences for sporulation-specific cell division in Streptomyces coelicolor. Electron and fluorescence microscopy demonstrated that ylmE mutants have a highly aberrant phenotype with defective septum synthesis, and produce very few spores with low viability and high heat sensitivity. FtsZ-ring formation was also highly disturbed in ylmE mutants. Deletion of ylmD had a far less severe effect on sporulation. Interestingly, the additional deletion of ylmD restored sporulation to the ylmE null mutant. YlmD and YlmE are not part of the divisome, but instead localize diffusely in aerial hyphae, with differential intensity throughout the sporogenic part of the hyphae. Taken together, our work reveals a function for YlmD and YlmE in the control of sporulation-specific cell division in S. coelicolor, whereby the presence of YlmD alone results in major developmental defects.

摘要

在链霉菌生命周期的繁殖阶段,细胞分裂需要多个隔膜的同步形成和 DNA 分离之间的紧密协调。与大多数其他细菌系统的一个显著区别是,链霉菌的细胞分裂是由 SsgB 招募 FtsZ 正向控制的。在这里,我们表明,删除 ylmD(SCO2081)或 ylmE(SCO2080),它们在放线菌的 dcw 簇中的 ftsZ 操纵子中,对链霉菌色氨酸的孢子特异性细胞分裂有重大影响。电子和荧光显微镜显示,ylmE 突变体具有高度异常的表型,隔膜合成缺陷,并产生很少的孢子,活力低,耐热性高。ylmE 突变体中的 FtsZ 环形成也受到高度干扰。删除 ylmD 对孢子形成的影响要小得多。有趣的是,ylmD 的额外缺失恢复了 ylmE 缺失突变体的孢子形成。YlmD 和 YlmE 不是分裂体的一部分,而是在气生菌丝中弥散定位,在菌丝的产孢部分强度不同。总之,我们的工作揭示了 YlmD 和 YlmE 在链霉菌色氨酸中控制孢子特异性细胞分裂的功能,其中仅存在 YlmD 会导致主要的发育缺陷。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/ddf5ca87ef4b/41598_2018_25782_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/a17cf7c6ed27/41598_2018_25782_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/9621d9bd896b/41598_2018_25782_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/4764b0b8cc96/41598_2018_25782_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/3a9ae84ec4a2/41598_2018_25782_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/920300cb92ac/41598_2018_25782_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/1db115ad7656/41598_2018_25782_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/ddf5ca87ef4b/41598_2018_25782_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/a17cf7c6ed27/41598_2018_25782_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/9621d9bd896b/41598_2018_25782_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/4764b0b8cc96/41598_2018_25782_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/3a9ae84ec4a2/41598_2018_25782_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/920300cb92ac/41598_2018_25782_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/1db115ad7656/41598_2018_25782_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7d7/5943314/ddf5ca87ef4b/41598_2018_25782_Fig7_HTML.jpg

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