Control of translation elongation in health and diseaseCitation formats

  • External authors:
  • Gavin Garland
  • Tuija Pöyry
  • Emma Mead
  • Nikola Vlahov
  • Aristeidis Sfakianos
  • Stefano Grosso
  • Fabio De-Lima-Hedayioglu
  • Giovanna Mallucci
  • Tobias von der Haar
  • C Mark Smales
  • Owen J Sansom
  • Anne E Willis

Standard

Control of translation elongation in health and disease. / Knight, John; Garland, Gavin; Pöyry, Tuija; Mead, Emma; Vlahov, Nikola; Sfakianos, Aristeidis; Grosso, Stefano; De-Lima-Hedayioglu, Fabio; Mallucci, Giovanna; von der Haar, Tobias; Smales, C Mark; Sansom, Owen J; Willis, Anne E.

In: Disease Models & Mechanisms, Vol. 13, No. 3, 01.03.2020.

Research output: Contribution to journalReview articlepeer-review

Harvard

Knight, J, Garland, G, Pöyry, T, Mead, E, Vlahov, N, Sfakianos, A, Grosso, S, De-Lima-Hedayioglu, F, Mallucci, G, von der Haar, T, Smales, CM, Sansom, OJ & Willis, AE 2020, 'Control of translation elongation in health and disease', Disease Models & Mechanisms, vol. 13, no. 3. https://doi.org/10.1242/dmm.043208

APA

Knight, J., Garland, G., Pöyry, T., Mead, E., Vlahov, N., Sfakianos, A., Grosso, S., De-Lima-Hedayioglu, F., Mallucci, G., von der Haar, T., Smales, C. M., Sansom, O. J., & Willis, A. E. (2020). Control of translation elongation in health and disease. Disease Models & Mechanisms, 13(3). https://doi.org/10.1242/dmm.043208

Vancouver

Knight J, Garland G, Pöyry T, Mead E, Vlahov N, Sfakianos A et al. Control of translation elongation in health and disease. Disease Models & Mechanisms. 2020 Mar 1;13(3). https://doi.org/10.1242/dmm.043208

Author

Knight, John ; Garland, Gavin ; Pöyry, Tuija ; Mead, Emma ; Vlahov, Nikola ; Sfakianos, Aristeidis ; Grosso, Stefano ; De-Lima-Hedayioglu, Fabio ; Mallucci, Giovanna ; von der Haar, Tobias ; Smales, C Mark ; Sansom, Owen J ; Willis, Anne E. / Control of translation elongation in health and disease. In: Disease Models & Mechanisms. 2020 ; Vol. 13, No. 3.

Bibtex

@article{1d841a05ba7d490897bb3f528f4408fd,
title = "Control of translation elongation in health and disease",
abstract = "Regulation of protein synthesis makes a major contribution to post-transcriptional control pathways. During disease, or under stress, cells initiate processes to reprogramme protein synthesis and thus orchestrate the appropriate cellular response. Recent data show that the elongation stage of protein synthesis is a key regulatory node for translational control in health and disease. There is a complex set of factors that individually affect the overall rate of elongation and, for the most part, these influence either transfer RNA (tRNA)- and eukaryotic elongation factor 1A (eEF1A)-dependent codon decoding, and/or elongation factor 2 (eEF2)-dependent ribosome translocation along the mRNA. Decoding speeds depend on the relative abundance of each tRNA, the cognate:near-cognate tRNA ratios and the degree of tRNA modification, whereas eEF2-dependent ribosome translocation is negatively regulated by phosphorylation on threonine-56 by eEF2 kinase. Additional factors that contribute to the control of the elongation rate include epigenetic modification of the mRNA, coding sequence variation and the expression of eIF5A, which stimulates peptide bond formation between proline residues. Importantly, dysregulation of elongation control is central to disease mechanisms in both tumorigenesis and neurodegeneration, making the individual key steps in this process attractive therapeutic targets. Here, we discuss the relative contribution of individual components of the translational apparatus (e.g. tRNAs, elongation factors and their modifiers) to the overall control of translation elongation and how their dysregulation contributes towards disease processes.",
author = "John Knight and Gavin Garland and Tuija P{\"o}yry and Emma Mead and Nikola Vlahov and Aristeidis Sfakianos and Stefano Grosso and Fabio De-Lima-Hedayioglu and Giovanna Mallucci and {von der Haar}, Tobias and Smales, {C Mark} and Sansom, {Owen J} and Willis, {Anne E}",
year = "2020",
month = mar,
day = "1",
doi = "10.1242/dmm.043208",
language = "English",
volume = "13",
journal = "DMM Disease Models and Mechanisms",
issn = "1754-8403",
publisher = "Company of Biologists Ltd",
number = "3",

}

RIS

TY - JOUR

T1 - Control of translation elongation in health and disease

AU - Knight, John

AU - Garland, Gavin

AU - Pöyry, Tuija

AU - Mead, Emma

AU - Vlahov, Nikola

AU - Sfakianos, Aristeidis

AU - Grosso, Stefano

AU - De-Lima-Hedayioglu, Fabio

AU - Mallucci, Giovanna

AU - von der Haar, Tobias

AU - Smales, C Mark

AU - Sansom, Owen J

AU - Willis, Anne E

PY - 2020/3/1

Y1 - 2020/3/1

N2 - Regulation of protein synthesis makes a major contribution to post-transcriptional control pathways. During disease, or under stress, cells initiate processes to reprogramme protein synthesis and thus orchestrate the appropriate cellular response. Recent data show that the elongation stage of protein synthesis is a key regulatory node for translational control in health and disease. There is a complex set of factors that individually affect the overall rate of elongation and, for the most part, these influence either transfer RNA (tRNA)- and eukaryotic elongation factor 1A (eEF1A)-dependent codon decoding, and/or elongation factor 2 (eEF2)-dependent ribosome translocation along the mRNA. Decoding speeds depend on the relative abundance of each tRNA, the cognate:near-cognate tRNA ratios and the degree of tRNA modification, whereas eEF2-dependent ribosome translocation is negatively regulated by phosphorylation on threonine-56 by eEF2 kinase. Additional factors that contribute to the control of the elongation rate include epigenetic modification of the mRNA, coding sequence variation and the expression of eIF5A, which stimulates peptide bond formation between proline residues. Importantly, dysregulation of elongation control is central to disease mechanisms in both tumorigenesis and neurodegeneration, making the individual key steps in this process attractive therapeutic targets. Here, we discuss the relative contribution of individual components of the translational apparatus (e.g. tRNAs, elongation factors and their modifiers) to the overall control of translation elongation and how their dysregulation contributes towards disease processes.

AB - Regulation of protein synthesis makes a major contribution to post-transcriptional control pathways. During disease, or under stress, cells initiate processes to reprogramme protein synthesis and thus orchestrate the appropriate cellular response. Recent data show that the elongation stage of protein synthesis is a key regulatory node for translational control in health and disease. There is a complex set of factors that individually affect the overall rate of elongation and, for the most part, these influence either transfer RNA (tRNA)- and eukaryotic elongation factor 1A (eEF1A)-dependent codon decoding, and/or elongation factor 2 (eEF2)-dependent ribosome translocation along the mRNA. Decoding speeds depend on the relative abundance of each tRNA, the cognate:near-cognate tRNA ratios and the degree of tRNA modification, whereas eEF2-dependent ribosome translocation is negatively regulated by phosphorylation on threonine-56 by eEF2 kinase. Additional factors that contribute to the control of the elongation rate include epigenetic modification of the mRNA, coding sequence variation and the expression of eIF5A, which stimulates peptide bond formation between proline residues. Importantly, dysregulation of elongation control is central to disease mechanisms in both tumorigenesis and neurodegeneration, making the individual key steps in this process attractive therapeutic targets. Here, we discuss the relative contribution of individual components of the translational apparatus (e.g. tRNAs, elongation factors and their modifiers) to the overall control of translation elongation and how their dysregulation contributes towards disease processes.

UR - http://dx.doi.org/10.1242/dmm.043208

U2 - 10.1242/dmm.043208

DO - 10.1242/dmm.043208

M3 - Review article

VL - 13

JO - DMM Disease Models and Mechanisms

JF - DMM Disease Models and Mechanisms

SN - 1754-8403

IS - 3

ER -