Bax Inhibitor-1, a conserved cell death suppressor, is a key molecular switch downstream from a variety of biotic and abiotic stress signals in plants.

Naohide Watanabe,Eric Lam

doi:10.3390/ijms10073149

Abstract

In Nature plants are constantly challenged by a variety of environmental stresses that could lead to disruptions in cellular homeostasis. Programmed cell death (PCD) is a fundamental cellular process that is often associated with defense responses to pathogens, during development and in response to abiotic stresses in fungi, animals and plants. Although there are many characteristics shared between different types of PCD events, it remains unknown whether a common mechanism drives various types of PCD in eukaryotes. One candidate regulator for such a mechanism is Bax Inhibitor-1 (BI-1), an evolutionary conserved, endoplasmic reticulum (ER)-resident protein that represents an ancient cell death regulator that potentially regulates PCD in all eukaryotes. Recent findings strongly suggested that BI-1 plays an important role in the conserved ER stress response pathway to modulate cell death induction in response to multiple types of cell death signals. As ER stress signaling pathways has been suggested to play important roles not only in the control of ER homeostasis but also in other biological processes such as the response to pathogens and abiotic stress in plants, BI-1 might function to control the convergence point that modulates the level of the “pro-survival and pro-death” signals under multiple stress conditions.

Highlights

Programmed cell death (PCD) comprises a series of genetically controlled cell suicide processes and plays a fundamental role in various biological processes including cell proliferation, generation of developmental patterns, defenses of eukaryotes against pathogens and environmental insults [1,2,3]
Accumulation of unfolded and misfolded proteins in the lumen of the endoplasmic reticulum (ER) can be triggered by a diverse array of cellular stresses that are induced by multiple stimuli and pathological conditions
We recently demonstrated that in Arabidopsis seedlings, strong PCD phenotypes such as nuclear condensation, DNA laddering and H2O2 production were observed in roots that have been challenged with various drugs known to induce ER stress such as the N-linked glycosylation inhibitor tunicamycin (TM), cyclopiazonic acid (CPA), and the proline analogue L-azetidine-2-carboxylic acid (AZC) [85]

Summary

Introduction

Programmed cell death (PCD) comprises a series of genetically controlled cell suicide processes and plays a fundamental role in various biological processes including cell proliferation, generation of developmental patterns, defenses of eukaryotes against pathogens and environmental insults [1,2,3]. It was shown that ectopic expression of the pro-apoptotic protein Bax can induce cell death with apoptotic features and overexpression of metazoan anti-apoptotic proteins such as IAP (Inhibitor of Apoptosis) and Bcl-XL proteins can suppress some types of plant PCD [17,18,19,20]. Recent emerging evidence demonstrated the existence of ER-dependent apoptosis pathway that is initiated when ER homeostasis is heavily impaired due to ER stress [39] It is evident from a number of studies that plants possess such defense mechanisms to cope with ER stress [40,41,42,43,44,45,46], the UPR in plants still remains unclear at the molecular and biochemical levels. Plant BI-1 may function downstream from the early steps of ROS-dependent cell death pathway

Role of Mammalian BI-1 in the ER-dependent PCD Pathway

Role of Plant BI-1 in ER-dependent PCD Pathway

Working Model of Plant BI-1 in PCD Induced by Biotic and Abiotic Stresses

Findings

Conclusions