Magnitude of modulation of gene expression in aneuploid maize depends on the extent of genomic imbalance
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA556850 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9843140.fastq.gz | Fastqsanger.gz | |||
| SRR9843150.fastq.gz | Fastqsanger.gz | |||
| SRR9843131.fastq.gz | Fastqsanger.gz | |||
| SRR9843141.fastq.gz | Fastqsanger.gz | |||
| SRR9843151.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 29 |
Similar Datasets
Project description:Aneuploidy has profound effects on an organism, typically more so than polyploidy, and the basis of this contrast is not fully understood. A dosage series of maize chromosome arm 1L was used to compare relative global gene expression in different types and degrees of aneuploidy to gain insight into how the magnitude of genomic imbalance as well as hypoploidy affect global gene expression. While previously available methods required a selective examination of specific genes, RNA sequencing provides a whole-genome view of gene expression in aneuploids. Most studies of global aneuploid effects have concentrated on trisomics because other types of aneuploids are difficult to produce in most model genetic organisms. The genetic toolkit of maize allows the examination of multiple ploidies and 1-4 doses of chromosome arms. Thus, a detailed examination of expression changes both on the varied chromosome arm and elsewhere in the genome is possible, in both hypoploids and hyperploids, compared with euploid controls. Previous studies observed the inverse trans effect, in which genes not varied in DNA dosage are expressed in a negative relationship to the varied chromosomal region. This response was also the major type of change found globally in this study. It was also found that the effects of aneuploidy are progressive, with more severe aneuploids producing effects of greater magnitude.
2020-02-17 | GSE134936 | GEO
Project description:Genomic imbalance refers to the more severe phenotypic consequences of changing a single chromosome compared to changing the whole genome set. Previous genome imbalance studies in maize have identified gene expression modulation in aneuploids of single chromosome arms. Here, the modulation of gene expression in more complex aneuploids, e.g. monosomy of one chromosome arm and trisomy of another. To determine the extent that combination aneuploids were additive, multiplicative, or rebalanced in terms of their effect on gene expression. A series of genetic crosses was performed to produce one, two, and three copies of one arm with independent one, two, and three copies of the other arm in each of the three genotypes for the opposite arm. In total, 31 combinations were analyzed. By examining RNA modulation, we discovered that cis genes on varied chromosome arms are generally more dosage-compensated in aneuploid combinations than in single aneuploidy even though some showed a clear dosage effect. For genes on the unvaried chromosomes (trans), there is greater modulation in most of the aneuploidy combinations. Finally, 22 of the 31 combinations were found to have an altered transcriptome size, suggesting that extensive stoichiometric changes of genomic regions upsets global mRNA transcription. Overall, these results have important implications for understanding the role of genomic stoichiometry for mechanisms of gene expression, the evolution of dosage-sensitive duplicated genes, the evolution of sex chromosomes, the rapid growth adaptation of aneuploid cancer cells, and the diploid of quantitative traits.
2025-04-27 | GSE284999 | GEO
Project description:Aneuploidy, an abnormal chromosome composition, results in a stoichiometric imbalance of protein complexes, which jeopardizes the fitness of aneuploid cells. Aneuploid cells thus need to compensate for the imbalanced DNA levels by regulating their RNA and protein levels, a phenomenon known as dosage compensation. However, the molecular mechanisms involved in dosage compensation in human cells – and whether they can be targeted to selectively kill aneuploid cancer cells – remain unknown. Here, we addressed this question via molecular dissection of multiple diploid vs. aneuploid cell models. Using genomic and functional profiling of a novel isogenic system of RPE1-hTERT cells with various degrees of aneuploidy, we found that aneuploid cells cope with both transcriptional burden and proteotoxic stress. At the mRNA level, aneuploid cells increased RNA synthesis, but concomitantly elevated several RNA degradation pathways, in particular the nonsense-mediated decay (NMD) and the microRNA-mediated mRNA silencing pathways. Consequently, aneuploid cells were more sensitive to the genetic or chemical perturbation of several key components of these RNA degradation pathways. At the protein level, aneuploid cells experienced proteotoxic stress, resulting in reduced translation and increased protein degradation, rendering them more sensitive to proteasome inhibition. These findings were recapitulated across hundreds of human cancer cell lines and primary tumors, confirming that both non-transformed and transformed cells alter their RNA and protein metabolism in order to adapt to the aneuploid state. Our results reveal that aneuploid cells are dependent on the over- or under-activation of several nodes along the gene expression process, identifying these pathways as clinically-actionable vulnerabilities of aneuploid cells.
2024-07-08 | GSE247267 | GEO
Project description:To identify the genes required to sustain aneuploid viability, we screened a deletion library of non-essential genes in the fission yeast Schizosaccharomyces pombe, in which most types of aneuploidy are eventually lethal to the cell. Aneuploids remain viable for a period time and can form colonies by reducing the extent of the aneuploidy. We hypothesized that a reduction in colony formation efficiency could be used to screen for gene deletions that compromise aneuploid viability. Deletion mutants were used to measure the effects on the viability of spores derived from triploid meiosis and from a chromosome instability mutant. We found that the CCR4-NOT complex, an evolutionarily conserved general regulator of mRNA turnover, and other related factors, including poly(A)-specific nuclease for mRNA decay, are involved in aneuploid viability. Defective mutations in CCR4-NOT complex components in the distantly related yeast Saccharomyces cerevisiae also affected the viability of spores produced from triploid cells, suggesting that this complex has a conserved role in aneuploids. In addition, our findings suggest that the genes required for homologous recombination repair are important for aneuploid viability.
2012-06-27 | GSE36454 | GEO
Project description:DNA aneuploid sublines in sporadic colorectal cancers (CRCs) are quite frequent (about 85%) and likely the consequence of chromosomal instability and DNA copy number aberrations (CNAs). In order to gain insight into the mechanisms of the diploid-aneuploid transition in CRCs, we compared the CNA status in both diploid and aneuploid sublines. We used fresh/frozen material from 17 aneuploid CRCs, which was separated into 17 DNA diploid and 17 aneuploid sublines using enrichment of the epithelial component by multiparameter flow cytometry and sorting. CNA status of both sublines was obtained by array comparative genomic hybridization. The DNA diploid sublines from the aneuploid CRCs showed already CNAs, in particular, gains at 20p and 20q. The same aberrations were detected at increased frequencies in the corresponding DNA aneuploid sublines. Moreover, the very frequent gains/losses of chromosomes 4, 7, 8, 13, 15, and 18 in the DNA aneuploid sublines were absent or rare in the DNA diploid sublines from the same sporadic aneuploid CRCs. The comparison of the DNA diploid and aneuploid sublines from aneuploid CRCs suggests that 20p and 20q gains may play a role in the diploid-aneuploid transition. The 20q chromosomal arm appears of particular interest since it harbors several genes implicated in chromosomal instability.
2014-10-20 | GSE47148 | GEO
Project description:Aneuploidy, a condition characterized by whole chromosome gains and losses, is often associated with significant cellular stress and decreased fitness. However, whether and how cells respond to the aneuploid state has remained controversial. In aneuploid budding yeast, two opposing gene expression patterns have been reported: an environmental stress response (ESR) and a “common aneuploidy gene-expression” (CAGE) signature, in which many ESR genes are oppositely regulated. Here, we investigate and bring clarity to this controversy. We show that the CAGE signature is not an aneuploidy-specific gene expression signature but is the result of euploid control cells, but not aneuploid cells, having grown into stationary phase. Because growth into stationary phase is amongst the strongest inducers of the ESR, the ESR in aneuploid cells was masked when stationary phase euploid cells were used for normalization in transcriptomic studies. When exponentially growing euploid cells are used in gene expression comparisons with aneuploid cells, the CAGE signature is no longer evident in aneuploid cells. Instead, aneuploid cells are found to exhibit the ESR. We further show that the ESR causes a selective loss of ribosomes in aneuploid cells, providing an explanation for the decreased cellular density in aneuploid cells. We conclude that aneuploid budding yeast cells mount the ESR, rather than a CAGE signature, in response to aneuploidy-induced cellular stresses that results in selective ribosome loss.
2020-06-16 | GSE146791 | GEO
Project description:To identify the genes required to sustain aneuploid viability, we screened a deletion library of non-essential genes in the fission yeast Schizosaccharomyces pombe, in which most types of aneuploidy are eventually lethal to the cell. Aneuploids remain viable for a period time and can form colonies by reducing the extent of the aneuploidy. We hypothesized that a reduction in colony formation efficiency could be used to screen for gene deletions that compromise aneuploid viability. Deletion mutants were used to measure the effects on the viability of spores derived from triploid meiosis and from a chromosome instability mutant. We found that the CCR4-NOT complex, an evolutionarily conserved general regulator of mRNA turnover, and other related factors, including poly(A)-specific nuclease for mRNA decay, are involved in aneuploid viability. Defective mutations in CCR4-NOT complex components in the distantly related yeast Saccharomyces cerevisiae also affected the viability of spores produced from triploid cells, suggesting that this complex has a conserved role in aneuploids. In addition, our findings suggest that the genes required for homologous recombination repair are important for aneuploid viability. Gene expression profile at exponentially-growing phase.in the fission yeast deletion mutants of the CCR4-NOT complex protein genes.
2012-06-26 | E-GEOD-36454 | biostudies-arrayexpress
Project description:Single-cell whole-genome sequencing of aneuploid cycling and aneuploid arrested cells
| PRJEB58407 | ENA
Project description:Transcriptome analysis to map transcriptomes of Mps1DK p53null-driven aneuploid T-ALL, to determine correlation between copy number changes and expression changes and to map the transcriptional response to CIN
2014-07-01 | GSE57333 | GEO
Project description:We used C. albicans diploid reference strain SC5314 to obtain aneuploid colonies via selection by drugs. We got a collection of aneuploid strains bearing trisomy of each homolog of each chromosome.
2020-11-16 | E-MTAB-9739 | biostudies-arrayexpress