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Physiological response dynamics of the brown tide organism Aureococcus anophagefferens treated with modified clay

Author:
Zhu, Jianan, Yu, Zhiming, He, Liyan, Cao, Xihua, Ji, Hena, Song, Xiuxian
Source:
Harmful algae 2019 v.86 pp. 1-9
ISSN:
1568-9883
Subject:
algal blooms, cell proliferation, clay, flocculation, gene expression regulation, genes, models, oxidative stress, phospholipids, photosynthesis, physiological response, poisonous algae, programmed cell death, quantitative polymerase chain reaction, reverse transcriptase polymerase chain reaction
Abstract:
On the basis of experiences in mitigating harmful algal blooms (HABs) with modified clay (MC), a bloom does not continue after the dispersal of the MC, even though the density of the residual cells in the water remains as high as 20–30% of the initial cell density. This interesting phenomenon indicates that in addition to flocculation, MC has additional mechanisms of HAB control. Here, Aureococcus anophagefferens was selected as a model organism to study the physiological response dynamics of residual cells treated with MC, and RT-qPCR was used to measure the differential expression of 40 genes involved in anti-oxidation, photosynthesis, phospholipid synthesis, programmed cell death and cell proliferation at five time points. The results showed that every functional gene category exhibited a "V" shaped pattern with a turning point. It was reflected that there were two processes for MC inhibiting the growth of residual cells. One is the oxidative stress process (OSP) caused by ineffective collision with MC, whose effect weakened gradually; another is the programmed cell death process (PCDP) caused by the lysis of damaged residual cells, whose effect enhanced two days after MC treatment. In addition, the scanning electron micrographs verified that some of the residual cells were deformed or even lysed. Combined with the effects of OSP and PCDP in dynamics, the growth of residual cells was inhibited and was followed by gradual bloom disappearance. This study further elucidates the mechanism of MC controlling HABs at the molecular level and enable a more comprehensive understanding of HAB mitigation using MC.
Agid:
6380990