Ploidy-specific transcriptomes shed light on the heterogeneous identity and metabolism of developing pericarp cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1030391 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26455000_1.fastq.gz | Fastqsanger.gz | |||
| SRR26455000_2.fastq.gz | Fastqsanger.gz | |||
| SRR26455001_1.fastq.gz | Fastqsanger.gz | |||
| SRR26455001_2.fastq.gz | Fastqsanger.gz | |||
| SRR26455002_1.fastq.gz | Fastqsanger.gz |
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Project description:A quantitative proteome analysis of four developmental stages of pericarp tissues of the açaí berry (Euterpe oleracea Mart.) was performed by the isobaric labeling of peptides with iTRAQ® 4-plex, HILIC pre-fractionation of labeled peptides and high-performance mass spectrometry analysis. This analysis resulted in the identification of 4286 proteins, of which 476 presented differential abundance between the stages. The differential abundance of these proteins was seen to be coordinated with the metabolic demands during cell division, lignification, and cell expansion at developmental stages 1 and 2, as well phenolic acids accumulation and metabolic changes in the fruit maturation, at developmental stages 3 and 4. The distinct accumulation of anthocyanins observed in the pericarp at developmental stage 4 was correlated with the increase in abundance of some key biosynthetic enzymes, such as leucoanthocyanidin dioxygenase, anthocyanidin O-3-glycosyltransferase and UDP-glycosyltransferase. Here evidence is also provided for the presence in the açaí berry of secondary metabolites not previously described in açaí, such as pterostilbene, matairesinol and furaneol. Together, these results will pave the way for studies aimed at the genetic improvement of the nutritional properties of this important fruit crop.
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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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Project description:Neuroblastic tumours (NBTs) represent a heterogeneous spectrum of neoplastic diseases associated with multiple genetic alterations. Structural and numerical chromosomal changes are frequent and are predictive parameters of NBTs outcome. We performed a comparative analysis of the biological entities constituted by NBTs with different ploidy status. Gene expression profiling of 49 diagnostic primary near-triploid (n= 22) and near-diploid/tetraploid (n=27) NBTs performed using Affymetrix U95Av2 arrays, revealed distinct expression profiles associated with each NBT subgroup. A statistically significant portion of genes mapped to 1p36 (P=0.01) and 17p13-q21 (P<0.0001). Specific chromosomal abnormalities observed in NBTs, 1p loss, 17q and whole chromosome 17 gains, were reflected in the gene expression profiles. This study demonstrates that NBTs with different cellular DNA content display distinct transcriptional profiles with a significant portion of differentially expressed genes mapping to specific chromosomal regions known to be associated with outcome. Furthermore, our results suggest that NBTs with different ploidy status may result from different mechanisms of aneuploidy driving tumourigenesis.
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