Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic analysis of Arabidopsis thaliana seedlings in response to impaired mitochondrial translation

ABSTRACT: Transcriptomic analysis of Arabidopsis thaliana seedlings in response to impaired mitochondrial translation

PROVIDER: PRJNA1111132 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Transcriptomic analysis of Arabidopsis thaliana seedlings in response to impaired mitochondrial translation

Project description:The goal of this study is to establish the global gene expression profiles of seedlings under doxycycline (Dox) treatment.

2025-04-20 | GSE267356 | GEO

Transcriptomic analysis of Arabidopsis thaliana seedlings in response to impaired mitochondrial translation

Project description:The goal of this study is to establish the global gene expression profiles of seedlings under doxycycline treatment or genetic silencing of MRPL1 (AT2G42710).

2017-11-02 | GSE78862 | GEO

Impaired age-associated mitochondrial translation is mitigated by exercise and PGC-1α

Project description:Impaired age-associated mitochondrial translation is mitigated by exercise and PGC-1α

| PRJNA976340 | ENA

Mitochondrial translation accuracy

Project description:Hyperaccurate mitochondrial translation increases cellular proteostatic capacity

| PRJEB17642 | ENA

bnsdp1 impaired seedling growth, especially in yellowed seedlings

Project description:impaired seedling growth, especially in yellowed seedlings, was not fully rescued in medium supplemented with exogenous sucrose.

2023-12-30 | GSE252072 | GEO

Arabidopsis thaliana

Project description:Transcriptomic analysis of Arabidopsis thaliana seedlings in response to impaired mitochondrial translation

| PRJNA314197 | ENA

bnsdp1 impaired seedling growth, especially in yellowed seedlings

Project description:bnsdp1 impaired seedling growth, especially in yellowed seedlings

| PRJNA1057264 | ENA

MicroRNA Directly Enhances Mitochondrial Translation during Muscle Differentiation.

Project description:MicroRNAs are well known to mediate translational repression and mRNA degradation in the cytoplasm. Various microRNAs have also been detected in membrane-compartmentalized organelles, but the functional significance has remained elusive. Here we report that miR-1, a microRNA specifically induced during myogenesis, efficiently enters the mitochondria where it unexpectedly stimulates, rather than represses, the translation of specific mitochondrial genome-encoded transcripts. We show that this positive effect requires specific miR:mRNA base-pairing and Ago2, but not its functional partner GW182, which is excluded from the mitochondria. We provide evidence for the direct action of Ago2 in mitochondrial translation by Ago2 CrossLinking ImmunoPrecipitation coupled with sequencing (CLIP-seq), functional rescue with mitochondria-targeted Ago2, and selective inhibition of the microRNA machinery in the cytoplasm. These findings unveil a positive function of microRNA in mitochondrial translation and suggest a highly coordinated myogenic program via miR-1 mediated translational stimulation in the mitochondria and repression in the cytoplasm. Examination of miRNA's regulation function in mitochondria in C2C12 myoblasts cells and myotubes cells with CLIP-seq (Ago2).

2014-08-01 | E-GEOD-57596 | biostudies-arrayexpress

Mitochondrial unfolded protein response controls matrix pre-RNA processing and translation

Project description:The mitochondrial matrix is unique in that it must integrate folding and assembly of proteins derived from nuclear and mitochondrial genomes. In C. elegans, the mitochondrial unfolded protein response (UPRmt) senses matrix protein misfolding and induces a program of nuclear gene expression, including mitochondrial chaperonins, to promote mitochondrial proteostasis. While misfolded mitochondrial matrix-localized ornithine trans-carbamylase (OTC) induces chaperonin expression, our understanding of mammalian UPRmt is rudimentary, reflecting a lack of acute triggers for UPRmt activation. This limitation has prevented analysis of the cellular responses to matrix protein misfolding and the effects of UPRmt on mitochondrial translation to control protein folding loads. Here, we combine pharmacological inhibitors of matrix-localized HSP90/TRAP1 or LON protease, which promote chaperonin expression, with global transcriptional and proteomic analysis to reveal an extensive and acute response of human cells to UPRmt. This response involved widespread induction of nuclear genes, including matrix-localized proteins involved in folding, pre-RNA processing and translation. Functional studies revealed rapid but reversible translation inhibition in mitochondria occurring concurrently with defects in pre-RNA processing due to transcriptional repression and LON-dependent turnover of the mitochondrial pre-RNA processing nuclease MRPP3. This study reveals that acute mitochondrial protein folding stress activates both increased chaperone availability within the matrix and reduced matrix-localized protein synthesis through translational inhibition, and provides a framework for further dissection of mammalian UPRmt. triplicate experiment of 3 conditions (untreated, GTPP treatment, CDDO treatment)

2016-06-28 | E-GEOD-75247 | biostudies-arrayexpress

Mitochondrial unfolded protein response controls matrix pre-RNA processing and translation

2016-06-28 | E-GEOD-75410 | biostudies-arrayexpress