Translational Control under Stress: Reshaping the Translatome

Adequate reprogramming of cellular metabolism in response to stresses or suboptimal growth conditions involves a myriad of coordinated changes that serve to promote cell survival. As protein synthesis is an energetically expensive process, its regulation under stress is of critical importance. Repro...

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Published in:BioEssays Vol. 41; no. 5; pp. e1900009 - n/a
Main Authors: Advani, Vivek M., Ivanov, Pavel
Format: Journal Article
Language:English
Published: United States Wiley Subscription Services, Inc 01.05.2019
Subjects:
Cell Survival
cell viability
Chemical synthesis
cytoplasmic granules
Eukaryotic Initiation Factor-2 - metabolism
Growth conditions
Kinases
messenger RNA
Metabolism
Molecular modelling
Phosphorylation
phosphotransferases (kinases)
Protein Biosynthesis
Protein synthesis
Proteins
Ribonucleic acid
RNA
RNA, Transfer - metabolism
Signal Transduction
stress
stress response
Stress, Physiological - genetics
Survival
TOR Serine-Threonine Kinases - metabolism
Transduction
Transfer RNA
Translation
translation (genetics)
Translation initiation
translational reprogramming
tRNA
translation
translation initiation
stress
tRNA
translational reprogramming
ISSN:0265-9247, 1521-1878, 1521-1878
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Abstract Adequate reprogramming of cellular metabolism in response to stresses or suboptimal growth conditions involves a myriad of coordinated changes that serve to promote cell survival. As protein synthesis is an energetically expensive process, its regulation under stress is of critical importance. Reprogramming of messenger RNA (mRNA) translation involves well‐understood stress‐activated kinases that target components of translation initiation machinery, resulting in the robust inhibition of general translation and promotion of the translation of stress‐responsive proteins. Translational arrest of mRNAs also results in the accumulation of transcripts in cytoplasmic foci called stress granules. Recent studies focus on the key roles of transfer RNA (tRNA) in stress‐induced translational reprogramming. These include stress‐specific regulation of tRNA pools, codon‐biased translation influenced by tRNA modifications, tRNA miscoding, and tRNA cleavage. In combination, signal transduction pathways and tRNA metabolism changes regulate translation during stress, resulting in adaptation and cell survival. This review examines molecular mechanisms that regulate protein synthesis in response to stress. Translational control contributes to various aspects of cell homeostasis. As messenger RNA (mRNA) translation is energy‐expensive, its regulation is critical. Reprogramming of mRNA translation during stress involves signal transduction pathways and transfer RNA metabolism changes that aim at cell survival. This review examines molecular mechanisms that regulate protein synthesis in response to stress.
AbstractList Adequate reprogramming of cellular metabolism in response to stresses or suboptimal growth conditions involves a myriad of coordinated changes that serve to promote cell survival. As protein synthesis is an energetically expensive process, its regulation under stress is of critical importance. Reprogramming of messenger RNA (mRNA) translation involves well‐understood stress‐activated kinases that target components of translation initiation machinery, resulting in the robust inhibition of general translation and promotion of the translation of stress‐responsive proteins. Translational arrest of mRNAs also results in the accumulation of transcripts in cytoplasmic foci called stress granules. Recent studies focus on the key roles of transfer RNA (tRNA) in stress‐induced translational reprogramming. These include stress‐specific regulation of tRNA pools, codon‐biased translation influenced by tRNA modifications, tRNA miscoding, and tRNA cleavage. In combination, signal transduction pathways and tRNA metabolism changes regulate translation during stress, resulting in adaptation and cell survival. This review examines molecular mechanisms that regulate protein synthesis in response to stress. Translational control contributes to various aspects of cell homeostasis. As messenger RNA (mRNA) translation is energy‐expensive, its regulation is critical. Reprogramming of mRNA translation during stress involves signal transduction pathways and transfer RNA metabolism changes that aim at cell survival. This review examines molecular mechanisms that regulate protein synthesis in response to stress.
Adequate reprogramming of cellular metabolism in response to stresses or suboptimal growth conditions involves a myriad of coordinated changes that serve to promote cell survival. As protein synthesis is an energetically expensive process, its regulation under stress is of critical importance. Reprogramming of messenger RNA (mRNA) translation involves well-understood stress-activated kinases that target components of translation initiation machinery, resulting in the robust inhibition of general translation and promotion of the translation of stress-responsive proteins. Translational arrest of mRNAs also results in the accumulation of transcripts in cytoplasmic foci called stress granules. Recent studies focus on the key roles of transfer RNA (tRNA) in stress-induced translational reprogramming. These include stress-specific regulation of tRNA pools, codon-biased translation influenced by tRNA modifications, tRNA miscoding, and tRNA cleavage. In combination, signal transduction pathways and tRNA metabolism changes regulate translation during stress, resulting in adaptation and cell survival. This review examines molecular mechanisms that regulate protein synthesis in response to stress.Adequate reprogramming of cellular metabolism in response to stresses or suboptimal growth conditions involves a myriad of coordinated changes that serve to promote cell survival. As protein synthesis is an energetically expensive process, its regulation under stress is of critical importance. Reprogramming of messenger RNA (mRNA) translation involves well-understood stress-activated kinases that target components of translation initiation machinery, resulting in the robust inhibition of general translation and promotion of the translation of stress-responsive proteins. Translational arrest of mRNAs also results in the accumulation of transcripts in cytoplasmic foci called stress granules. Recent studies focus on the key roles of transfer RNA (tRNA) in stress-induced translational reprogramming. These include stress-specific regulation of tRNA pools, codon-biased translation influenced by tRNA modifications, tRNA miscoding, and tRNA cleavage. In combination, signal transduction pathways and tRNA metabolism changes regulate translation during stress, resulting in adaptation and cell survival. This review examines molecular mechanisms that regulate protein synthesis in response to stress.
Adequate reprogramming of cellular metabolism in response to stresses or suboptimal growth conditions involves a myriad of coordinated changes that serve to promote cell survival. As protein synthesis is an energetically expensive process, its regulation under stress is of critical importance. Reprogramming of messenger RNA (mRNA) translation involves well-understood stress-activated kinases that target components of translation initiation machinery, resulting in the robust inhibition of general translation and promotion of the translation of stress-responsive proteins. Translational arrest of mRNAs also results in the accumulation of transcripts in cytoplasmic foci called stress granules. Recent studies focus on the key roles of transfer RNA (tRNA) in stress-induced translational reprogramming. These include stress-specific regulation of tRNA pools, codon-biased translation influenced by tRNA modifications, tRNA miscoding, and tRNA cleavage. In combination, signal transduction pathways and tRNA metabolism changes regulate translation during stress, resulting in adaptation and cell survival. This review examines molecular mechanisms that regulate protein synthesis in response to stress.
Adequate reprogramming of cellular metabolism in response to stresses or suboptimal growth conditions involves a myriad of coordinated changes that serve to promote cell survival. As protein synthesis is an energetically expensive process, its regulation under stress is of critical importance. Reprogramming of mRNA translation involves well-understood stress-activated kinases that target components of translation initiation machinery resulting in the robust inhibition of general translation and promotion of the translation of stress-responsive proteins. Translational arrest of mRNAs also results in the accumulation of transcripts in cytoplasmic foci called stress granules. Recent studies point on the key roles of transfer RNA (tRNA) in the stress-induced translational reprogramming. These include stress-specific regulation of tRNA pools, codon-biased translation influenced by tRNA modifications, tRNA miscoding, and tRNA cleavage. In combination, signal transduction pathways and tRNA metabolism changes regulate translation during stress resulting in the adaptation and cell survival. This review will examine molecular mechanisms that regulate protein synthesis in response to stress. Translational control contributes to various aspects of cell homeostasis. As mRNA translation is energy-expensive, its regulation is critical. Reprogramming of mRNA translation during stress involves signal transduction pathways and tRNA metabolism changes that aim on cell survival. This review examines molecular mechanisms that regulate protein synthesis in response to stress.
Author Ivanov, Pavel
Advani, Vivek M.
AuthorAffiliation 3 The Broad Institute of Harvard and M.I.T., Cambridge, Massachusetts, United States of America
1 Division of Rheumatology, Immunology and Allergy, Brigham and Women’s Hospital, Boston, Massachusetts, United States of America
2 Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America
AuthorAffiliation_xml – name: 2 Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America
– name: 1 Division of Rheumatology, Immunology and Allergy, Brigham and Women’s Hospital, Boston, Massachusetts, United States of America
– name: 3 The Broad Institute of Harvard and M.I.T., Cambridge, Massachusetts, United States of America
Author_xml – sequence: 1
  givenname: Vivek M.
  surname: Advani
  fullname: Advani, Vivek M.
  email: vadvani@bwh.harvard.edu
  organization: Harvard Medical School
– sequence: 2
  givenname: Pavel
  surname: Ivanov
  fullname: Ivanov, Pavel
  email: pivanov@rics.bwh.harvard.edu
  organization: The Broad Institute of Harvard and MIT
BackLink https://www.ncbi.nlm.nih.gov/pubmed/31026340$$D View this record in MEDLINE/PubMed
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Issue 5
Keywords translation
translation initiation
stress
tRNA
translational reprogramming
Language English
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Snippet Adequate reprogramming of cellular metabolism in response to stresses or suboptimal growth conditions involves a myriad of coordinated changes that serve to...
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pubmed
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Aggregation Database
Index Database
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Publisher
StartPage e1900009
SubjectTerms Cell Survival
cell viability
Chemical synthesis
cytoplasmic granules
Eukaryotic Initiation Factor-2 - metabolism
Growth conditions
Kinases
messenger RNA
Metabolism
Molecular modelling
Phosphorylation
phosphotransferases (kinases)
Protein Biosynthesis
Protein synthesis
Proteins
Ribonucleic acid
RNA
RNA, Transfer - metabolism
Signal Transduction
stress
stress response
Stress, Physiological - genetics
Survival
TOR Serine-Threonine Kinases - metabolism
Transduction
Transfer RNA
Translation
translation (genetics)
Translation initiation
translational reprogramming
tRNA
Title Translational Control under Stress: Reshaping the Translatome
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fbies.201900009
https://www.ncbi.nlm.nih.gov/pubmed/31026340
https://www.proquest.com/docview/2215217067
https://www.proquest.com/docview/2216292812
https://www.proquest.com/docview/2253240173
https://pubmed.ncbi.nlm.nih.gov/PMC6541386
Volume 41
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