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Functional characterization of a Drosophila melanogaster mitochondrial deoxynucleotide transporter dRIM2.

ABSTRACT: We have studied the deoxynucleotide transport in Drosophila melanogaster. On the basis of homology with the S. cerevisiae RIM2 gene, encoding a pyrimidine deoxynucleotide carrier (Marrobbio et al. 2006), the CG18317 gene (dRIM2) in the fruit fly may code for a deoxynucleotide carrier. We demonstrated that Drosophila S2R+ cells, silenced for the dRIM2 expression, had a marked defect in the amounts of all mitochondrial dNTPs, both purines and pyrimidines. In vivo dRIM2 homozygous knockout produced a larval lethal phenotype. dRIM2-/- larvae showed (i) impairments in the locomotor behavior, (ii) a decrease in the rates of oxygen consumption and (iii) a depletion of the mtDNA. Following a detailed morphological characterization carried out in dRIM2-/- larvae evidenced an ongoing mitochondrial biogenesis accompanied by an alteration of mitochondria shaping. Additionally, the role of dRIM2 in the purine and pyrimidine metabolism was supported by a microarray analysis. We conclude that dRIM2 is a Drosophila deoxynucleotide carrier, essential for maintaining the mitochondrial functionality.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE48012 | GEO | 2014/05/02

SECONDARY ACCESSION(S): PRJNA208661

REPOSITORIES: GEO

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Functional characterization of a Drosophila melanogaster mitochondrial deoxynucleotide transporter dRIM2.

Project description:We have studied the deoxynucleotide transport in Drosophila melanogaster. On the basis of homology with the S. cerevisiae RIM2 gene, encoding a pyrimidine deoxynucleotide carrier (Marrobbio et al. 2006), the CG18317 gene (dRIM2) in the fruit fly may code for a deoxynucleotide carrier. We demonstrated that Drosophila S2R+ cells, silenced for the dRIM2 expression, had a marked defect in the amounts of all mitochondrial dNTPs, both purines and pyrimidines. In vivo dRIM2 homozygous knockout produced a larval lethal phenotype. dRIM2-/- larvae showed (i) impairments in the locomotor behavior, (ii) a decrease in the rates of oxygen consumption and (iii) a depletion of the mtDNA. Following a detailed morphological characterization carried out in dRIM2-/- larvae evidenced an ongoing mitochondrial biogenesis accompanied by an alteration of mitochondria shaping. Additionally, the role of dRIM2 in the purine and pyrimidine metabolism was supported by a microarray analysis. We conclude that dRIM2 is a Drosophila deoxynucleotide carrier, essential for maintaining the mitochondrial functionality. Gene expression profiling was carried out on dRIM-/- and dRIM+/- Drosophila larvae using the Drosophila 1.0 custom platform (Agilent). Total RNA was obtained from the whole body of 3rd instar larvae for each genotype. Four and three biological replicates were analyzed for dRIM-/- and dRIM+/- samples respectively for a total of 7 microarray experiments.

2014-05-02 | E-GEOD-48012 | biostudies-arrayexpress

Drosophila melanogaster

Project description:Functional characterization of a Drosophila melanogaster mitochondrial deoxynucleotide transporter dRIM2.

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Cellular pyrimidine imbalance triggers mitochondrial DNA-dependent innate immunity [WT_vs_Yme1lKO_MEF_RNA-seq]

Project description:Cytosolic mitochondrial DNA (mtDNA) elicits a type I interferon response, but signals triggering the release of mtDNA from mitochondria remain enigmatic. Here, we show that mtDNA-dependent immune signalling via the cyclic GMP–AMP syn- thase‒stimulator of interferon genes‒TANK-binding kinase 1 (cGAS–STING–TBK1) pathway is under metabolic control and is induced by cellular pyrimidine deficiency. The mitochondrial protease YME1L preserves pyrimidine pools by supporting de novo nucleotide synthesis and by proteolysis of the pyrimidine nucleotide carrier SLC25A33. Deficiency of YME1L causes inflamma- tion in mouse retinas and in cultured cells. It drives the release of mtDNA and a cGAS–STING–TBK1-dependent inflammatory response, which requires SLC25A33 and is suppressed upon replenishment of cellular pyrimidine pools. Overexpression of SLC25A33 is sufficient to induce immune signalling by mtDNA. Similarly, depletion of cytosolic nucleotides upon inhibition of de novo pyrimidine synthesis triggers mtDNA-dependent immune responses in wild-type cells. Our results thus identify mtDNA release and innate immune signalling as a metabolic response to cellular pyrimidine deficiencies.

2021-02-26 | GSE161735 | GEO

Cellular pyrimdine imbalance triggers mitochondrial DNA-dependent innate immunity [Scr_vs_Yme1l-si_RNA-seq]

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Cellular pyrimidine imbalance triggers mitochondrial DNA-dependent innate immunity [HeLa_CAD_RNA-seq]

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Leigh Syndrome in Drosophila melanogaster: morphological and biochemical characterization of Surf1 post-transcriptional silencing.

Project description:Leigh Syndrome (LS) is the most common early-onset, progressive mitochondrial encephalopathy usually leading to early death. The single most prevalent cause of LS is occurrence of mutations in the hSurf1 gene. LSSurf1 patients show a marked and specific decrease in the activity of mitochondrial respiratory chain complex IV (cytochrome c oxidase, COX). hSurf1 encodes an inner membrane mitochondrial protein involved in COX assembly. We established a D. melanogaster model of LS based on the post-transcriptional silencing of CG9943, the Drosophila homolog of hSurf1. Knock down of Surf1 was induced (i) ubiquitously, which led to larval lethality; (ii) in the mesodermal derivatives, which led to pupal lethality; (iii) in the central nervous system, which allowed survival; and (iv) at specific developmental stages. A biochemical characterization was carried out in knock down individuals, which unexpectedly revealed defects in all complexes of the mitochondrial respiratory chain (MRC) included the F-ATP synthase (complex V) in larvae, and a COX-specific impairment in adults. Silencing of Surf1 expression in Drosophila S2R+ cells led to loss of COX activity associated with decreased oxygen consumption. We conclude that Surf1 is essential for COX activity and mitochondrial function in D. melanogaster, and provide a new tool to clarify the pathogenic mechanisms of LS.

2014-11-04 | GSE58301 | GEO

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Project description:The genomic distribution of a novel transcription factor called M1BP was determined in Drosophila S2R+ cells

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Project description:The goal of this experiment was to identify genomic dCAP-D3 binding sites in Drosophila S2R+ cells

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Project description:The goal of this study was to determine how decreased mitochondrial citrate export influences gene expression in Drosophila larvae. RNA was isolated from Drosopohila sea mutants, which exhibiti decreased mitochondrial citrate transport activity, and a genetically-matched control strain during mid-L3 development.

2018-09-07 | GSE117117 | GEO

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