Calamaria berezowskii
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ABSTRACT:
PROVIDER: PRJNA1105319 | ENA |
REPOSITORIES: ENA
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Project description:Calamaria berezowskii Raw sequence reads
| PRJNA1105351 | ENA
Project description:Electron transport chain (ETC) biogenesis is tightly coupled to energy levels and availability of ETC subunits. Coenzyme Q: cytochrome c oxidoreductase (complex III or CIII) occupies a central position in the ETC, receiving electrons from diverse fuel sources to control the ubiquinol:ubiquinone (CoQH2/CoQ) ratio. As such, CIII is an attractive node for controlling ETC biogenesis during metabolic stress. Here, we report the discovery of mammalian CoOrdinator of Mitochondrial CYTB or “COM” complexes that regulate CIII biogenesis in a step-wise fashion in response to nutrient and nuclear-encoded ETC subunit availability. The COMA complex, consisting of UQCC1/2 and the membrane anchor C16ORF91 (UQCC4), facilitates the translation of CIII enzymatic core subunit CYTB. Subsequently, microproteins SMIM4 and BRAWNIN, together with COMA subunits form the COMB complex that stabilizes nascent CYTB. Finally, UQCC3-containing COMC promotes CTYB maturation and association with downstream CIII subunits. This stepwise assembly enables cells to adapt to metabolic stress by increasing CIII biogenesis and inducing an integrated stress response when challenged. Furthermore, when nuclear CIII subunits are unavailable for assembly, COMB is required to chaperone nascent CYTB to prevent OXPHOS collapse. Our studies highlight CYTB synthesis as a key regulatory node of ETC biogenesis, and uncover the roles of mito-SEPs in mitochondrial homeostasis during energy stress.
2022-09-25 | PXD030258 | Pride
Project description:Sarda orientalis isolate CF-2 cytochrome b (cytb) gene, partial cds mitochondrial Raw sequence reads
| PRJNA541341 | ENA
Project description:Mitochondrial gene expression needs to be balanced with cytosolic translation to produce oxidative phosphorylation complexes. In yeast, translational feedback loops involving lowly expressed proteins called translational activators help to achieve this balance. Synthesis of cytochrome b (Cytb or COB), a core subunit of complex III in the respiratory chain, is controlled by three translational activators and the assembly factor Cbp3-Cbp6. However, the molecular interface between the COB translational feedback loop and complex III assembly is yet unknown. Here, using protein-proximity mapping combined with selective mitoribosome profiling, we reveal the components and dynamics of the molecular switch controlling COB translation. Specifically, we demonstrate that Mrx4, a previously uncharacterized ligand of the mitoribosomal polypeptide tunnel exit, interacts with either the assembly factor Cbp3-Cbp6 or with the translational activator Cbs2. These reciprocal interactions determine whether the translational activator complex with bound COB mRNA can interact with the mRNA channel exit on the small ribosomal subunit for translation initiation. Organization of the feedback loop at the tunnel exit therefore orchestrates mitochondrial translation with respiratory chain biogenesis
2025-07-11 | PXD061279 | Pride
Project description:The mitochondrial respiratory chain is composed of lipoprotein complexes imbedded in the inner mitochondrial membrane. This chain of enzymes transfers electrons from NADH and FADH2, provided from divers metabolic pathways, to oxygen. It couples the transfer of electrons to the translocation of protons across the membrane. Several clinical syndromes have been associated with respiratory dysfunction caused by mitochondrial or nuclear mutations. A number of mutations in the mitochondrial genes encoding for cytochrome b (CYTB) and cytochrome oxidase (COX 1, 2 and 3) have been linked with diseases. We are using yeast mutants to characterize the deleterious effect of mutations reported in patients on the assembly and catalytic properties of the affected enzymes, and to study the impact of mutations in nuclear genes, such as OXA1, encoding for factors required for the assembly of the respiratory complexes. In this work, we monitored the effects of the mutations causing respiratory defect on the whole genome expression. We compared the change in gene expression in rho0 cells (with a complete deletion of the mitochondrial genome, and by consequence without respiratory chain), in cells with either a single defective enzyme or several, and in cells after prolonged treatment with the bc1 inhibitors myxothiazol or antimycin. The impact of the mutations on the respiratory function ranged from mild to severe. The expression of approx. 350 genes was changed in at least one mutant. Cluster analysis was performed using the Cluster program (Eisen, 1998, PNAS 95:14863). Four groups of genes were studied in more details: Group A, the most repressed genes; Group B, the most over-expressed genes; Group C, genes more repressed in rho0 and Doxa1 cells; and Group D, genes more over-expressed in Doxa1.
2009-02-20 | E-MEXP-585 | biostudies-arrayexpress