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Cytoplasmic translocation of tumor suppressor HINT1 and its impact on cell shape during density transition

ABSTRACT: Cytoplasmic translocation of tumor suppressor HINT1 and its impact on cell shape during density transition

PROVIDER: PRJNA1129113 | ENA |

REPOSITORIES: ENA

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Cytoplasmic translocation of tumor suppressor HINT1 and its impact on cell shape during density transition

Project description:Cells at low density exhibit spreading and migration behaviors with more spread-out morphologies, while high-density cultures show confined, rounded morphologies. During this transition, the actin cytoskeleton rearranges from oriented stress fibers to a cortical actin shell, supporting cell movement and shape maintenance. This transition also halts cell proliferation to prevent uncontrolled growth, as seen in tumors. However, the molecular mechanism behind actin cytoskeleton remodeling by cell density is not well understood. Using proteomics of purified open chromatin, we identified the tumor suppressor HINT1 as a key molecule whose nucleocytoplasmic shuttling depends on cell density. RNA-seq analysis of wild-type (WT) and knock-out (KO) HEK293A cells revealed that HINT1 is involved in morphogensis and development.

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Project description:Developmental Cytoplasmic-to-Nuclear Translocation of RNA-Binding Protein HuR Is Required for Adult Neurogenesis

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Project description:Although neurogenesis in the adult brain recapitulates processes that occur during embryonic development, adult neurogenesis exhibits distinct characteristics from its embryonic counterpart. However, the intrinsic mechanism underlying the differential regulation of neurogenesis between these two stages remains unclear. Herein, we show that the ablation of RNA-binding protein HuR in neural stem cells (NSCs) impairs adult, but not embryonic, neurogenesis. HuR is predominantly expressed in the cytoplasm of embryonic NSCs but translocates into the nucleus of adult NSCs. Transcriptomic analysis of HuR-deficient adult NSCs revealed that nuclear HuR primarily regulates alternative splicing of numerous premRNA transcripts, including focal adhesion kinase (FAK). HuR-deficient adult NSCs generate increased FAK mRNA isoforms with shorter 5’ UTRs, leading to enhanced FAK mRNA translation and hyperactivated FAK signaling, and inhibition of FAK ameliorates defective adult neurogenesis and impaired hippocampus-dependent learning in HuR-deficient mice. Taken together, these findings reveal novel mechanistic insights into the differential regulation of embryonic and adult neurogenesis through developmental cytoplasmic-to-nuclear translocation of HuR in NSCs.

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