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Cell disruption of Chlorella vulgaris using active extracellular substances from Bacillus thuringiensis ITRI-G1 is a programmed cell death event

Microalgae are rich resources for high-value nutrients and biodiesel production. However, extraction of these valuable compounds from them requires costly energy-consuming procedures due to their rigid cell walls. Application of cell-disruptive agents, the AES-Bt agents, extracted from an algicidal...

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Bibliographic Details
Published in:Journal of applied phycology 2017-06, Vol.29 (3), p.1307-1315
Main Authors: Bai, Ming-Der, Hsu, Hui-Ju, Wu, Shao-I, Lu, Wen-Chang, Wan, Hou-Peng, Chen, Jen-Chih
Format: Article
Language:English
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Summary:Microalgae are rich resources for high-value nutrients and biodiesel production. However, extraction of these valuable compounds from them requires costly energy-consuming procedures due to their rigid cell walls. Application of cell-disruptive agents, the AES-Bt agents, extracted from an algicidal bacterium, Bacillus thuringiensis ITRI-G1, are a promising way to reduce the cost of cell disruption. Treatment with AES-Bt agents resulted in a rapid decline of photosynthesis ability and caused cell death in Chlorella vulgaris . Hallmarks of programmed cell death (PCD), including chromatin condensation, DNA fragmentation, and phosphatidylserine externalization, were detected in C. vulgaris cells treated with the AES-Bt agents. Therefore, the cell disruption effect caused by application of the AES-Bt agents can be due to the occurrence of PCD. Similar to other PCDs, the PCD caused by AES-Bt agents was also associated with increased reactive oxygen species (ROS). However, co-treatments with diphenyleneiodonium chloride (DPI), an NAD(P)H oxidase inhibitor, or N , N ′-dimethylthiourea (DMTU), a hydrogen peroxide (H 2 O 2 ) trap, with the AES-Bt agents successfully reduced ROS production, and more cells displayed a feature of PCD detected after the co-treatments. In conclusion, the AES-Bt agents can promote PCD of microalgae; however, the mechanism may not be through induction of ROS.
ISSN:0921-8971
1573-5176
DOI:10.1007/s10811-017-1058-x