ER stress response, peroxisome proliferation, mitochondrial unfolded protein response and Golgi stress response

Abstract

The endoplasmic reticulum (ER) response has been thought a cytoprotective mechanism to cope with accumulation of unfolded proteins in the ER. Recent progress has made a quantum leap revealing that ER stress response can be regarded as an autoregulatory system adjusting the ER capacity to cellular demand. This Copernican change raised a novel fundamental question in cell biology: how do cells regulate the capacity of each organelle in accordance with cellular needs? Although this fundamental question has not been fully addressed yet, research about each organelle has been advancing. The proliferation of the peroxisome is regulated by the PPARα pathway, whereas the abundance of mitochondria appears to be regulated by mitochondrial retrograde signaling and the mitochondrial unfolded protein response. The functional capacity of the Golgi apparatus may be regulated by the mechanism of the Golgi stress response. These observations strongly suggest the existence of an elaborate network of organelle autoregulation in eukaryotic cells. © 2009 IUBMB IUBMB Life 61(9): 871–879, 2009

Transcriptomic response of Arabidopsis thaliana to tunicamycin-induced endoplasmic reticulum stress

“…It was also reported that a deficient ER stress response results in poor ER development in pancreatic and salivary gland acinar cells, accompanied by decreased expression of ER chaperone genes (Lee et al 2005). These observations support the notion that the ER stress response modulates the capacity of the ER and subsequent secretory pathway in response to cellular demands (Yoshida 2009).…”

SalA Attenuates Hypoxia-Induced Endothelial Endoplasmic Reticulum Stress and Apoptosis via Down-Regulation of VLDL Receptor Expression

“…Besides its important function of regulating blood coagulation, the endothelium has been shown to play an essential role in the inflammatory processes, development of atherosclerotic lesions, and regulation of blood pressure. The endoplasmic reticulum (ER) is a complex membranous framework found in all eukaryotic cells [18]. The biology processes of folding of secretory and membrane proteins, calcium homeostasis, and lipid biosynthesis were implemented in ER lumen.…”

TFE3 Is a bHLH-ZIP-type Transcription Factor that Regulates the Mammalian Golgi Stress Response

“…When the synthesis of secretory proteins increases and overwhelms the capacity of ER chaperones and ERAD, unfolded proteins accumulate in the lumen of the ER, which could lead to apoptotic cell death. To cope with such an insufficiency of ER function (ER stress), eukaryotic cells activate homeostatic mechanisms called the ER stress response (also called the unfolded protein response) and increase the protein-folding capacity of the ER (Kimata and Kohno, 2011;Mori, 2009;Ron and Harding, 2012;Walter and Ron, 2011;Wang and Kaufman, 2012;Yoshida, 2009). The mammalian ER stress response consists of three main mechanisms: the ATF6, IRE1 and PERK pathways.…”