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作 者:Vahid Fallahzadeh-Mamaghami Hannah Weber Birgit Kemmerling
机构地区:[1]ZMBP,University Tubingen,Auf der Morgenstelle 32,Tübingen 72076,Germany
出 处:《Stress Biology》2023年第1期463-467,共5页逆境生物学(英文)
基 金:supported by the SFB1101 D03 and the TRR356 B02,funded by the German science foundation DFG.
摘 要:BRI1-ASSOCIATED KINASE 1(BAK1/SERK3)and its closest homolog BAK1-LIKE 1(BKK1/SERK4)are leucine-rich repeat receptor kinases(LRR-RKs)belonging to the SOMATIC EMBRYOGENESIS RECEPTOR KINASE(SERK)family.They act as co-receptors of various other LRR-RKs and participate in multiple signaling events by complexing and transphosphorylating ligand-binding receptors.Initially identified as the brassinosteroid receptor BRASSINOSTEROID INSENSITIVE 1(BRI1)co-receptor,BAK1 also functions in plant immunity by interacting with pattern recognition receptors.Mutations in BAK1 and BKK1 cause severely stunted growth and cell death,characterized as autoimmune cell death.Several factors play a role in this type of cell death,including RKs and components of effector-triggered immunity(ETI)signaling pathways,glycosylation factors,ER quality control components,nuclear trafficking components,ion channels,and Nod-like receptors(NLRs).The Shan lab has recently discovered a novel RK BAK-TO-LIFE 2(BTL2)that interacts with BAK1 and triggers cell death in the absence of BAK1 and BKK1.This RK compensates for the loss of BAK1-mediated pattern-triggered immunity(PTI)by activating phytocytokine-mediated immune and cell death responses.
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