ArticlePlant physiology2015
Overexpression of BAX INHIBITOR-1 Links Plasma Membrane Microdomain Proteins to Stress.
Article in Plant physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Bax inhibitor-1 confers resistance to Phytophthora parasitica and is antagonized by RTP1 in Arabidopsis.Stress biology · 2026Article
- γ-Aminobutyric Acid Alleviates Programmed Cell Death in TwoInternational journal of molecular sciences · 2024Article
- Genome wide identification and characterization of Bax inhibitor-1 gene family in cucumber (Cucumis sativus) under biotic and abiotic stress.BMC genomics · 2024Article
- Lipid Rafts and Plant Gravisensitivity.Life (Basel, Switzerland) · 2022Review
- Sphingolipids are involved in insect egg-induced cell death in Arabidopsis.Plant physiology · 2022Article
- Membrane nanodomains and transport functions in plant.Plant physiology · 2021Review
- Transcriptomics of Biostimulation of Plants Under Abiotic Stress.Frontiers in genetics · 2021Review
- Organization and dynamics of functional plant membrane microdomains.Cellular and molecular life sciences : CMLS · 2020Review
- Sphingolipids: towards an integrated view of metabolism during the plant stress response.The New phytologist · 2020Review
- Plant-UniquePlants (Basel, Switzerland) · 2019Article
- Uncovering Bax inhibitor-1 dual role in the legume-rhizobia symbiosis in common bean roots.Journal of experimental botany · 2019Article
- Arabidopsis Bax inhibitor-1 interacts with enzymes related to very-long-chain fatty acid synthesis.Journal of plant research · 2019Article
- Mapping of Plasma Membrane Proteins Interacting WithFrontiers in plant science · 2018Article
- The Wheat Bax Inhibitor-1 Protein Interacts with an Aquaporin TaPIP1 and Enhances Disease Resistance inFrontiers in plant science · 2018Article
- Melatonin restricts Pb-induced PCD by enhancing BI-1 expression in tobacco suspension cells.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2016Article
- Plasma Membrane Microdomains Are Essential for Rac1-RbohB/H-Mediated Immunity in Rice.The Plant cell · 2016Article
- How Very-Long-Chain Fatty Acids Could Signal Stressful Conditions in Plants?Frontiers in plant science · 2016Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BAX INHIBITOR-1 (BI-1) is a cell death suppressor widely conserved in plants and animals. Overexpression of BI-1 enhances tolerance to stress-induced cell death in plant cells, although the molecular mechanism behind this enhancement is unclear. We recently found that Arabidopsis (Arabidopsis thaliana) BI-1 is involved in the metabolism of sphingolipids, such as the synthesis of 2-hydroxy fatty acids, suggesting the involvement of sphingolipids in the cell death regulatory mechanism downstream of BI-1. Here, we show that BI-1 affects cell death-associated components localized in sphingolipid-enriched microdomains of the plasma membrane in rice (Oryza sativa) cells. The amount of 2-hydroxy fatty acid-containing glucosylceramide increased in the detergent-resistant membrane (DRM; a biochemical counterpart of plasma membrane microdomains) fraction obtained from BI-1-overexpressing rice cells. Comparative proteomics analysis showed quantitative changes of DRM proteins in BI-1-overexpressing cells. In particular, the protein abundance of FLOTILLIN HOMOLOG (FLOT) and HYPERSENSITIVE-INDUCED REACTION PROTEIN3 (HIR3) markedly decreased in DRM of BI-1-overexpressing cells. Loss-of-function analysis demonstrated that FLOT and HIR3 are required for cell death by oxidative stress and salicylic acid, suggesting that the decreased levels of these proteins directly contribute to the stress-tolerant phenotypes in BI-1-overexpressing rice cells. These findings provide a novel biological implication of plant membrane microdomains in stress-induced cell death, which is negatively modulated by BI-1 overexpression via decreasing the abundance of a set of key proteins involved in cell death.
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