Programmed cell death regulator BAP2 is required for IRE1-mediated unfolded protein response in Arabidopsis

Noelia Pastor-Cantizano, Evan R. Angelos, Cristina Ruberti, Tao Jiang, Xiaoyu Weng, Brandon C. Reagan, Taslima Haque, Thomas E. Juenger and Federica Brandizzi ()
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Noelia Pastor-Cantizano: Michigan State University
Evan R. Angelos: Michigan State University
Cristina Ruberti: Michigan State University
Tao Jiang: Michigan State University
Xiaoyu Weng: University of Texas
Brandon C. Reagan: Michigan State University
Taslima Haque: University of Texas
Thomas E. Juenger: University of Texas
Federica Brandizzi: Michigan State University

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract Environmental and physiological situations can challenge the balance between protein synthesis and folding capacity of the endoplasmic reticulum (ER) and cause ER stress, a potentially lethal condition. The unfolded protein response (UPR) restores ER homeostasis or actuates programmed cell death (PCD) when ER stress is unresolved. The cell fate determination mechanisms of the UPR are not well understood, especially in plants. Here, we integrate genetics and ER stress profiling with natural variation and quantitative trait locus analysis of 350 natural accessions of the model species Arabidopsis thaliana. Our analyses implicate a single nucleotide polymorphism to the loss of function of the general PCD regulator BON-ASSOCIATED PROTEIN2 (BAP2) in UPR outcomes. We establish that ER stress-induced BAP2 expression is antagonistically regulated by the UPR master regulator, inositol-requiring enzyme 1 (IRE1), and that BAP2 controls adaptive UPR amplitude in ER stress and ignites pro-death mechanisms in conditions of UPR insufficiency.

Date: 2024
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DOI: 10.1038/s41467-024-50105-6

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