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铜绿微囊藻的自漂白过程被共生菌假单胞菌 MAE1-K 延迟,而蛋氨酸缺乏则促进了这一过程。

The Self-Bleaching Process of Microcystis aeruginosa is Delayed by a Symbiotic Bacterium Pseudomonas sp. MAE1-K and Promoted by Methionine Deficiency.

机构信息

Department of Life Science, Chung-Ang Universitygrid.254224.7, Seoul, Republic of Korea.

Department of Food Science and Biotechnology, CHA University, Pocheon, Gyeonggi-do, Republic of Korea.

出版信息

Microbiol Spectr. 2022 Aug 31;10(4):e0181422. doi: 10.1128/spectrum.01814-22. Epub 2022 Jun 30.

DOI:10.1128/spectrum.01814-22
PMID:35771009
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9430746/
Abstract

Various interactions between marine cyanobacteria and heterotrophic bacteria have been known, but the symbiotic relationships between and heterotrophic bacteria remain unclear. An axenic culture (NIES-298) was quickly bleached after exponential growth, whereas a xenic culture (KW) showed a normal growth curve, suggesting that some symbiotic bacteria may delay this bleaching. The bleaching process of was distinguished from the phenomena of previously proposed chlorosis and programmed cell death in various characteristics. Bleached cultures of NIES-298 quickly bleached actively growing cultures, suggesting that itself produces bleach-causing compounds. Pseudomonas sp. MAE1-K delaying the bleaching of NIES-298 cultures was isolated from the KW culture. Bleached cultures of NIES-298 treated with strain MAE1-K lost their bleaching ability, suggesting that strain MAE1-K rescues from bleaching via inactivation of bleaching compounds. From Tn5 transposon mutant screening, a mutant of strain MAE1-K (F-D3) unable to synthesize methionine, promoting the bleaching of NIES-298 cultures but capable of inactivating bleaching compounds, was obtained. The bleaching process of NIES-298 cultures was promoted with the coculture of mutant F-D3 and delayed by methionine supplementation, suggesting that the bleaching process of is promoted by methionine deficiency. Cyanobacterial blooms in freshwaters represent serious global concerns for the ecosystem and human health. In this study, we found that one of the major species in cyanobacterial blooms, Microcystis aeruginosa, was quickly collapsed after exponential growth by producing self-bleaching compounds and that a symbiotic bacterium, Pseudomonas sp. MAE1-K delayed the bleaching process via the inactivation of bleaching compounds. In addition, we found that a mutant of strain MAE1-K (F-D3) causing methionine deficiency promoted the bleaching process of , suggesting that methionine deficiency may induce the production of bleaching compounds. These results will provide insights into the symbiotic relationships between and heterotrophic bacteria that will contribute to developing novel strategies to control cyanobacterial blooms.

摘要

海洋蓝藻与异养细菌之间存在着多种相互作用,但蓝藻与异养细菌之间的共生关系尚不清楚。无菌培养的(NIES-298)在指数生长期后迅速变白,而共生培养的(KW)则显示出正常的生长曲线,这表明某些共生细菌可能会延迟这种白化现象。蓝藻的白化过程在各种特性上与先前提出的黄化和程序性细胞死亡现象不同。从快速生长的 NIES-298 培养物中分离出 Pseudomonas sp. MAE1-K 可以延迟 NIES-298 培养物的白化。用菌株 MAE1-K 处理的 NIES-298 漂白培养物失去了漂白能力,这表明菌株 MAE1-K 通过使漂白化合物失活来拯救 NIES-298 免于漂白。从 Tn5 转座子突变体筛选中,获得了一株不能合成蛋氨酸的 MAE1-K 突变株(F-D3),该突变株能够促进 NIES-298 培养物的白化,但能够使漂白化合物失活。与突变株 F-D3 的共培养促进了 NIES-298 培养物的白化过程,而蛋氨酸的补充则延迟了白化过程,这表明 中蓝藻的白化过程是由蛋氨酸缺乏引起的。淡水富营养化蓝藻水华对生态系统和人类健康构成了严重的全球威胁。在这项研究中,我们发现,蓝藻水华的主要物种之一铜绿微囊藻在指数生长期后通过产生自漂白化合物而迅速崩溃,共生细菌 Pseudomonas sp. MAE1-K 通过使漂白化合物失活来延迟漂白过程。此外,我们发现,一株 MAE1-K 菌株(F-D3)的突变株,由于蛋氨酸缺乏而导致的突变株,促进了 的白化过程,这表明蛋氨酸缺乏可能会诱导漂白化合物的产生。这些结果将为蓝藻与异养细菌之间的共生关系提供新的见解,这将有助于开发控制蓝藻水华的新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/a9253a802dfe/spectrum.01814-22-f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/4c68a1ef5716/spectrum.01814-22-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/e5f24cb9acf2/spectrum.01814-22-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/e4fe31dbea59/spectrum.01814-22-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/5edc3e4cb071/spectrum.01814-22-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/c9936f0b8040/spectrum.01814-22-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/e6bc2fcda9ca/spectrum.01814-22-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/a9253a802dfe/spectrum.01814-22-f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/4c68a1ef5716/spectrum.01814-22-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/e5f24cb9acf2/spectrum.01814-22-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/e4fe31dbea59/spectrum.01814-22-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/5edc3e4cb071/spectrum.01814-22-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/c9936f0b8040/spectrum.01814-22-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/e6bc2fcda9ca/spectrum.01814-22-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7123/9430746/a9253a802dfe/spectrum.01814-22-f007.jpg

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