Total proteins were probed with α-Ub and α-NPR1. (K) Col-0 and npr1–2 plants were treated with SA for 6 hr. (I-J) Ws-2 (I) or Col-0 and npr1–2 (J), were treated as in (E-G) before inoculation with Pf Pf0–1/AvrRps4 or Pf Pf0–1/AvrRps4 KRVY-AAAA. (H) Plants expressing dex:AvrRpt2 in Col-0, npr1–2 and rps2 were treated as in (E-G) before treatment with 25 μM dexamethasone (dex). Data are presented as mean ± SD (F), and mean ± 95% confidence intervals (G). Bacterial growth was measured at 1 dpi (G). Cell death was assessed by trypan blue staining (E) and conductivity assay (F).
(E-G) Col-0, rps2 and npr1–2 plants were treated with water (mock) or 1 mM SA 24 hr before inoculation with Psm ES4326/AvrRpt2. At 2 dpi, the adjacent leaf halves were infiltrated with 25 μM dexamethasone (dex) and cell death was assessed as in (B). (D) Half leaves of plants expressing dex:AvrRpt2 in Col-0, npr1–2, and rps2 were inoculated as in (B). Data are presented as mean ± SD (B), and mean ± 95% confidence intervals (C). Growth of Psm ES4326/AvrRpt2 (Tet r) was measured in the adjacent leaf halves after the first inoculation with Psm ES4326/AvrRpm1 (Avr Kan r) (C). Cell death was assessed by tissue collapse at 1 dpi (A) and conductivity assay (B). At 2 dpi, the adjacent leaf halves were infiltrated with the same pathogen. (A-C) Half leaves (left side) of Col-0, npr1–2 and sid2–2 plants were infiltrated with MgSO 4 (mock) or Psm ES4326/AvrRpt2 (Avr). NPR1 cell survival cullin 3 RING E3 ligase effector-triggered immunity plant immunity protein homeostasis salicylic acid-induced NPR1 condensate (SINC) systemic acquired resistance ubiquitination.Ĭopyright © 2020 Elsevier Inc. Our analysis of SINCs suggests that NPR1 is centrally integrated into the cell death or survival decisions in plant immunity by modulating multiple stress-responsive processes in this quasi-organelle. Transition of NPR1 into condensates is required for formation of the NPR1-Cullin 3 E3 ligase complex to ubiquitinate SINC-localized substrates, such as EDS1 and specific WRKY transcription factors, and promote cell survival during ETI. SINCs are enriched with stress response proteins, including nucleotide-binding leucine-rich repeat immune receptors, oxidative and DNA damage response proteins, and protein quality control machineries. Here we show that NPR1 promotes cell survival by targeting substrates for ubiquitination and degradation through formation of salicylic acid-induced NPR1 condensates (SINCs). However, the biochemical activities of NPR1 enabling it to promote defense and restrict cell death remain unclear.
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In plants, pathogen effector-triggered immunity (ETI) often leads to programmed cell death, which is restricted by NPR1, an activator of systemic acquired resistance.
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