Gymnogobius isaza
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB14773 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gymnogobius petschiliensis overview
| PRJNA660830 | ENA
Project description:Transcriptome sequence of Gymnogobius petschiliensis
| PRJDB10494 | ENA
Project description:Gymnogobius scrobiculatus mitochondrial Metagenomic assembly
| PRJNA1109288 | ENA
Project description:Transcriptome of goby fish larvae reared in fresh- and seawater
| PRJDB12996 | ENA
Project description:The goal of this analysis was to utilize microarray profiling to identify basal alterations in gene expression in response to TFAM depletion and mtDNA stress. Mitochondrial DNA (mtDNA) is normally present at thousands of copies per cell and is packaged into several hundred higher-order structures termed nucleoids. The abundant mtDNA-binding protein, TFAM (transcription factor A,mitochondrial), regulates nucleoid architecture, abundance and segregation. Complete mtDNA depletion profoundly impairs oxidative phosphorylation, triggering calcium-dependent stress signalling and adaptive metabolic responses. However, the cellular responses to mtDNA instability, a physiologically relevant stress observed in many human diseases and ageing, remain poorly defined. Here we show that moderate mtDNA stress elicited by TFAM deficiency engages cytosolic antiviral signalling to enhance the expression of a subset of interferon-stimulated genes. Mechanistically, we find that aberrant mtDNA packaging promotes escape of mtDNA into the cytosol, where it engages the DNA sensor cGAS (also known as MB21D1) and promotes STING (also known as TMEM173)–IRF3-dependent signalling to elevate interferon-stimulated gene expression, potentiate type I interferon responses and confer broad viral resistance. Furthermore, we demonstrate that herpesviruses induce mtDNA stress, which enhances antiviral signalling and type I interferon responses during infection. Our results further demonstrate that mitochondria are central participants in innate immunity, identify mtDNA stress as a cell-intrinsic trigger of antiviral signaling and suggest that cellular monitoring of mtDNA homeostasis cooperates with canonical virus sensing mechanisms to fully engage antiviral innate immunity. Murine embryonic fibroblasts were isolated from wild-type or Tfam+/- E13.5 littermate embryos. RNA from passage-matched wild-type and Tfam+/- MEF lines was extracted in duplicate and hybridized onto Affymetrix microarrays. Four arrays were performed in total with two technical replicates per genotype.
2015-01-26 | E-GEOD-63767 | biostudies-arrayexpress
Project description:Maternal inheritance of mitochondrial DNA (mtDNA) is highly conserved in metazoans. While many species eliminate paternal mtDNA during late sperm development to foster maternal inheritance, the regulatory mechanisms governing this process remain elusive. Through a large-scale genetic screen in Drosophila, we identified 47 mutant lines exhibiting substantial retention of mtDNA in mature sperm. We mapped one line to Poldip2, a gene predominantly expressed in the testis. Disruption of Poldip2 led to pronounced mtDNA retention in mature sperm and subsequent paternal transmission to progeny. Further investigation via imaging, biochemical analyses and ChIP assays revealed that POLDIP2 is a mitochondrial matrix protein capable of binding to mtDNA. Moreover, we uncovered that CLPX, a key component of the major mitochondrial protease, binds to POLDIP2 to co-regulate mtDNA elimination in Drosophila spermatids. This study shed light on the mechanisms underlying mtDNA removal during spermatogenesis, underscoring the pivotal role of this process in safeguarding maternal inheritance.
2024-06-04 | E-MTAB-14100 | biostudies-arrayexpress
Project description:Background: Developments in DNA resequencing microarrays include mitochondrial DNA (mtDNA) sequencing and mutation detection. During automated analysis to sequence mtDNA, bases can be identified as wildtype, variant, or there may be a failure to assign a base (N-call) when compared to the mtDNA reference sequence (rCRS). The purpose of our study was to re-examine the N-call distribution of mtDNA samples, based on the hypothesis that N-calls may represent insertions or deletions in mtDNA. Findings: We analysed mtDNA from 16 patient samples (8 blood/bone marrow origin and 8 from cultured fibroblasts) using the Affymetrix MitoChip v.2.0 which has 2 probe areas, one for sequencing compared to the rCRS and one for 500 common haplotypes. N-calls by the proprietary GSEQ software were significantly reduced when the freeware on-line algorithm M-bM-^@M-^XsPROFILERM-bM-^@M-^Y was utilized. Interestingly, this decrease in N-calls, in both sections of the MitoChip, had no effect on the homoplasmic or heteroplasmic mutation levels compared to GSEQ software. We then used conventional DNA sequencing to analyse continuous N-call stretches identified by sPROFILER, ranging from 2 to 22 bases, to identify changes resulting in base calling failures. Conclusions: Our study is the first to analyse N-calls produced from GSEQ software for the MitoChip v2.0. We found that by narrowing the focus to stretches of N-calls revealed by sPROFILER, conventional sequencing was able to identify unique deletions and insertions. This study also appeared to support the contention that the GSEQ is more capable of assigning bases when used in conjunction with sPROFILER. mtDNA from 16 patient samples were analysed using Mitochip v2.0. Eight samples were DNA extractions directly from blood/bone marrow. The other eight samples were DNA extractions from primary cultured fibroblasts. Results were generated in GSEQ and reanalysed in sPROFILER for comparison.
2012-05-17 | E-GEOD-29550 | biostudies-arrayexpress