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

Journal Article · · Nature Communications
 [1];  [2];  [3];  [4];  [5];  [6];  [7];  [5];  [6]
  1. Univ. of Valencia (Spain); Michigan State Univ., East Lansing, MI (United States)
  2. Univ. of California, Riverside, CA (United States); Michigan State Univ., East Lansing, MI (United States)
  3. Univ. of Milan (Italy); Michigan State Univ., East Lansing, MI (United States)
  4. Univ. of Florida, Apopka, FL (United States); Michigan State Univ., East Lansing, MI (United States)
  5. Univ. of Texas, Austin, TX (United States)
  6. Michigan State Univ., East Lansing, MI (United States)
  7. Univ. of Michigan, Ann Arbor, MI (United States); Univ. of Texas, Austin, TX (United States)
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.
Research Organization:
Chicago Office, Argonne, IL (United States)
Sponsoring Organization:
AgBioResearch, Michigan State University; Generalitat Valenciana; National Institutes of Health; USDOE; USDOE Office of Science (SC), Basic Energy Sciences (BES). Chemical Sciences, Geosciences & Biosciences Division (CSGB); USDOE Office of Science (SC), Biological and Environmental Research (BER)
Grant/Contract Number:
FG02-91ER20021; SC0018409
OSTI ID:
2396775
Alternate ID(s):
OSTI ID: 2569089
Journal Information:
Nature Communications, Journal Name: Nature Communications Journal Issue: 1 Vol. 15; ISSN 2041-1723
Publisher:
Nature Publishing GroupCopyright Statement
Country of Publication:
United States
Language:
English

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