Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1251291 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33154775_1.fastq.gz | Fastqsanger.gz | |||
| SRR33154775_2.fastq.gz | Fastqsanger.gz | |||
| SRR33154776_1.fastq.gz | Fastqsanger.gz | |||
| SRR33154776_2.fastq.gz | Fastqsanger.gz | |||
| SRR33154777_1.fastq.gz | Fastqsanger.gz |
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Project description:Autophagy, a critical process for the vacuolar degradation of proteins and organelles, is governed by multiple conserved autophagy-related (ATG) proteins. The central component of the ATG machinery is the ubiquitin-like protein ATG8, which is essential for multiple steps of the autophagy process, including phagophore expansion, autophagosome closure, trafficking and fusion with the lysosome/vacuole, and selective cargo recruitment. Currently, our understanding of the roles of ATG8 in plant autophagy and the functional specialization of ATG8 family members is limited due to genetic redundancy. To assess the roles of ATG8 genes in plant autophagy, here we used CRISPR/Cas9 technology to systematically knockout the Arabidopsis ATG8 genes. By analyzing the atg8 mutants, we found that in contrast to mammalian ATG8s, in which the LC3s and GABARAP subfamilies play distinct roles in the autophagic process, Arabidopsis ATG8s perform an overlapping function in controlling autophagic flux. Combinatorial mutations of Clade I and Clade II ATG8s resulted in severely impaired autophagy under nutrient-starved conditions. Furthermore, we found that RABG3 proteins, members of the RAB7/RABG GTPase family, interact with ATG8s through AIM-LDS interfaces, and that such interaction is essential for the association of RABG3 proteins with the autophagosomal membrane and probably for the fusion of autophagosome with the vacuole, but is not required for endosomal trafficking. With the collection of multiple high-order atg8 mutants generated in this study, we now provide a venue to study the roles of ATG8 genes in canonical autophagy and non-canonical autophagy in Arabidopsis.
2025-01-15 | PXD059803 | Pride
Project description:In this study, we performed RNA sequencing on tibialis anterior muscle of male mice. WT and Mtm1 deficient (Mtm1-/y) mice as well as on Dnm2+/- mice and on Mtm1-/y mice crossed with Dnm2+/- (Mtm1-/yDnm2+/-) were sequenced. A longitudinal follow up was established by sequencing all the genotypes at E18.5, 2w and 7w.
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Project description:In this study, we performed RNA sequencing on tibialis anterior muscle of male mice of 7 weeks of age. WT and Mtm1 deficient (Mtm1-/y) mice as well as tamoxifen-treated WT and tamoxifen-treated Mtm1-/y mice were sequenced.
2020-12-15 | GSE160083 | GEO
Project description:In this study, we performed RNA sequencing on tibialis anterior muscle of male mice at 7 weeks of age. WT and Mtm1 deficient (Mtm1-/y) mice were sequenced. The rescued mice, Mtm1-/y mice crossed with TgBIN1 mice (Mmt1-/yTgBIN1) and the associated control mice TgBIN1 were also sequenced.
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Project description:The arabidopsis L-type lectin receptor kinase-VI.2 positively regulates bacterial PAMP-triggered immunity. We used microarrays and performed genome-wide transcriptome analysis of LecRKVI.2 over-expressing plants and identified number of upregulated genes involved against bacterial resistance. Total RNA was isolated from 5-week-old Arabidopsis plants for RNA extraction and hybridisation on Affymetrix microarrays.
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Project description:Karrikin Receptor KARRIKIN INSENSITIVE2 Positively Regulates Heat Stress Tolerance in Arabidopsis thaliana
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Project description:Purpose: The goal of this study was to investigate the transcriptional profile of genes expressed in the quadriceps muscle of myotubularin deficient (Mtm1-/-) mice, and determine whether improvements in the pathophysiology of tamoxifen treated Mtm1-/- mice are a consequence of ER-dependent transcriptional modulation. Methods: Muscle mRNA profiles from quadriceps of 36-day-old wild-type (WT), myotubularin deficient (Mtm1-/-) mice, and tamoxifen treated WT and Mtm1-/- mice were generated by deep sequencing, in triplicate or quadruplicate, using Illumina HiSeq 2500. Read sets from each of the 14 samples across the four conditions were aligned to the reference genome (GRCm38/MM10 version of the Mus musculus genome) and transcriptome using STAR (Dobin et al. Bioinformatics 2013 PMID: 23104886) two-step alignment to generate a Binary Alignment Map file (BAM file). Coordinate sorted BAM files were used to quantify transcript abundance (count data) using HTSeq (Anders et al. Bioinformatics 2014, PMID: 25260700). Raw read counts generated were used as input for differential gene expression analysis, carried out using both DESeq (Anders and Huber 2010) and edgeR (Robinson, McCarthy, and Smyth 2010) R/Bioconductor packages. This was carried out in a pair-wise manner between any two conditions that were considered. FDR adjusted p-values from both edgeR and DESeq was used to determine genes that are significantly differentially expressed between the conditions tested. Finally, we used the GoSeq R/Bioconductor package (Young MD, et al Genome Biology, 11, pp. R14) to identify pathways that were significantly enriched for differentially expressed genes between any two conditions. Results: Using an established data analysis workflow, 65 million reads were aligned per sample (>90% exonic). We observed 849 differentially expressed transcripts in untreated mtm1-/-mice (p< 0.01) in comparison to wild-type (WT) controls. Furthermore, we identified 29 differentially expressed genes (p<0.01) between mtm1-/- mice and their TAM-treated mtm1-/- mice. In particular, we observed that the transcriptional profiles of mtm1 -/- mice and tamoxifen-treated mtm1-/- mice cluster together and are distinct from wild-type contros. Moreover, no significant changes were observed in the expression of estrogen-response genes that are known gene targets of tamoxifen; no significant transcriptional changes were observed in well-known MTM-related genes.This strongly indicates that, contrary to its well-established function as a transcriptional modulator, tamoxifen improves the pathophysiology of myotubular myopathy in a post-transcriptional manner. Concusions: Our study represents the first comprehensive analysis of the whole transcriptome of the Mtm1-/- and tamoxifen treated Mtm1-/- mouse, generated by RNA-seq technology. The data reported here provides a framework a comparative investigation of the expression profiles in Mtm1-/- mice and tamoxifen treated Mtm1-/- mice. Importantly, our results demonstrate that in our MTM murine model, tamoxifen does not appear to alter the transcriptional profile of many estrogen-receptor (ER) related genes, and moreover does not appear to alter the transcriptional profile of genes that are abnormally expressed in Mtm1-/- mice alone. This suggests that tamoxifen is acting to improve the pathophysiology of the MTM mouse model in a transcriptionally-indepedent manner.
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2018-05-18 | GSE108858 | GEO