Ontology highlight
ABSTRACT:
PROVIDER: PRJNA766754 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16093744_1.fastq.gz | Fastqsanger.gz | |||
| SRR16093744_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 2 of 2 |
Similar Datasets
Project description:The thiolation modification of tRNA is essential for plant immunity
| PRJNA759143 | ENA
Project description:Plants have evolved sophisticated mechanisms to regulate gene expression to activate immune responses against pathogen infections. However, how the translation system contributes to plant immunity is largely unknown. The evolutionarily conserved thiolation modification of tRNA ensures efficient decoding during translation. Here we show that tRNA thiolation is required for plant immunity in Arabidopsis. The Arabidopsis cgb mutant is hyper-susceptible to the pathogen Pseudomonas syringae. CGB encodes ROL5, a homolog of yeast NCS6 required for tRNA thiolation. ROL5 physically interacts with CTU2, a homolog of yeast NCS2. Mutations in either ROL5 or CTU2 result in loss of tRNA thiolation. Further analyses reveal that tRNA thiolation is required for both transcriptional reprogramming and translational reprogramming during immune responses. The translation efficiency of immune-related proteins reduces when tRNA thiolation is absent. Our study not only uncovers a new biological function of tRNA thiolation but also reveals a new mechanism for plant immunity.
2022-08-31 | GSE183087 | GEO
Project description:Plants have evolved sophisticated mechanisms to regulate gene expression to activate immune responses against pathogen infections. However, how the translation system contributes to plant immunity is largely unknown. The evolutionarily conserved thiolation modification of tRNA ensures efficient decoding during translation. Here we show that tRNA thiolation is required for plant immunity in Arabidopsis. The Arabidopsis cgb mutant is hyper-susceptible to the pathogen Pseudomonas syringae. CGB encodes ROL5, a homolog of yeast NCS6 required for tRNA thiolation. ROL5 physically interacts with CTU2, a homolog of yeast NCS2. Mutations in either ROL5 or CTU2 result in loss of tRNA thiolation. Further analyses reveal that tRNA thiolation is required for both transcriptional reprogramming and translational reprogramming during immune responses. The translation efficiency of immune-related proteins reduces when tRNA thiolation is absent. Our study not only uncovers a new biological function of tRNA thiolation but also reveals a new mechanism for plant immunity.
2022-07-05 | PXD028189 |
Project description:The tRNA N7-methylguanosine (m7G) modification is not essential for yeast growth, but in mammals mis-regulations of tRNA m7G modification cause stem cell defect and developmental disorders. Here we found that tRNA m7G methyltransferase complex components METTL1 and WDR4 are elevated in lung cancer tissues and associated with poor lung cancer prognosis. Functionally, depletion of METTL1 or WDR4 suppresses proliferation, migration, and invasion of lung cancer cells. In addition, forced expression of METTL1 or WDR4 promotes lung cancer progression depending on the tRNA m7G methyltransferase activity. Mechanistically, METTL1 knockdown leads to reduced tRNA m7G modification and decreased expression of m7G-modified tRNAs. Depletion of METTL1 selectively reduces the translation of a subset of oncogenic transcripts, including the genes related to cell proliferation in a m7G related codon dependent manner. Our study uncovered a new layer of translation regulation mechanism mediated by tRNA m7G modification, provided strong evidence to support the important physiological function of mis-regulated tRNA modification in cancer, and suggested that targeting METTL1 could be a promising strategy for lung cancer treatment.
2022-12-31 | GSE173760 | GEO
Project description:While performing mitochondrial isolations and recently developed tRNA-seq methods (AlkB treatment and YAMAT-Seq) in plant tissue, we inadvertently sequenced the mitochondrial tRNAs from a common plant pest, the acariform mite Tetranychus urticae, to a high enough coverage to detect all previously annotated T. urticae tRNA regions. The results not only confirm expression, CCA-tailing and post-transcriptional base modification of these highly divergent tRNAs, but also revealed paired sense and antisense expression of multiple T. urticae mitochondrial tRNAs.
2020-12-10 | GSE162913 | GEO
Project description:Suppressor mutant screening lacking growth-essential tRNA modification in bacteria
| PRJEB56046 | ENA
Project description:The tRNA N7-methylguanosine (m7G) modification is not essential for yeast growth, but in mammals mis-regulations of tRNA m7G modification cause stem cell defect and developmental disorders. Here we found that homozygous mutated WDR4 caused microcephaly, retardation in motor coordination and spatial learning ability in mice, which mimics the symptom in human patients with WDR4 mutation. Further analysis revealed that homozygous mutation of WDR4 impaired tRNA m7G modification and reduced the translation level of genes involved in mTOR signaling pathway in mouse brain, which further caused endoplasmic reticulum (ER) stress and cell death. Our study uncovered a new layer of translation regulation mechanism mediated by tRNA m7G modification, provided strong evidence to support the important physiological function of mis-regulated tRNA modification in neuron disorders.
2024-10-16 | GSE229610 | GEO
Project description:The tRNA N7-methylguanosine (m7G) modification is not essential for yeast growth, but in mammals mis-regulations of tRNA m7G modification cause stem cell defect and developmental disorders. Here we found that homozygous mutated WDR4 caused microcephaly, retardation in motor coordination and spatial learning ability in mice, which mimics the symptom in human patients with WDR4 mutation. Further analysis revealed that homozygous mutation of WDR4 impaired tRNA m7G modification and reduced the translation level of genes involved in mTOR signaling pathway in mouse brain, which further caused endoplasmic reticulum (ER) stress and cell death. Our study uncovered a new layer of translation regulation mechanism mediated by tRNA m7G modification, provided strong evidence to support the important physiological function of mis-regulated tRNA modification in neuron disorders.
2024-10-16 | GSE229243 | GEO
Project description:The tRNA N7-methylguanosine (m7G) modification is not essential for yeast growth, but in mammals mis-regulations of tRNA m7G modification cause stem cell defect and developmental disorders. Here we found that homozygous mutated WDR4 caused microcephaly, retardation in motor coordination and spatial learning ability in mice, which mimics the symptom in human patients with WDR4 mutation. Further analysis revealed that homozygous mutation of WDR4 impaired tRNA m7G modification and reduced the translation level of genes involved in mTOR signaling pathway in mouse brain, which further caused endoplasmic reticulum (ER) stress and cell death. Our study uncovered a new layer of translation regulation mechanism mediated by tRNA m7G modification, provided strong evidence to support the important physiological function of mis-regulated tRNA modification in neuron disorders.
2024-10-16 | GSE229242 | GEO
Project description:The tRNA N7-methylguanosine (m7G) modification is not essential for yeast growth, but in mammals mis-regulations of tRNA m7G modification cause stem cell defect and developmental disorders. Here we found that homozygous mutated WDR4 caused microcephaly, retardation in motor coordination and spatial learning ability in mice, which mimics the symptom in human patients with WDR4 mutation. Further analysis revealed that homozygous mutation of WDR4 impaired tRNA m7G modification and reduced the translation level of genes involved in mTOR signaling pathway in mouse brain, which further caused endoplasmic reticulum (ER) stress and cell death. Our study uncovered a new layer of translation regulation mechanism mediated by tRNA m7G modification, provided strong evidence to support the important physiological function of mis-regulated tRNA modification in neuron disorders.
2024-10-16 | GSE229240 | GEO