Regulation of apoptosis by Pacific oyster Crassostrea gigas reveals acclimation strategy to CO2 driven acidification

Ocean acidification (OA) has posed formidable threats to marine calcifiers. In response to elevated CO2 levels, marine calcifiers have developed multiple strategies to survive, such as taking advantage of apoptosis, but its regulation mechanism remains largely unknown. Here, we used the Pacific oyst...

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Bibliographic Details
Published in:Ecotoxicology and Environmental Safety
Main Authors: Wang, Xiudan, Li, Changmei, Jia, Zhihao, Xu, Tongxiao, Wang, Yilin, Sun, Mingzhu, Han, Shuhui, Wang, Xia, Qiu, Limei
Format: Report
Language:English
Published: ACADEMIC PRESS INC ELSEVIER SCIENCE 2021
Subjects:
Ocean acidification
Crassostrea gigas
Apoptosis
CgBcl-XL
Environmental Sciences & Ecology
Toxicology
Environmental Sciences
Pacific
Pacific oyster
Online Access:http://ir.qdio.ac.cn/handle/337002/170983
http://ir.qdio.ac.cn/handle/337002/170984
https://doi.org/10.1016/j.ecoenv.2021.112235
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Summary:Ocean acidification (OA) has posed formidable threats to marine calcifiers. In response to elevated CO2 levels, marine calcifiers have developed multiple strategies to survive, such as taking advantage of apoptosis, but its regulation mechanism remains largely unknown. Here, we used the Pacific oyster Crassostrea gigas as model to understand the apoptotic responses and regulation mechanism at short- (7 d) to long-term (56 d) CO2 exposure (pH = 7.50). The apoptosis of hemocytes was significantly induced after short-term treatment (7-21 d) but was suppressed under long-term CO2 exposure (42-56 d). Similarly, caspase-3 and caspase-9 were also increased post short-term exposure and fell back to normal levels after long-term exposure. These data together indicated diverse regulation mechanisms of apoptosis through different exposure periods. Through analysis of the B-cell lymphoma 2 (Bcl-2) family mitochondrial apoptosis regulators, we showed that only CgBcl-XL's expression kept at high levels after 42- and 56-day CO2 exposure. CgBcl-XL shared sequence, and structural similarity with its mammalian counterpart, and knockdown of CgBcl-XL in hemocytes via RNA interference promoted apoptosis. The protein level of CgBcl-XL was significantly increased after long-term CO2 exposure (28-56 d), and its distribution in hemocytes became more concentrated and dense. Therefore, CgBcl-XL serves as an essential antiapoptotic protein for tipping the balance of cell apoptosis, which may play a key role in survival under longterm CO2 exposure. These results reveal a potential adaptation strategy of oysters towards OA and the variable environment changes through the modulation of apoptosis.

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