Abstract
The binding protein (BiP) has been demonstrated to participate in innate immunity and attenuate endoplasmic reticulum- and osmotic stress-induced cell death. Here, we employed transgenic plants with manipulated levels of BiP to assess whether BiP also controlled developmental and hypersensitive programmed cell death (PCD). Under normal conditions, the BiP-induced transcriptome revealed a robust down-regulation of developmental PCD genes and an up-regulation of the genes involved in hypersensitive PCD triggered by nonhost-pathogen interactions. Accordingly, the BiP-overexpressing line displayed delayed leaf senescence under normal conditions and accelerated hypersensitive response triggered by Pseudomonas syringae pv tomato in soybean (Glycine max) and tobacco (Nicotiana tabacum), as monitored by measuring hallmarks of PCD in plants. The BiP-mediated delay of leaf senescence correlated with the attenuation of N-rich protein (NRP)-mediated cell death signaling and the inhibition of the senescence-associated activation of the unfolded protein response (UPR). By contrast, under biological activation of salicylic acid (SA) signaling and hypersensitive PCD, BiP overexpression further induced NRP-mediated cell death signaling and antagonistically inhibited the UPR. Thus, the SA-mediated induction of NRP cell death signaling occurs via a pathway distinct from UPR. Our data indicate that during the hypersensitive PCD, BiP positively regulates the NRP cell death signaling through a yet undefined mechanism that is activated by SA signaling and related to ER functioning. By contrast, BiP's negative regulation of leaf senescence may be linked to its capacity to attenuate the UPR activation and NRP cell death signaling. Therefore, BiP can function either as a negative or positive modulator of PCD events.
Highlights
The binding protein (BiP) has been demonstrated to participate in innate immunity and attenuate endoplasmic reticulum- and osmotic stress-induced cell death
Using criteria of a corrected P value less than 0.05 and log2-fold change greater than 1.5, we identified 310 genes that were differentially expressed in BiP-overexpressing leaves compared with control untransformed leaves (Supplemental Fig. S2B)
Because the gene expression profile was assessed under normal conditions and because BiP overexpression down-regulated genes associated with programmed cell death (PCD), we examined whether BiP would regulate aging or leaf senescence under normal developmental conditions
Summary
The binding protein (BiP) has been demonstrated to participate in innate immunity and attenuate endoplasmic reticulum- and osmotic stress-induced cell death. An enhanced accumulation of NRPs up-regulates the cell death effector Glycine max NAC-domain containing protein (GmNAC81) (formerly designated GmNAC6; Faria et al, 2011) to induce a programmed cell death (PCD) event, which can be monitored by an induction of caspase-like activity, DNA fragmentation, chlorophyll loss, elevated peroxidation, and senescence-associated marker gene expression (Costa et al, 2008; Faria et al, 2011) We discovered another member of the GmNAC family, GmNAC30, which binds to GmNAC81 in the nucleus of plant cells to coordinately regulate the caspase1-like vacuolar processing enzyme gene expression, underlying a mechanism for the execution of the ER stress- and osmotic stress-induced cell death program (Mendes et al, 2013). Whether BiP would control PCD under developmental conditions remains unanswered
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