Journal
NATURE PLANTS
Volume 2, Issue 2, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/NPLANTS.2015.218
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Funding
- National Institutes of Health (NIH) [R01GM092893]
- National Science Foundation (NSF) [IOS-1252539]
- NIH [R01GM097247]
- Robert A. Welch Foundation [A 1795]
- NSF [IOS 1547551]
- China Scholarship Council (CSC)
- CAPES Foundation (Coordination for the Improvement of Higher Education Personnel), Brazil
- Rio de Janeiro State Research Foundation (FAPERJ), Brazil
- NSF Research Experiences for Undergraduates (REU) programme
- Texas AgriLife Genomics
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [1547551] Funding Source: National Science Foundation
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Precise control of cell death is essential for the survival of all organisms. Arabidopsis thaliana BRASSINOSTEROID INSENSITIVE 1-associated receptor kinase 1 (BAK1) and somatic embryogenesis receptor kinase 4 (SERK4) redundantly and negatively regulate cell death through elusive mechanisms. By deploying a genetic screen for suppressors of cell death triggered by virus-induced gene silencing of BAK1/SERK4 on Arabidopsis knockout collections, we identified STT3a, a protein involved in N-glycosylation modification, as an important regulator of bak1/serk4 cell death. Systematic investigation of glycosylation pathway and endoplasmic reticulum (ER) quality control (ERQC) components revealed distinct and overlapping mechanisms of cell death regulated by BAK1/SERK4 and their interacting protein BIR1. Genome-wide transcriptional analysis revealed the activation of members of cysteine-rich receptor-like kinase (CRK) genes in the bak1/serk4 mutant. Ectopic expression of CRK4 induced STT3a/N-glycosylation-dependent cell death in Arabidopsis and Nicotiana benthamiana. Therefore, N-glycosylation and specific ERQC components are essential to activate bak1/serk4 cell death, and CRK4 is likely to be among client proteins of protein glycosylation involved in BAK1/SERK4-regulated cell death.
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