Ontology highlight
ABSTRACT:
PROVIDER: PRJNA553311 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To study the expression profiles of hexaploid wheat chromosome 3B genes during the life cycle of a wheat plant and establish a transcriptome atlas for this chromosome, deep transcriptome sequencing was conducted in duplicates in 15 wheat samples corresponding to five different organs (leaf, shoot, root, spike, and grain) at three developmental stages each. Strand-non-specific and strand-specific libraries were used to produce 2.52 billion paired-end reads (232 Gb) and 615.3 single-end reads (62 Gb), respectively.
2014-09-08 | E-MTAB-4484 | biostudies-arrayexpress
Project description:We report the transcriptome profile of different cultivars of Fusarium graminearum-infected wheat grains, aiming to search for some different expression genes and pathways to reveal the difference between wheat cultivars.
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Project description:The goals of this study are to compare transcriptome profiling (RNA-seq) between two wheat cultivars with different antioxidant actvity and to clarify the differences of these two wheat cultivars.
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Project description:While most eukaryotic cells are diploid, with two chromosome sets, variances in ploidy are common. Despite the relative prevalence of ploidy changes and their relevance for pathology and evolution, a complete picture of consequences of altered ploidy is missing. We analyzed transcriptome and proteome changes in budding yeast Saccharomyces cerevisiae from haploid to tetraploid and found that the mRNA and protein abundance increases linearly with ploidy, but does not double with doubling the DNA content. Besides this linear increase, we found that pathways related to mitochondria and to cytoplasmic ribosomes and translation are differentially regulated. Indeed, with increasing ploidy the cells reduce mitochondrial content and this effect can be rescued by antioxidants. Moreover, cells of higher ploidy reduce their ribosome content while maintaining constant translational output. We show that this is an active process regulated via the Tor1 and Sch9 kinases and a transcriptional corepressor of rDNA transcription, Tup1. Similarly, human tetraploid cells downregulate their ribosome content via Tle1, a Tup1 homolog, demonstrating that the proteome remodeling is a conserved response to increased ploidy.
2022-08-15 | PXD022605 | Pride
Project description:To investigate whether rat adult hepatocytes would exhibit different characteristics dependent on their ploidy statuses, we compared the transcriptome profile of 2c, 4c and 8c hepatocytes by mRNA microarray.
2019-08-01 | GSE132409 | GEO
Project description:Transcriptome of adult rat hepatocytes with different ploidy statuses
| PRJNA547946 | ENA
Project description:Whereas most eukaryotic cells are diploid, carrying two chromosome sets, variances in ploidy are common. Despite the relative prevalence of ploidy changes and their relevance for pathology and evolution, the consequences of altered ploidy for cellular gene expression remain poorly understood. We quantified changes in the transcriptome and proteome of the yeast Saccharomyces cerevisiae with different ploidy, from the haploid to the tetraploid state. We found that the abundance of proteins increases with ploidy, but does not scale proportionally with increasing DNA content, suggesting a compensatory, cellular response to increases in ploidy. We further found that pathways related to cytoplasmic ribosomes and translation are differentially regulated. With increasing ploidy the cells reduced the rRNA and ribosomal protein abundance, although they maintained a constant translational output. These adaptations stem from an active process that involves the kinases Tor1 and Sch9 and the transcriptional corepressor of rDNA transcription, Tup1. Consistent with our results in yeast, human tetraploid cells show reduced mTORC1 activity and downregulated their ribosome content via the Tup1 homolog Tle1, demonstrating that the proteome remodeling pathway discovered here constitutes a conserved response pathway to increased ploidy.
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