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Cell cycle duration determines oncogenic transformation capacity

ABSTRACT: Cell cycle duration determines oncogenic transformation capacity

PROVIDER: PRJNA1026993 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26359915.fastq.gz	Fastqsanger.gz
	SRR26359916.fastq.gz	Fastqsanger.gz

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Cell cycle duration determines oncogenic transformation capacity

Project description:We present single-cell RNA sequencing data of P8 mouse retina with Rb/p107 double knockout (DKO), or Rb/p107 DKO with Skp2+/-.

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A Tunable Mechanism Determines the Transgenerational Duration of Small RNA Inheritance in C.elegans

Project description:In C.elegans nematodes small RNAs enable transmission of epigenetic responses across multiple generations. While RNA interference (RNAi) inheritance mechanisms that enable “memorization” of ancestral responses are being elucidated, it is not known why or how, after a few generations, epigenetic effects are “forgotten”. We show that exposure to dsRNA activates a feedback loop that determines the duration of inherited silencing. We find that gene-specific RNAi responses dictate the transgenerational duration of RNAi responses mounted against unrelated genes, elicited separately in previous generations. RNA-seq analysis reveals that aside from silencing of genes with complementary sequences, dsRNA-induced RNAi affects the production of heritable endogenous small RNAs, which regulate the expression of RNAi factors. Manipulating genes in this feedback pathway changes the duration of heritable silencing. Active control of transgenerational effects could be adaptive, since ancestral responses would be detrimental if the environments of the progeny and the ancestors would differ.

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Epigenetic enhancer changes during oncogenic transformation

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STRIPAK directs PP2A activity to promote oncogenic transformation

Project description:We evaluated the effects of suppressing MAP4K4 on transcriptome and YAP1 pathway based on the observation that partial suppression of MAP4K4 leads to transformation through activation of YAP1. Mutations and deletions involving subunits of the serine-threonine phosphatase PP2A occur in a broad range of human cancers, and partial loss of PP2A function contributes to cell transformation. In particular, displacement of regulatory B subunits by the viral oncoprotein SV40 small-t antigen (ST) or mutation or deletion of PP2A subunits alters the abundance and types of PP2A complexes in cells and induces cell transformation in human cells. Here we show that ST not only displaces common PP2A B subunits but also promotes PP2A A-C subunit interactions with a set of alternative B subunits (B’’’, striatins) that are components of the Striatin-interacting phosphatase and kinase (STRIPAK) complex. We found that members of the STRIPAK complex are required for ST-PP2A induced cell transformation. PP2A interacts with and dephosphorylates the STRIPAK-associated kinase MAP4K4, which induces cell transformation in part through the regulation of the Hippo pathway effector YAP1. These observations identify an unanticipated role of MAP4K4 in transformation and show that the STRIPAK complex plays a key role in defining PP2A specificity and activity.

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Kim et al. STRIPAK directs PP2A activity towards MAP4K4 to promote oncogenic transformation

Project description:STRIPAK directs PP2A activity towards MAP4K4 to promote oncogenic transformation

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Upregulation of Antioxidant Capacity and Nucleotide Precursor Availability Suffices for Oncogenic Transformation.

Project description: Not available

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Reprogramming-associated aberrant DNA methylation determines hematopoietic differentiation capacity of human induced pluripotent stem cells

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