scholarly journals Mitochondrial RNA granules: Compartmentalizing mitochondrial gene expression

2016 ◽  
Vol 212 (6) ◽  
pp. 611-614 ◽  
Author(s):  
Alexis A. Jourdain ◽  
Erik Boehm ◽  
Kinsey Maundrell ◽  
Jean-Claude Martinou
Keyword(s):  
Gene Expression ◽  
Dna Replication ◽  
Mitochondrial Gene ◽  
Regulation Of Gene Expression ◽  
Rna Degradation ◽  
Mitochondrial Rna ◽  
Mitochondrial Gene Expression ◽  
Rna Granules ◽  
Mitochondria Dna ◽  
Replication Gene

In mitochondria, DNA replication, gene expression, and RNA degradation machineries coexist within a common nondelimited space, raising the question of how functional compartmentalization of gene expression is achieved. Here, we discuss the recently characterized “mitochondrial RNA granules,” mitochondrial subdomains with an emerging role in the regulation of gene expression.

scholarly journals The Mitochondrial RNA-Binding Protein GRSF1 Localizes to RNA Granules and Is Required for Posttranscriptional Mitochondrial Gene Expression

2013 ◽  
Vol 17 (3) ◽  
pp. 386-398 ◽  
Author(s):  
Hana Antonicka ◽  
Florin Sasarman ◽  
Tamiko Nishimura ◽  
Vincent Paupe ◽  
Eric A. Shoubridge
Keyword(s):  
Gene Expression ◽  
Rna Binding ◽  
Binding Protein ◽  
Mitochondrial Gene ◽  
Rna Binding Protein ◽  
Mitochondrial Rna ◽  
Mitochondrial Gene Expression ◽  
Rna Granules

scholarly journals Quantitative proteomics revealed C6orf203/MTRES1 as a factor preventing stress-induced transcription deficiency in human mitochondria

2019 ◽  
Vol 47 (14) ◽  
pp. 7502-7517 ◽  
Author(s):  
Anna V Kotrys ◽  
Dominik Cysewski ◽  
Sylwia D Czarnomska ◽  
Zbigniew Pietras ◽  
Lukasz S Borowski ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rna Binding ◽  
Mitochondrial Gene ◽  
Binding Activity ◽  
Stress Conditions ◽  
Mitochondrial Rna ◽  
Mitochondrial Gene Expression ◽  
Compensatory Mechanisms ◽  
Temporary Reduction ◽  
Mitochondrial Transcription

AbstractMaintenance of mitochondrial gene expression is crucial for cellular homeostasis. Stress conditions may lead to a temporary reduction of mitochondrial genome copy number, raising the risk of insufficient expression of mitochondrial encoded genes. Little is known how compensatory mechanisms operate to maintain proper mitochondrial transcripts levels upon disturbed transcription and which proteins are involved in them. Here we performed a quantitative proteomic screen to search for proteins that sustain expression of mtDNA under stress conditions. Analysis of stress-induced changes of the human mitochondrial proteome led to the identification of several proteins with poorly defined functions among which we focused on C6orf203, which we named MTRES1 (Mitochondrial Transcription Rescue Factor 1). We found that the level of MTRES1 is elevated in cells under stress and we show that this upregulation of MTRES1 prevents mitochondrial transcript loss under perturbed mitochondrial gene expression. This protective effect depends on the RNA binding activity of MTRES1. Functional analysis revealed that MTRES1 associates with mitochondrial RNA polymerase POLRMT and acts by increasing mitochondrial transcription, without changing the stability of mitochondrial RNAs. We propose that MTRES1 is an example of a protein that protects the cell from mitochondrial RNA loss during stress.

scholarly journals A link between mitochondrial gene expression and life stage morphologies in Trypanosoma cruzi

2019 ◽  
Author(s):  
Roger Ramirez-Barrios ◽  
Emily K. Susa ◽  
Sean P. Faacks ◽  
Charles K. Liggett ◽  
Sara L. Zimmer
Keyword(s):  
Gene Expression ◽  
Trypanosoma Cruzi ◽  
Mitochondrial Gene ◽  
Life Stage ◽  
Mitochondrial Rna ◽  
Mitochondrial Gene Expression ◽  
Signaling Mechanism ◽  
Transport Chain ◽  
Host Life ◽  
Induced Changes

SummaryThe protozoan Trypanosoma cruzi has a complicated dual-host life cycle, and starvation can trigger transition from the replicating insect stage to the mammalian-infectious nonreplicating insect stage (epimastigote to trypomastigote differentiation). Abundance of some mature RNAs derived from its mitochondrial genome increase during culture starvation of T. cruzi for unknown reasons. Here we examine T. cruzi mitochondrial gene expression in the mammalian intracellular replicating life stage (amastigote), and uncover implications of starvation-induced changes in gene expression in insect-stage cells. Mitochondrial RNA levels in general were found to be lowest in actively replicating amastigotes. We discovered that mitochondrial respiration decreases during starvation, despite the previously-observed increases in mitochondrial mRNAs encoding electron transport chain components. Surprisingly, T. cruzi epimastigotes in replete medium grow at normal rates when we genetically compromised their ability to perform insertion/deletion editing and thereby generate mature forms of some mitochondrial mRNAs. However, these cells, when starved, were impeded in the epimastigote to trypomastigote transition. Further, they experience a short-flagella phenotype that may also be linked to differentiation. We hypothesize a scenario where levels of mature RNA species or editing in the single T. cruzi mitochondrion are linked to differentiation by a yet-unknown signaling mechanism.

scholarly journals Mitochondrial RNA and its eccentricities

2015 ◽  
Vol 37 (2) ◽  
pp. 28-32
Author(s):  
Zofia M. ChrzanowskaLightowlers
Keyword(s):  
Gene Expression ◽  
Molecular Mechanisms ◽  
Maternal Inheritance ◽  
Mitochondrial Gene ◽  
Mitochondrial Rna ◽  
Mitochondrial Gene Expression ◽  
Mitochondrial Evolution ◽  
Inheritance Patterns ◽  
Rna Elements

For those who do not work on mitochondria, their knowledge is often restricted to eubacterial origins, production of ATP and perhaps an appreciation of the non-Mendelian maternal inheritance patterns. These features are true enough, but things then start to get more complicated. Although the origins of mitochondria are accepted as a eubacterial endosymbiont of evolving eukaryotic cells1, there were organisms that were described as having jettisoned these ‘organelles’, referred to as amitochondriate eukaryotes. This concept has been challenged, and rudimentary mitochondria, or mitosomes, have now been found in those eukaryotes, which are apparently reluctant to lose this organelle2. The consequences of mitochondrial evolution can be seen in the divergence from the standard repertoire of RNA elements. These eccentricities pose challenges to our understanding of molecular mechanisms underlying mitochondrial gene expression.

scholarly journals Mitochondrial Gene Expression Is Responsive to Starvation Stress and Developmental Transition in Trypanosoma cruzi

mSphere ◽  
2016 ◽  
Vol 1 (2) ◽  
Author(s):  
Aubie K. Shaw ◽  
Murat C. Kalem ◽  
Sara L. Zimmer
Keyword(s):  
Gene Expression ◽  
Life Cycle ◽  
Mitochondrial Genome ◽  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Mitochondrial Gene ◽  
Mitochondrial Rna ◽  
Life Stages ◽  
Mitochondrial Gene Expression ◽  
Content Type

ABSTRACT Chagas disease is caused by insect-transmitted Trypanosoma cruzi. Halting T. cruzi’s life cycle in one of its various human and insect life stages would effectively stop the parasite’s infection cycle. T. cruzi is exposed to a variety of environmental conditions in its different life stages, and gene expression must be remodeled to survive these changes. In this work, we look at the impact that one of these changes, nutrient depletion, has on the expression of the 20 gene products encoded in the mitochondrial genome that is neglected by whole-genome studies. We show increases in mitochondrial RNA abundances in starved insect-stage cells, under two conditions in which transition to the infectious stage occurs or does not. This report is the first to show that T. cruzi mitochondrial gene expression is sensitive to environmental perturbations, consistent with mitochondrial gene expression regulatory pathways being potential antiparasitic targets. Trypanosoma cruzi parasites causing Chagas disease are passed between mammals by the triatomine bug vector. Within the insect, T. cruzi epimastigote-stage cells replicate and progress through the increasingly nutrient-restricted digestive tract, differentiating into infectious, nonreplicative metacyclic trypomastigotes. Thus, we evaluated how nutrient perturbations or metacyclogenesis affects mitochondrial gene expression in different insect life cycle stages. We compared mitochondrial RNA abundances in cultures containing fed, replicating epimastigotes, differentiating cultures containing both starved epimastigotes and metacyclic trypomastigotes and epimastigote starvation cultures. We observed increases in mitochondrial rRNAs and some mRNAs in differentiating cultures. These increases predominated only for the edited CYb mRNA in cultures enriched for metacyclic trypomastigotes. For the other transcripts, abundance increases were linked to starvation and were strongest in culture fractions with a high population of starved epimastigotes. We show that loss of both glucose and amino acids results in rapid increases in RNA abundances that are quickly reduced when these nutrients are returned. Furthermore, the individual RNAs exhibit distinct temporal abundance patterns, suggestive of multiple mechanisms regulating individual transcript abundance. Finally, increases in mitochondrial respiratory complex subunit mRNA abundances were not matched by increases in abundances of nucleus-encoded subunit mRNAs, nor were there statistically significant increases in protein levels of three nucleus-encoded subunits tested. These results show that, similarly to that in T. brucei, the mitochondrial genome in T. cruzi has the potential to alter gene expression in response to environmental or developmental stimuli but for an as-yet-unknown purpose. IMPORTANCE Chagas disease is caused by insect-transmitted Trypanosoma cruzi. Halting T. cruzi’s life cycle in one of its various human and insect life stages would effectively stop the parasite’s infection cycle. T. cruzi is exposed to a variety of environmental conditions in its different life stages, and gene expression must be remodeled to survive these changes. In this work, we look at the impact that one of these changes, nutrient depletion, has on the expression of the 20 gene products encoded in the mitochondrial genome that is neglected by whole-genome studies. We show increases in mitochondrial RNA abundances in starved insect-stage cells, under two conditions in which transition to the infectious stage occurs or does not. This report is the first to show that T. cruzi mitochondrial gene expression is sensitive to environmental perturbations, consistent with mitochondrial gene expression regulatory pathways being potential antiparasitic targets.

scholarly journals Mitochondrial Glucocorticoid Receptors and Their Actions

2021 ◽  
Vol 22 (11) ◽  
pp. 6054
Author(s):  
Ioanna Kokkinopoulou ◽  
Paraskevi Moutsatsou
Keyword(s):  
Gene Expression ◽  
Glucocorticoid Receptors ◽  
Mitochondrial Gene ◽  
Cell Types ◽  
Ros Generation ◽  
Mitochondrial Gene Expression ◽  
Mitochondrial Energy Metabolism ◽  
Bcl2 Family ◽  
Cellular Processes ◽  
Almost All

Mitochondria are membrane organelles present in almost all eukaryotic cells. In addition to their well-known role in energy production, mitochondria regulate central cellular processes, including calcium homeostasis, Reactive Oxygen Species (ROS) generation, cell death, thermogenesis, and biosynthesis of lipids, nucleic acids, and steroid hormones. Glucocorticoids (GCs) regulate the mitochondrially encoded oxidative phosphorylation gene expression and mitochondrial energy metabolism. The identification of Glucocorticoid Response Elements (GREs) in mitochondrial sequences and the detection of Glucocorticoid Receptor (GR) in mitochondria of different cell types gave support to hypothesis that mitochondrial GR directly regulates mitochondrial gene expression. Numerous studies have revealed changes in mitochondrial gene expression alongside with GR import/export in mitochondria, confirming the direct effects of GCs on mitochondrial genome. Further evidence has made clear that mitochondrial GR is involved in mitochondrial function and apoptosis-mediated processes, through interacting or altering the distribution of Bcl2 family members. Even though its exact translocation mechanisms remain unknown, data have shown that GR chaperones (Hsp70/90, Bag-1, FKBP51), the anti-apoptotic protein Bcl-2, the HDAC6- mediated deacetylation and the outer mitochondrial translocation complexes (Tom complexes) co-ordinate GR mitochondrial trafficking. A role of mitochondrial GR in stress and depression as well as in lung and hepatic inflammation has also been demonstrated.

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