Contribution of ERMES subunits to mature peroxisome abundance.

Eukaryotic organelles share different components and establish physical contacts to communicate throughout the cell. One of the best-recognized examples of such interplay is the metabolic cooperation and crosstalk between mitochondria and peroxisomes, both organelles being functionally and physicall...

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Main Authors: Michela Esposito, Sylvie Hermann-Le Denmat, Agnès Delahodde
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2019-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0214287
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spelling doaj-6dfe1d4f64b3420f905e9b5d7dc865012021-03-03T20:47:32ZengPublic Library of Science (PLoS)PLoS ONE1932-62032019-01-01143e021428710.1371/journal.pone.0214287Contribution of ERMES subunits to mature peroxisome abundance.Michela EspositoSylvie Hermann-Le DenmatAgnès DelahoddeEukaryotic organelles share different components and establish physical contacts to communicate throughout the cell. One of the best-recognized examples of such interplay is the metabolic cooperation and crosstalk between mitochondria and peroxisomes, both organelles being functionally and physically connected and linked to the endoplasmic reticulum (ER). In Saccharomyces cerevisiae, mitochondria are linked to the ER by the ERMES complex that facilitates inter-organelle calcium and phospholipid exchanges. Recently, peroxisome-mitochondria contact sites (PerMit) have been reported and among Permit tethers, one component of the ERMES complex (Mdm34) was shown to interact with the peroxin Pex11, suggesting that the ERMES complex or part of it may be involved in two membrane contact sites (ER-mitochondria and peroxisome- mitochondria). This opens the possibility of exchanges between these three membrane compartments. Here, we investigated in details the role of each ERMES subunit on peroxisome abundance. First, we confirmed previous studies from other groups showing that absence of Mdm10 or Mdm12 leads to an increased number of mature peroxisomes. Secondly, we showed that this is not simply due to respiratory function defect, mitochondrial DNA (mtDNA) loss or mitochondrial network alteration. Finally, we present evidence that the contribution of ERMES subunits Mdm10 and Mdm12 to peroxisome number involves two different mechanisms.https://doi.org/10.1371/journal.pone.0214287
collection DOAJ
language English
format Article
sources DOAJ
author Michela Esposito
Sylvie Hermann-Le Denmat
Agnès Delahodde
spellingShingle Michela Esposito
Sylvie Hermann-Le Denmat
Agnès Delahodde
Contribution of ERMES subunits to mature peroxisome abundance.
PLoS ONE
author_facet Michela Esposito
Sylvie Hermann-Le Denmat
Agnès Delahodde
author_sort Michela Esposito
title Contribution of ERMES subunits to mature peroxisome abundance.
title_short Contribution of ERMES subunits to mature peroxisome abundance.
title_full Contribution of ERMES subunits to mature peroxisome abundance.
title_fullStr Contribution of ERMES subunits to mature peroxisome abundance.
title_full_unstemmed Contribution of ERMES subunits to mature peroxisome abundance.
title_sort contribution of ermes subunits to mature peroxisome abundance.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2019-01-01
description Eukaryotic organelles share different components and establish physical contacts to communicate throughout the cell. One of the best-recognized examples of such interplay is the metabolic cooperation and crosstalk between mitochondria and peroxisomes, both organelles being functionally and physically connected and linked to the endoplasmic reticulum (ER). In Saccharomyces cerevisiae, mitochondria are linked to the ER by the ERMES complex that facilitates inter-organelle calcium and phospholipid exchanges. Recently, peroxisome-mitochondria contact sites (PerMit) have been reported and among Permit tethers, one component of the ERMES complex (Mdm34) was shown to interact with the peroxin Pex11, suggesting that the ERMES complex or part of it may be involved in two membrane contact sites (ER-mitochondria and peroxisome- mitochondria). This opens the possibility of exchanges between these three membrane compartments. Here, we investigated in details the role of each ERMES subunit on peroxisome abundance. First, we confirmed previous studies from other groups showing that absence of Mdm10 or Mdm12 leads to an increased number of mature peroxisomes. Secondly, we showed that this is not simply due to respiratory function defect, mitochondrial DNA (mtDNA) loss or mitochondrial network alteration. Finally, we present evidence that the contribution of ERMES subunits Mdm10 and Mdm12 to peroxisome number involves two different mechanisms.
url https://doi.org/10.1371/journal.pone.0214287
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