Adaptation to ER stress is mediated by differential stabilities of pro-survival and pro-apoptotic mRNAs and proteins.

Adaptation to ER stress is mediated by differential stabilities of pro-survival and pro-apoptotic mRNAs and proteins. Research Abstract Details 

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Adaptation to ER stress is mediated by differential stabilities of pro-survival and pro-apoptotic mRNAs and proteins. Abstract Text:

D Thomas Rutkowski,Stacey M Arnold,Corey N Miller,Jun Wu,Jack Li,Kathryn M Gunnison,Kazutoshi Mori,Amir A Sadighi Akha,David Raden,Randal J Kaufman,

The accumulation of unfolded proteins in the endoplasmic reticulum (ER) activates a signaling cascade known as the unfolded protein response (UPR). Although activation of the UPR is well described, there is little sense of how the response, which initiates both apoptotic and adaptive pathways, can selectively allow for adaptation. Here we describe the reconstitution of an adaptive ER stress response in a cell culture system. Monitoring the activation and maintenance of representative UPR gene expression pathways that facilitate either adaptation or apoptosis, we demonstrate that mild ER stress activates all UPR sensors. However, survival is favored during mild stress as a consequence of the intrinsic instabilities of mRNAs and proteins that promote apoptosis compared to those that facilitate protein folding and adaptation. As a consequence, the expression of apoptotic proteins is short-lived as cells adapt to stress. We provide evidence that the selective persistence of ER chaperone expression is also applicable to at least one instance of genetic ER stress. This work provides new insight into how a stress response pathway can be structured to allow cells to avert death as they adapt. It underscores the contribution of posttranscriptional and posttranslational mechanisms in influencing this outcome.

Adaptation to ER stress is mediated by differential stabilities of pro-survival and pro-apoptotic mRNAs and proteins. Publishing Authors By Initials

DT Rutkowski,SM Arnold,CN Miller,J Wu,J Li,KM Gunnison,K Mori,AA Sadighi Akha,D Raden,RJ Kaufman,

For similar pathological conditions, signs and symptoms: pathologic processes: stress research abstracts see: pathological conditions, signs and symptoms: pathologic processes: stress research

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Adaptation to ER stress is mediated by differential stabilities of pro-survival and pro-apoptotic mRNAs and proteins. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: PLoS biology

VOLUME: 4

Page Numbers: e374

Journal Abbreviation: PLoS Biol.

ISSN: 1545-7885

DAY: 3

MONTH: Nov

YEAR: 2006

Adaptation to ER stress is mediated by differential stabilities of pro-survival and pro-apoptotic mRNAs and proteins. Information

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LANGUAGE: eng

NlmUniqueID: 101183755

Adaptation to ER stress is mediated by differential stabilities of pro-survival and pro-apoptotic mRNAs and proteins. Keywords Mesh Terms:

KEYWORDS: Stress

MESH TERMS: metabolism

Chemical & Substance for Abstract: Adaptation to ER stress is mediated by differential stabilities of pro-survival and pro-apoptotic mRNAs and proteins. Information

Substance Name: RNA, Messenger

Registry Number: 0

Grant and Affiliation Information for Adaptation to ER stress is mediated by differential stabilities of pro-survival and pro-apoptotic mRNAs and proteins.

AFFILIATION: Howard Hughes Medical Institute, University of Michigan Medical Center, Ann Arbor, Michigan, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: R01 HL052173–06

ACRONYM: HL

MEDLINETA: PLoS Biol

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