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Rotenone complex i mutants-Effect of the inhibition of the mitochondrial respiratory chain complex I (CI) on shoot initiation on protoplast-derived calli

ABSTRACT: ra16-03_rotenone - rotenone_complex i mutants - How does inhibition of CI enhance organogenesis

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE117269 | GEO | 2019/01/01

REPOSITORIES: GEO

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rotenone-Effect of the inhibition of the mitochondrial respiratory chain complex I (CI) on shoot initiation on protoplast-derived calli

Project description:ra16-03_rotenone - rotenone - How does inhibition of CI enhance organogenesis? - NA

2019-01-01 | GSE107673 | GEO

rotenone-Effect of the inhibition of the mitochondrial respiratory chain complex I (CI) on shoot initiation on protoplast-derived calli

Project description:rotenone-Effect of the inhibition of the mitochondrial respiratory chain complex I (CI) on shoot initiation on protoplast-derived calli

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Rotenone complex i mutants-Effect of the inhibition of the mitochondrial respiratory chain complex I (CI) on shoot initiation on protoplast-derived calli

Project description:Rotenone complex i mutants-Effect of the inhibition of the mitochondrial respiratory chain complex I (CI) on shoot initiation on protoplast-derived calli

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Salvage pathway maintains functional respiratory complex I

Project description:Regulation of the turnover of complex I (CI), the largest mitochondrial respiratory chain complex remains enigmatic, despite huge advancement in understanding its structure and the assembly steps in recent years. Although some studies indicated that CI might be remodelled in response to various stimuli, the mechanism mediating these putative changes is unknown. Here, we report that the NADH-oxidising N-module which sits on the tip of the CI peripheral arm is turned over at a higher rate and largely independently of the rest of the complex. The N-module turnover is mediated by mitochondrial matrix protease ClpXP, which selectively removes and degrades damaged core subunits. The observed mechanism seems to be a safeguard against accumulation of dysfunctional CI arising from inactivation of the N-module subunits due to attrition caused by extensive redox activity. This CI salvage pathway maintains highly functional CI and healthy mitochondria through an energetically favourable mechanism that demands much lower energetic cost than de novo synthesis and reassembly of the entire CI.

2020-03-05 | PXD014897 | Pride

Loss of COX4i1 leads to combined respiratory chain deficiency and impaired mitochondrial protein synthesis

Project description:The oxidative phosphorylation (OXPHOS) system localized in the inner mitochondrial membrane secures production of the majority of ATP in mammalian organisms. Individual OXPHOS complexes form supramolecular assemblies termed supercomplexes. The complexes are linked not only by their function but also by interdependence of individual complex biogenesis or maintenance. For instance, cytochrome c oxidase (cIV, COX) or cytochrome bc1 complex (cIII) deficiencies affect the level of fully assembled NADH dehydrogenase (cI) in monomeric as well as supercomplex forms. It was hypothesized that cI is affected at the level of enzyme assembly as well as at the level of cI stability and maintenance. However, the true nature of interdependency between cI and cIV is not fully understood yet. We used a HEK293 cellular model where the COX4 subunit was completely knocked out, serving as an ideal system to study interdependency of cI and cIV, as early phases of cIV assembly process are disrupted. Total absence of cIV was accompanied by profound deficiency of cI, documented by decrease in the levels of cI subunits and significantly reduced amount of assembled cI. Supercomplexes assembled from cI, cIII and cIV were missing in COX4 KO due to loss of cIV and decrease in cI amount. Pulse-chase metabolic labelling of mtDNA-encoded proteins uncovered a decrease in the translation of cIV and cI subunits. Moreover, partial impairment of mitochondrial protein synthesis correlated with decreased content of mitochondrial ribosomal proteins. In addition, complexome profiling revealed accumulation of cI assembly intermediates indicating that cI biogenesis, rather than stability, was the affected process. We propose, that impairment of mitochondrial protein synthesis caused by cIV deficiency represents one of the mechanisms which may couple biogenesis of cI and cIV.

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Selective Mitochondrial Respiratory Complex I Subunit Deficiency Causes Tumor Immunogenicity

Project description:Targeting of specific metabolic pathways in tumor cells has the potential to sensitize them to immune-mediated attack. Here we provide evidence for a specific means of mitochondrial respiratory Complex I (CI) inhibition that improves tumor immunogenicity and sensitivity to immune checkpoint blockade (ICB). Targeted genetic deletion of the CI subunits Ndufs4 and Ndufs6, but not other subunits, induces an immune-dependent tumor growth attenuation in mouse melanoma models. We show that deletion of Ndufs4 induces expression of the transcription factor Nlrc5 and genes in the MHC class-I antigen presentation and processing pathway. This induction of MHC-related genes is driven by an accumulation of pyruvate dehydrogenase-dependent mitochondrial acetyl-CoA downstream of CI subunit deletion. This work provides a novel functional modality by which selective CI inhibition restricts tumor growth, suggesting that specific targeting of Ndufs4, or related CI subunits, increases T-cell mediated immunity and sensitivity to ICB.

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Optimizing Protocols for Arabidopsis Shoot and Root Protoplast Cultivation.

Project description:Procedures for the direct regeneration of entire plants from a shoot and root protoplasts of Arabidopsis thaliana have been optimized. The culture media for protoplast donor-plant cultivation and protoplast culture have been adjusted for optimal plant growth, plating efficiency, and promotion of shoot regeneration. Protocols have been established for the detection of all three steps in plant regeneration: (i) chromatin relaxation and activation of auxin biosynthesis, (ii) cell cycle progression, and (iii) conversion of cell-cycle active cells to totipotent ones. The competence for cell division was detected by DNA replication events and required high cell density and high concentrations of the auxinic compound 2,4-D. Cell cycle activity and globular structure formation, with subsequent shoot induction, were detected microscopically and by labeling with fluorescent dye Rhodamine123. The qPCR results demonstrated significantly upregulated expression of the genes responsible for nuclear reorganization, auxin responses, and auxin biosynthesis during the early stage of cell reprogramming. We further optimized cell reprogramming with this protocol by applying glutathione (GSH), which increases the sensitivity of isolated mesophyll protoplasts to cell cycle activation by auxin. The developed protocol allows us to investigate the molecular mechanism of the de-differentiation of somatic plant cells.

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The respiratory chain inhibitor rotenone affects peroxisomal dynamics via its microtubule-destabilising activity.

Project description:Peroxisomes and mitochondria in mammalian cells are closely linked subcellular organelles, which maintain a redox-sensitive relationship. Their interplay and role in ROS signalling are supposed to impact on age-related and degenerative disorders. Whereas the generation of peroxisome-derived oxidative stress can affect mitochondrial morphology and function, little is known about the impact of mitochondria-derived oxidative stress on peroxisomes. Here, we investigated the effect of the mitochondrial complex I inhibitor rotenone on peroxisomal and mitochondrial membrane dynamics. We show that rotenone treatment of COS-7 cells alters peroxisome morphology and distribution. However, this effect is related to its microtubule-destabilising activity rather than to the generation of oxidative stress. Rotenone also induced alterations in mitochondrial morphology, which-in contrast to its effect on peroxisomes-were dependent on the generation of ROS but independent of its microtubule-active properties. The importance of our findings for the peroxisome-mitochondria redox relationship and the interpretation of in cellulo and in vivo studies with rotenone, which is widely used to study Parkinson's disease, are discussed.

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