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|a 10.1093/jxb/erae344
|2 doi
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|a pubmed25n1253.xml
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
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|a Tang, Xiao-Han
|e verfasserin
|4 aut
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| 245 |
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|a Interaction of PASTICCINO2 with Golgi anti-apoptotic proteins confers resistance to endoplasmic reticulum stress and is dependent on very-long-chain fatty acids
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|c 2024
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
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|2 rdamedia
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|a ƒa Online-Ressource
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|2 rdacarrier
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|a Date Completed 10.12.2024
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|a Date Revised 10.12.2024
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|a published: Print
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|a Citation Status MEDLINE
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|a © The Author(s) 2024. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved. For commercial re-use, please contact reprintsoup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.
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|a The endoplasmic reticulum (ER) is crucial for maintaining cell homeostasis because it is the primary site for synthesizing secreted and transmembrane proteins and lipids. The unfolded protein response (UPR) is activated to restore the homeostasis of the ER when it is under stress; however, the relationship between lipids and the ER stress response in plants is not well understood. Arabidopsis GOLGI ANTI-APOPTOTIC PROTEINS (GAAPs) are involved in resisting ER stress, and in this study, we found that PASTICCINO2 (PAS2), which is involved in very-long-chain fatty acid (VLCFA) synthesis, interacts with GAAPs and INOSITOL REQUIRING ENZYME 1. The pas2 single-mutant and the gaap1 pas2 and gaap2 pas2 double-mutants exhibited increased seedling damage and an impaired UPR response under chronic ER stress. Site mutation combined with genetic analysis revealed that the role of PAS2 in resisting ER stress depended on its VLCFA synthesis domain. VLCFA contents were increased under ER stress, and this required GAAPs. Exogenous VLCFAs partially restored the defect in the activation of the UPR caused by mutation of PAS2 or GAAP under chronic ER stress. Our findings demonstrate that the association of PAS2 with GAAPs confers plant resistance to ER stress by regulating VLCFA synthesis and the UPR. This provides a basis for further studies on the connection between lipids and cell-fate decisions under stress
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|a Journal Article
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|a Arabidopsis thaliana
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|a Golgi anti-apoptotic proteins (GAAPs)
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|a PASTICCINO2
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|a endoplasmic reticulum stress
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|a unfolded protein response (UPR)
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| 650 |
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|a very-long-chain fatty acids
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| 650 |
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|a Arabidopsis Proteins
|2 NLM
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| 650 |
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|a Fatty Acids
|2 NLM
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| 700 |
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|a Zhou, Yan
|e verfasserin
|4 aut
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| 700 |
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|a He, Yu-Ting
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zhang, Wei
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Chen, Xi
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Tan, Jing
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Guo, Kun
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Liu, Yu-Ting
|e verfasserin
|4 aut
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| 700 |
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|a Zhao, Shu-Heng
|e verfasserin
|4 aut
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| 700 |
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|a Ning, Yi-Qiu
|e verfasserin
|4 aut
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| 700 |
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|a Sun, Yue
|e verfasserin
|4 aut
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| 700 |
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|a Li, Xiao-Fang
|e verfasserin
|4 aut
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| 773 |
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|i Enthalten in
|t Journal of experimental botany
|d 1985
|g 75(2024), 22 vom: 04. Dez., Seite 7267-7283
|w (DE-627)NLM098182706
|x 1460-2431
|7 nnas
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| 773 |
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|g volume:75
|g year:2024
|g number:22
|g day:04
|g month:12
|g pages:7267-7283
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|u http://dx.doi.org/10.1093/jxb/erae344
|3 Volltext
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|h 7267-7283
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