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

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

PROVIDER: PRJNA890164 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21890614.fastq.gz	Fastqsanger.gz
	SRR21890615.fastq.gz	Fastqsanger.gz

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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.

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

Project description:This SuperSeries is composed of the SubSeries listed below.

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

Project description:To understand differential gene expression between wildtype and c-Myc null mouse trophoblast giant cells.

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

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

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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]

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

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

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Myc promotes polyploidy in murine trophoblast cells and suppresses senescence.

Project description:The placenta is essential for reproductive success. The murine placenta includes polyploid giant cells that are crucial for its function. Polyploidy occurs broadly in nature but its regulators and significance in the placenta are unknown. We have discovered that many murine placental cell types are polyploid and have identified factors that license polyploidy using single-cell RNA sequencing. Myc is a key regulator of polyploidy and placental development, and is required for multiple rounds of DNA replication, likely via endocycles, in trophoblast giant cells. Furthermore, MYC supports the expression of DNA replication and nucleotide biosynthesis genes along with ribosomal RNA. Increased DNA damage and senescence occur in trophoblast giant cells without Myc, accompanied by senescence in the neighboring maternal decidua. These data reveal Myc is essential for polyploidy to support normal placental development, thereby preventing premature senescence. Our study, combined with available literature, suggests that Myc is an evolutionarily conserved regulator of polyploidy.

| S-EPMC10309589 | biostudies-literature

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