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Somatic polyploidy supports biosynthesis and tissue function by increasing transcriptional output [ChIP-seq]

ABSTRACT: Somatic polyploidy supports biosynthesis and tissue function by increasing transcriptional output [ChIP-seq]

PROVIDER: PRJNA1181025 | ENA |

REPOSITORIES: ENA

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Somatic polyploidy supports biosynthesis and tissue function by increasing transcriptional output [RNA-seq]

Project description:Somatic polyploidy supports biosynthesis and tissue function by increasing transcriptional output [RNA-seq]

| PRJNA1181026 | ENA

Somatic polyploidy supports biosynthesis and tissue function by increasing transcriptional output [ChIP-seq]

Project description:Cell size and biosynthetic capacity generally increase with increased DNA content. Somatic polyploidy has therefore been proposed to be an adaptive strategy to increase cell size in specialized tissues with high biosynthetic demands. However, if and how DNA concentration limits cellular biosynthesis in vivo is not well understood. Here, we show that polyploidy in the C. elegans intestine is critical for cell growth and yolk biosynthesis, a central role of this organ. Artificially lowering the DNA/cytoplasm ratio by reducing polyploidization in the intestine gave rise to smaller cells with dilute mRNA. Highly-expressed transcripts were more sensitive to this mRNA dilution, whereas lowly-expressed genes were partially compensated – in part by loading more RNA Polymerase II on the remaining genomes. Polyploidy-deficient animals produced fewer and slower growing offspring, consistent with reduced synthesis of highly-expressed yolk proteins. DNA-dilute cells had normal total protein concentration, which we propose is achieved by increasing expression of translational machinery at the expense of specialized, cell-type specific proteins.

2024-11-03 | GSE280912 | GEO

Somatic polyploidy supports biosynthesis and tissue function by increasing transcriptional output [RNA-seq]

2024-11-03 | GSE280911 | GEO

c-Myc supports polyploidy and prevents senescence in the murine placenta

Project description:c-Myc supports polyploidy and prevents senescence in the murine placenta

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c-Myc supports polyploidy and prevents senescence in the murine placenta [scRNA-Seq]

Project description:Placenta is essential for reproductive success and placental abnormalities are the leading cause of low birth weight and preterm birth. The placenta includes polyploid cells that are crucial for its function. Polyploidy occurs broadly in nature but the regulators that enable polyploidy to arise in a spatiotemporally regulated manner in the placenta are unknown. We used scRNA seq to understand molecular regulators of polyploidy.

2023-05-12 | GSE215381 | GEO

c-Myc supports polyploidy and prevents senescence in the murine placenta [scRNA-Seq]

Project description:c-Myc supports polyploidy and prevents senescence in the murine placenta [scRNA-Seq]

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c-Myc supports polyploidy and prevents senescence in the murine placenta [RNA-seq]

Project description:c-Myc supports polyploidy and prevents senescence in the murine placenta [RNA-seq]

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Polyploidy in the adult Drosophila melanogaster brain

Project description:Polyploidy in the adult Drosophila melanogaster brain

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Development of decidual cell polyploidy and bi-nucleation necessitates mitochondrial activity

Project description:In the present study, to better define the aspects of decidual cell polyploidy, we isolated pure polyploid and non-polyploid decidual cell populations from the in vivo decidual bed. Three independent RNA pools prepared for each population were then subjected to the Affymetrix gene chip analysis for the whole mouse genome transcripts. Our data revealed up-regulation of 1015 genes and down-regulation of 1207 genes in the polyploid populations, as compared to the non-polyploid group. We analyzed whole gnenome transcription from non-polyploid and polyploid cell populations using the Affymetrix GeneChip® Mouse Gene 1.0 ST Array . 3 replicates were performed.

2011-04-29 | E-GEOD-28917 | biostudies-arrayexpress

Mechanotransduction regulates adipose estrogen output and its impact on tumor cell growth

Project description:Adipose stromal cells (ASCs) are the primary source of local estrogens in adipose tissue, aberrant production of which promotes estrogen receptor-positive (ER+) breast cancer. Here we show that extracellular matrix (ECM) rigidity and cell contractility are two opposing determinants for estrogen output of ASCs. Using synthetic ECMs and elastomeric micropost arrays with tunable rigidity, we find that increasing matrix compliance induces transcription of aromatase, a rate-limiting enzyme in estrogen biosynthesis. This mechanical cue is transduced sequentially by Discoidin Domain Receptor 1 (DDR1), c-Jun N-terminal kinase 1 (JNK1), and phosphorylated JunB, which binds to and activates two breast cancer-associated aromatase promoters. In contrast, elevated cell contractility due to actin stress fiber formation dampens aromatase transcription. Mechanically stimulated stromal estrogen production enhances estrogen-dependent transcription in ER+ tumor cells and promotes their growth. This novel mechanotransduction pathway underlies communications between ECM, stromal hormone output, and cancer cell growth within the same microenvironment. Total RNA was isolated from primary adipose stromal cells after 2d culture or 3d Collagen gel for 21 hours. Triplicates for each conditioned were analyzed

2013-03-04 | E-GEOD-44811 | biostudies-arrayexpress

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