ArticlePloS one2015
ER quality control components UGGT and STT3a are required for activation of defense responses in bir1-1.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- The Hrd1-Mediated ERAD Pathway in Plants: Conserved Principles and Plant-Specific Innovations.International journal of molecular sciences · 2026Review
- Overexpression of TaSTT3b-2B improves resistance to sharp eyespot and increases grain weight in wheat.Plant biotechnology journal · 2022Article
- The Crucial Role of Demannosylating Asparagine-Linked Glycans in ERADicating Misfolded Glycoproteins in the Endoplasmic Reticulum.Frontiers in plant science · 2020Review
- Arabidopsis Endoplasmic Reticulum-Localized UBAC2 Proteins Interact with PAMP-INDUCED COILED-COIL to Regulate Pathogen-Induced Callose Deposition and Plant Immunity.The Plant cell · 2019Article
- Article
- Plant protein glycosylation.Glycobiology · 2016Review
- Specific control of Arabidopsis BAK1/SERK4-regulated cell death by protein glycosylation.Nature plants · 2016Article
- Danger peptide receptor signaling in plants ensures basal immunity upon pathogen-induced depletion of BAK1.The EMBO journal · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The receptor-like kinase SUPPRESSOR OF BIR1, 1 (SOBIR1) functions as a critical regulator in plant immunity. It is required for activation of cell death and defense responses in Arabidopsis bak1-interacting receptor-like kinase 1,1 (bir1-1) mutant plants. Here we report that the ER quality control component UDP-glucose:glycoprotein glucosyltransferase (UGGT) is required for the biogenesis of SOBIR1 and mutations in UGGT suppress the spontaneous cell death and constitutive defense responses in bir1-1. Loss of function of STT3a, which encodes a subunit of the oligosaccharyltransferase complex, also suppresses the autoimmune phenotype in bir1-1. However, it has no effect on the accumulation of SOBIR1, suggesting that additional signaling components other than SOBIR1 may be regulated by ER quality control. Our study provides clear evidence that ER quality control play critical roles in regulating defense activation in bir1-1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.