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DDX3 DEAD-box RNA helicase plays a central role in mitochondrial protein quality control in Leishmania
DDX3 is a highly conserved member of ATP-dependent DEAD-box RNA helicases with multiple functions in RNA metabolism and cellular signaling. Here, we describe a novel function for DDX3 in regulating the mitochondrial stress response in the parasitic protozoan Leishmania. We show that genetic inactiva...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133982/ https://www.ncbi.nlm.nih.gov/pubmed/27735940 http://dx.doi.org/10.1038/cddis.2016.315 |
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author | Padmanabhan, Prasad Kottayil Zghidi-Abouzid, Ouafa Samant, Mukesh Dumas, Carole Aguiar, Bruno Guedes Estaquier, Jerome Papadopoulou, Barbara |
author_facet | Padmanabhan, Prasad Kottayil Zghidi-Abouzid, Ouafa Samant, Mukesh Dumas, Carole Aguiar, Bruno Guedes Estaquier, Jerome Papadopoulou, Barbara |
author_sort | Padmanabhan, Prasad Kottayil |
collection | PubMed |
description | DDX3 is a highly conserved member of ATP-dependent DEAD-box RNA helicases with multiple functions in RNA metabolism and cellular signaling. Here, we describe a novel function for DDX3 in regulating the mitochondrial stress response in the parasitic protozoan Leishmania. We show that genetic inactivation of DDX3 leads to the accumulation of mitochondrial reactive oxygen species (ROS) associated with a defect in hydrogen peroxide detoxification. Upon stress, ROS production is greatly enhanced, causing mitochondrial membrane potential loss, mitochondrial fragmentation, and cell death. Importantly, this phenotype is exacerbated upon oxidative stress in parasites forced to use the mitochondrial oxidative respiratory machinery. Furthermore, we show that in the absence of DDX3, levels of major components of the unfolded protein response as well as of polyubiquitinated proteins increase in the parasite, particularly in the mitochondrion, as an indicator of mitochondrial protein damage. Consistent with these findings, immunoprecipitation and mass-spectrometry studies revealed potential interactions of DDX3 with key components of the cellular stress response, particularly the antioxidant response, the unfolded protein response, and the AAA-ATPase p97/VCP/Cdc48, which is essential in mitochondrial protein quality control by driving proteosomal degradation of polyubiquitinated proteins. Complementation studies using DDX3 deletion mutants lacking conserved motifs within the helicase core support that binding of DDX3 to ATP is essential for DDX3's function in mitochondrial proteostasis. As a result of the inability of DDX3-depleted Leishmania to recover from ROS damage and to survive various stresses in the host macrophage, parasite intracellular development was impaired. Collectively, these observations support a central role for the Leishmania DDX3 homolog in preventing ROS-mediated damage and in maintaining mitochondrial protein quality control. |
format | Online Article Text |
id | pubmed-5133982 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-51339822016-12-16 DDX3 DEAD-box RNA helicase plays a central role in mitochondrial protein quality control in Leishmania Padmanabhan, Prasad Kottayil Zghidi-Abouzid, Ouafa Samant, Mukesh Dumas, Carole Aguiar, Bruno Guedes Estaquier, Jerome Papadopoulou, Barbara Cell Death Dis Original Article DDX3 is a highly conserved member of ATP-dependent DEAD-box RNA helicases with multiple functions in RNA metabolism and cellular signaling. Here, we describe a novel function for DDX3 in regulating the mitochondrial stress response in the parasitic protozoan Leishmania. We show that genetic inactivation of DDX3 leads to the accumulation of mitochondrial reactive oxygen species (ROS) associated with a defect in hydrogen peroxide detoxification. Upon stress, ROS production is greatly enhanced, causing mitochondrial membrane potential loss, mitochondrial fragmentation, and cell death. Importantly, this phenotype is exacerbated upon oxidative stress in parasites forced to use the mitochondrial oxidative respiratory machinery. Furthermore, we show that in the absence of DDX3, levels of major components of the unfolded protein response as well as of polyubiquitinated proteins increase in the parasite, particularly in the mitochondrion, as an indicator of mitochondrial protein damage. Consistent with these findings, immunoprecipitation and mass-spectrometry studies revealed potential interactions of DDX3 with key components of the cellular stress response, particularly the antioxidant response, the unfolded protein response, and the AAA-ATPase p97/VCP/Cdc48, which is essential in mitochondrial protein quality control by driving proteosomal degradation of polyubiquitinated proteins. Complementation studies using DDX3 deletion mutants lacking conserved motifs within the helicase core support that binding of DDX3 to ATP is essential for DDX3's function in mitochondrial proteostasis. As a result of the inability of DDX3-depleted Leishmania to recover from ROS damage and to survive various stresses in the host macrophage, parasite intracellular development was impaired. Collectively, these observations support a central role for the Leishmania DDX3 homolog in preventing ROS-mediated damage and in maintaining mitochondrial protein quality control. Nature Publishing Group 2016-10 2016-10-13 /pmc/articles/PMC5133982/ /pubmed/27735940 http://dx.doi.org/10.1038/cddis.2016.315 Text en Copyright © 2016 The Author(s) http://creativecommons.org/licenses/by/4.0/ Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Original Article Padmanabhan, Prasad Kottayil Zghidi-Abouzid, Ouafa Samant, Mukesh Dumas, Carole Aguiar, Bruno Guedes Estaquier, Jerome Papadopoulou, Barbara DDX3 DEAD-box RNA helicase plays a central role in mitochondrial protein quality control in Leishmania |
title | DDX3 DEAD-box RNA helicase plays a central role in mitochondrial protein quality control in Leishmania |
title_full | DDX3 DEAD-box RNA helicase plays a central role in mitochondrial protein quality control in Leishmania |
title_fullStr | DDX3 DEAD-box RNA helicase plays a central role in mitochondrial protein quality control in Leishmania |
title_full_unstemmed | DDX3 DEAD-box RNA helicase plays a central role in mitochondrial protein quality control in Leishmania |
title_short | DDX3 DEAD-box RNA helicase plays a central role in mitochondrial protein quality control in Leishmania |
title_sort | ddx3 dead-box rna helicase plays a central role in mitochondrial protein quality control in leishmania |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133982/ https://www.ncbi.nlm.nih.gov/pubmed/27735940 http://dx.doi.org/10.1038/cddis.2016.315 |
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