YelA, a putative Dictyostelium translational regulator, acts as antagonist of DIF-1 signaling to control cell-type proportioning

Yoko Yamada (Lead / Corresponding author), Chris Sugden, Jeffrey G. Williams

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Abstract

DIF-1 (differentiation-inducing factor1) is a polyketide produced by Dictyostelium prespore cells which induces initially uncommitted cells to differentiate as prestalk cells. Exposure of cells to DIF-1 causes transitory hypo-phosphorylation of seven serine residues in YelA, a protein with a region of strong homology to the MIF4G domain of the eukaryotic initiation factor eIF4G. Based upon its domain architecture, which in one important aspect closely resembles that of Death-Associated Protein 5 (DAP5), we predict a role in stimulating internal ribosome entry-driven mRNA translation. The two paradigmatic DIF-1 inducible genes are ecmA (extracellular matrixA) and ecmB. In support of a YelA function in DIF-1 signaling, a YelA null strain showed greatly increased expression of ecmA and ecmB in response to DIF-1. Also, during normal development in the null strain, expression of the two genes is accelerated. This is particularly evident for ecmB, a marker of stalk tube and supporting structure differentiation. Mutants in DIF-1 bio-synthesis or signaling display a rudimentary or no basal disc and, conversely, YelA null mutants produce fruiting bodies with a highly enlarged basal disc that ectopically expresses a stalk tube-specific marker. Thus YelA acts as an antagonist of DIF-1 signaling, with a consequent effect on cell type proportioning and it is predicted to act as a translational regulator.

Original languageEnglish
Pages (from-to)35-42
Number of pages8
JournalInternational Journal of Developmental Biology
Volume61
Issue number1-2
DOIs
Publication statusPublished - 2017

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Dictyostelium
Eukaryotic Initiation Factors
Polyketides
Protein Biosynthesis
Ribosomes
Serine
Cell Differentiation
Proteins
Phosphorylation
Gene Expression
Genes

Keywords

  • Journal article
  • Dictyostelium
  • DIF-1
  • MIF4G domain
  • Translational regulation
  • DAP5

Cite this

@article{4ecc2f85ad0944ffbcbeb99e7a004462,
title = "YelA, a putative Dictyostelium translational regulator, acts as antagonist of DIF-1 signaling to control cell-type proportioning",
abstract = "DIF-1 (differentiation-inducing factor1) is a polyketide produced by Dictyostelium prespore cells which induces initially uncommitted cells to differentiate as prestalk cells. Exposure of cells to DIF-1 causes transitory hypo-phosphorylation of seven serine residues in YelA, a protein with a region of strong homology to the MIF4G domain of the eukaryotic initiation factor eIF4G. Based upon its domain architecture, which in one important aspect closely resembles that of Death-Associated Protein 5 (DAP5), we predict a role in stimulating internal ribosome entry-driven mRNA translation. The two paradigmatic DIF-1 inducible genes are ecmA (extracellular matrixA) and ecmB. In support of a YelA function in DIF-1 signaling, a YelA null strain showed greatly increased expression of ecmA and ecmB in response to DIF-1. Also, during normal development in the null strain, expression of the two genes is accelerated. This is particularly evident for ecmB, a marker of stalk tube and supporting structure differentiation. Mutants in DIF-1 bio-synthesis or signaling display a rudimentary or no basal disc and, conversely, YelA null mutants produce fruiting bodies with a highly enlarged basal disc that ectopically expresses a stalk tube-specific marker. Thus YelA acts as an antagonist of DIF-1 signaling, with a consequent effect on cell type proportioning and it is predicted to act as a translational regulator.",
keywords = "Journal article, Dictyostelium, DIF-1 , MIF4G domain, Translational regulation , DAP5",
author = "Yoko Yamada and Chris Sugden and Williams, {Jeffrey G.}",
note = "This work was initially supported by Wellcome Trust Program Grant 053640/Z to J.G.W and completed while he was in receipt of Leverhulme Emeritus Fellowship EM-2013-024.",
year = "2017",
doi = "10.1387/ijdb.160160yy",
language = "English",
volume = "61",
pages = "35--42",
journal = "International Journal of Developmental Biology",
issn = "0214-6282",
publisher = "University of the Basque Country Press",
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TY - JOUR

T1 - YelA, a putative Dictyostelium translational regulator, acts as antagonist of DIF-1 signaling to control cell-type proportioning

AU - Yamada, Yoko

AU - Sugden, Chris

AU - Williams, Jeffrey G.

N1 - This work was initially supported by Wellcome Trust Program Grant 053640/Z to J.G.W and completed while he was in receipt of Leverhulme Emeritus Fellowship EM-2013-024.

PY - 2017

Y1 - 2017

N2 - DIF-1 (differentiation-inducing factor1) is a polyketide produced by Dictyostelium prespore cells which induces initially uncommitted cells to differentiate as prestalk cells. Exposure of cells to DIF-1 causes transitory hypo-phosphorylation of seven serine residues in YelA, a protein with a region of strong homology to the MIF4G domain of the eukaryotic initiation factor eIF4G. Based upon its domain architecture, which in one important aspect closely resembles that of Death-Associated Protein 5 (DAP5), we predict a role in stimulating internal ribosome entry-driven mRNA translation. The two paradigmatic DIF-1 inducible genes are ecmA (extracellular matrixA) and ecmB. In support of a YelA function in DIF-1 signaling, a YelA null strain showed greatly increased expression of ecmA and ecmB in response to DIF-1. Also, during normal development in the null strain, expression of the two genes is accelerated. This is particularly evident for ecmB, a marker of stalk tube and supporting structure differentiation. Mutants in DIF-1 bio-synthesis or signaling display a rudimentary or no basal disc and, conversely, YelA null mutants produce fruiting bodies with a highly enlarged basal disc that ectopically expresses a stalk tube-specific marker. Thus YelA acts as an antagonist of DIF-1 signaling, with a consequent effect on cell type proportioning and it is predicted to act as a translational regulator.

AB - DIF-1 (differentiation-inducing factor1) is a polyketide produced by Dictyostelium prespore cells which induces initially uncommitted cells to differentiate as prestalk cells. Exposure of cells to DIF-1 causes transitory hypo-phosphorylation of seven serine residues in YelA, a protein with a region of strong homology to the MIF4G domain of the eukaryotic initiation factor eIF4G. Based upon its domain architecture, which in one important aspect closely resembles that of Death-Associated Protein 5 (DAP5), we predict a role in stimulating internal ribosome entry-driven mRNA translation. The two paradigmatic DIF-1 inducible genes are ecmA (extracellular matrixA) and ecmB. In support of a YelA function in DIF-1 signaling, a YelA null strain showed greatly increased expression of ecmA and ecmB in response to DIF-1. Also, during normal development in the null strain, expression of the two genes is accelerated. This is particularly evident for ecmB, a marker of stalk tube and supporting structure differentiation. Mutants in DIF-1 bio-synthesis or signaling display a rudimentary or no basal disc and, conversely, YelA null mutants produce fruiting bodies with a highly enlarged basal disc that ectopically expresses a stalk tube-specific marker. Thus YelA acts as an antagonist of DIF-1 signaling, with a consequent effect on cell type proportioning and it is predicted to act as a translational regulator.

KW - Journal article

KW - Dictyostelium

KW - DIF-1

KW - MIF4G domain

KW - Translational regulation

KW - DAP5

U2 - 10.1387/ijdb.160160yy

DO - 10.1387/ijdb.160160yy

M3 - Article

VL - 61

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EP - 42

JO - International Journal of Developmental Biology

JF - International Journal of Developmental Biology

SN - 0214-6282

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ER -