Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cardiac mitochondrial function depends on BUD23 mediated ribosome programming

ABSTRACT: Cardiac mitochondrial function depends on BUD23 mediated ribosome programming

PROVIDER: PRJEB36241 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR3814200_1.fastq.gz	Fastqsanger.gz
	ERR3814200_2.fastq.gz	Fastqsanger.gz
	ERR3814210_1.fastq.gz	Fastqsanger.gz
	ERR3814210_2.fastq.gz	Fastqsanger.gz
	ERR3814201_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 36

Similar Datasets

Cardiac mitochondrial function depends on BUD23 mediated ribosome programming

2020-01-23 | E-MTAB-8673 | biostudies-arrayexpress

Cardiac mitochondrial function depends on BUD23 mediated ribosome programming.

Project description:Efficient mitochondrial function is required in tissues with high energy demand such as the heart, and mitochondrial dysfunction is associated with cardiovascular disease. Expression of mitochondrial proteins is tightly regulated in response to internal and external stimuli. Here we identify a novel mechanism regulating mitochondrial content and function, through BUD23-dependent ribosome generation. BUD23 was required for ribosome maturation, normal 18S/28S stoichiometry and modulated the translation of mitochondrial transcripts in human A549 cells. Deletion of Bud23 in murine cardiomyocytes reduced mitochondrial content and function, leading to severe cardiomyopathy and death. We discovered that BUD23 selectively promotes ribosomal interaction with low GC-content 5'UTRs. Taken together we identify a critical role for BUD23 in bioenergetics gene expression, by promoting efficient translation of mRNA transcripts with low 5'UTR GC content. BUD23 emerges as essential to mouse development, and to postnatal cardiac function.

| S-EPMC7002040 | biostudies-literature

Analysis of mitochondrial gene expression with Ribosome Profiling

Project description:Ribosome profiling (RiboSeq) maps positions of translating ribosomes on the transcriptome. Here we optimized ribosome profiling for footprinting mitochondrial ribosomes, and profiled three human cell-lines - HEK293, a PDE12-/- knockout, and a deltaFLP 143B cybrid.

2017-07-25 | E-MTAB-5519 | biostudies-arrayexpress

Ribosome profiling reveals features of normal and disease-associated mitochondrial translation

Project description:Ribosome profiling and RNAseq data on human BJ fibroblasts and cybrid cells using an adapted ribosome profiling protocol to improve detection of mitochondrial ribosome protected fragments 51-base length single read ribosome profiling data on human fibroblasts and cybrid cells using an adapted ribosome profiling protocol; and 51-base length single read RNAseq on polyA enriched RNA

2013-10-17 | E-GEOD-48933 | biostudies-arrayexpress

Intrauterine growth restriction is associated with cardiac ultrastructural and gene expression changes related to the energetic metabolism in a rabbit model

Project description:Intrauterine growth restriction (IUGR) affects 7-10% of pregnancies and is associated with cardiovascular remodeling and dysfunction which persists into adulthood. The underlying subcellular remodeling and cardiovascular programming events are still poorly documented. Cardiac muscle is central in the fetal adaptive mechanism to IUGR given its high energetic demands. The energetic homeostasis depends on the correct interaction of several molecular pathways and the adequate arrangement of intracellular energetic units (ICEUs), where mitochondria interact with the contractile machinery and the main cardiac ATPases to enable a quick and efficient energy transfer. We studied subcellular cardiac adaptations to IUGR in an experimental rabbit model. We evaluated the ultrastructure of ICEUs with transmission electron microscopy and observed an altered spatial arrangement in IUGR, with significant increases in cytosolic space between mitochondria and myofilaments. A global decrease of mitochondrial density was also observed. In addition, we conducted a global gene expression profile by advanced bioinformatics tools to assess the expression of genes involved in the cardiomyocyte energetic metabolism, and identified four gene modules with a coordinated over-representation in IUGR: oxygen homeostasis (GO: 0032364), mitochondrial respiratory chain complex I (GO:0005747), oxidative phosphorylation (GO: 0006119) and NADH dehydrogenase activity (GO:0003954). These findings might contribute to changes in energetic homeostasis in IUGR. The potential persistence and role of these changes in long term cardiovascular programming deserves further investigation. In this study, we used gene expression arrays to investigate differences between two experimental groups: IUGR and control. The design includes paired samples.

2013-10-30 | E-GEOD-37860 | biostudies-arrayexpress

Klf9 is essential for cardiac mitochondrial homeostasis

Project description:Mitochondrial dynamics and mitophagy are intimately linked physiological processes that are essential for cardiac homeostasis. Here we show that cardiac Klf9 is dysregulated in human and rodent cardiomyopathy. Young adult global Klf9-knockout mice displayed hypertrophic cardiomyopathy that was characterized by depressed systolic function, increased left ventricular mass and pulmonary congestion. Klf9 knockout led to mitochondrial disarray and fragmentation in cardiomyocytes. Biochemical analysis confirmed that mitochondrial respiratory function was impaired in Klf9-knockout cardiomyocytes, with reduced myocardial ATP levels and elevated ROS. Furthermore, cardiac-specific Klf9-deficient mice phenocopied global Klf9-knockout mice, suggesting that cardiac Klf9 is essential for mitochondrial homeostasis and heart function. Moreover, cardiac Klf9 deficiency inhibited mitophagy induced by angiotensin II (ANGII), thereby leading to accumulation of dysfunctional mitochondria and acceleration of heart failure in mice in response to ANGII treatment. In contrast, cardiac-specific Klf9 transgene improved cardiac systolic function via promoting mitophagy in mice in response to ANGII treatment. Molecular mechanism studies indicated that Klf9 knockout decreased the expression of PGC-1α and its target genes involved in mitochondrial energy metabolism. Moreover, Klf9 controlled the expression of Mfn2 by directly binding to its promoter region, thereby regulating mitochondrial dynamics and mitophagy. Finally, we performed Mfn2 rescue experiments in Klf9-CKO mice and found that AAV-mediated Mfn2 rescue in heart improved cardiac mitochondrial and systolic function in Klf9-CKO mice treated with or without ANGII. Thus, Klf9 integrates cardiac energy metabolism, mitochondrial dynamics and mitophagy. Modulating Klf9 activity may have therapeutic potential in the treatment of heart failure.

2024-10-03 | GSE278326 | GEO

Ribosome profiling reveals features of normal and disease-associated mitochondrial translation

2013-10-17 | GSE48933 | GEO

Small is big in Arabidopsis mitochondrial ribosome

Project description:Small is big in Arabidopsis mitochondrial ribosome

| PRJNA489863 | ENA

Analysis of mitochondrial gene expression with Ribosome Profiling

Project description:Analysis of mitochondrial gene expression with Ribosome Profiling

| PRJEB19678 | ENA

Analysis of the Chlamydomonas mitochondrial ribosome RNA content

Project description:Analysis of the Chlamydomonas mitochondrial ribosome RNA content

| PRJNA718484 | ENA