ATF6 aggravates apoptosis in early porcine embryonic development by regulating organelle homeostasis under high-temperature conditions

Ming-Hong Sun; Wen-Jie Jiang; Xiao-Han Li; Song-Hee Lee; Geun Heo; Dongjie Zhou; Zhi Chen; Xiang-Shun Cui

doi:10.24272/j.issn.2095-8137.2023.080

Volume 44 Issue 5

Sep. 2023

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Article Navigation > Zoological Research > 2023 > 44(5): 848-859

Ming-Hong Sun, Wen-Jie Jiang, Xiao-Han Li, Song-Hee Lee, Geun Heo, Dongjie Zhou, Zhi Chen, Xiang-Shun Cui. ATF6 aggravates apoptosis in early porcine embryonic development by regulating organelle homeostasis under high-temperature conditions. Zoological Research, 2023, 44(5): 848-859. doi: 10.24272/j.issn.2095-8137.2023.080

Citation:

Ming-Hong Sun, Wen-Jie Jiang, Xiao-Han Li, Song-Hee Lee, Geun Heo, Dongjie Zhou, Zhi Chen, Xiang-Shun Cui. ATF6 aggravates apoptosis in early porcine embryonic development by regulating organelle homeostasis under high-temperature conditions. Zoological Research, 2023, 44(5): 848-859. doi: 10.24272/j.issn.2095-8137.2023.080

Citation:

Ming-Hong Sun, Wen-Jie Jiang, Xiao-Han Li, Song-Hee Lee, Geun Heo, Dongjie Zhou, Zhi Chen, Xiang-Shun Cui. ATF6 aggravates apoptosis in early porcine embryonic development by regulating organelle homeostasis under high-temperature conditions. Zoological Research, 2023, 44(5): 848-859. doi: 10.24272/j.issn.2095-8137.2023.080

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ATF6 aggravates apoptosis in early porcine embryonic development by regulating organelle homeostasis under high-temperature conditions

doi: 10.24272/j.issn.2095-8137.2023.080

1.
Department of Animal Science, Chungbuk National University, Cheongju, South Korea 28644, Korea
2.
College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu 225009, China

The authors declare that they have no competing interests.
M.H.S. and X.S.C. designed the experiments; M.H.S. performed most of the experiments; D.Z., W.J.J., X.H.L., S.H.L., G.H., and Z.C. contributed to the materials; M.H.S. wrote the manuscript; and X.S.C. revised the manuscript. All authors read and approved the final version of the manuscript.

Funds: This work was supported by the National Research Foundation (NRF) of Korea Grant funded by the Korean Government (MSIT) (2020R1A4A1017552, 2022R1A2C300769), Republic of Korea

More Information

Corresponding author: E-mail: xscui@cbnu.ac.kr
Received Date: 2023-05-04
Accepted Date: 2023-07-19

Published Online: 2023-07-25

Publish Date: 2023-09-18

Abstract

Abstract

Activating transcription factor 6 (ATF6), one of the three sensor proteins in the endoplasmic reticulum (ER), is an important regulator of ER stress-induced apoptosis. ATF6 resides in the ER and, upon activation, is translocated to the Golgi apparatus, where it is cleaved by site-1 protease (S1P) to generate an amino-terminal cytoplasmic fragment. Although recent studies have made progress in elucidating the regulatory mechanisms of ATF6, its function during early porcine embryonic development under high-temperature (HT) stress remains unclear. In this study, zygotes were divided into four groups: control, HT, HT+ATF6 knockdown, and HT+PF (S1P inhibitor). Results showed that HT exposure induced ER stress, which increased ATF6 protein expression and led to a decrease in the blastocyst rate. Next, ATF6 expression was knocked down in HT embryos under microinjection of ATF6 double-stranded RNA (dsRNA). Results revealed that ATF6 knockdown (ATF6-KD) attenuated the increased expression of CHOP, an ER stress marker, and Ca²⁺ release induced by HT. In addition, ATF6-KD alleviated homeostasis dysregulation among organelles caused by HT-induced ER stress, and further reduced Golgi apparatus and mitochondrial dysfunction in HT embryos. AIFM2 is an important downstream effector of ATF6. Results showed that ATF6-KD reduced the occurrence of AIFM2-mediated embryonic apoptosis at HT. Taken together, our findings suggest that ATF6 is a crucial mediator of apoptosis during early porcine embryonic development, resulting from HT-induced ER stress and disruption of organelle homeostasis.
- ATF6,
- Embryo,
- High temperature,
- ER stress,
- Organelle homeostasis

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References(42)

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