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YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis

ABSTRACT: YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis

PROVIDER: PRJNA860801 | ENA |

REPOSITORIES: ENA

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YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [ChIP-Seq]

Project description:YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [ChIP-Seq]

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YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [RNA-Seq]

Project description:YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [RNA-Seq]

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YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [MeDIP-Seq]

Project description:YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [MeDIP-Seq]

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YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [MeDIP-Seq]

Project description:We use m6A-seq to report the most comprehensive survey to date of mRNA in spermatogonial stem cells (SSCs) and neural stem cell-like cells (iNSCs)

2025-07-21 | GSE208724 | GEO

YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [ChIP-Seq]

Project description:We use ChIP-seq to report the most comprehensive survey to date of chromatin organization in spermatogonial stem cells (SSCs) and neural stem cell-like cells (iNSCs)

2025-07-21 | GSE208723 | GEO

YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis

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

2025-07-21 | GSE208726 | GEO

YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [RNA-Seq]

Project description:The expression profile data was obtained by RNA-Seq data.

2025-07-21 | GSE208725 | GEO

Distinct roles for NFκB in hematopoietic stem cells and the bone marrow milieu in promoting hematopoietic aging

Project description:Hematopoietic aging is characterized by chronic inflammation associated with myeloid bias, HSC accumulation, and functional HSC impairment. Yet it remains unclear how inflammation promotes aging phenotypes. NFκB both responds to and directs inflammation, and we present an experimental model of elevated NFκB activity (“IκB–”) to dissect its role in hematopoietic aging phenotypes. We find that while elevated NFκB activity is not sufficient for HSC accumulation, HSC-autonomous NFκB activity impairs their functionality, leading to reduced bone marrow reconstitution. In contrast, myeloid bias is driven by the IκB– proinflammatory bone marrow milieu as observed functionally, epigenomically, and transcriptomically. A scRNA-seq HSPC labeling framework enables comparisons with aged murine and human HSC datasets, documenting an association between HSC-intrinsic NFκB activity and quiescence, but not myeloid bias. These findings delineate separate regulatory mechanisms that underlie the three hallmarks of hematopoietic aging, suggesting that they are specifically and independently therapeutically targetable.

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YTHDF1-N6-methyladenosine-ARHGEF2 axis promoted colorectal tumorigenesis and metastasis

Project description:N6-methyladenosine (m6A) governs the fate of RNAs through m6A readers. Colorectal cancer (CRC) exhibits aberrant m6A modifications and expression of m6A regulators. However, little is known about how m6A readers interpret oncogenic m6A methylome for malignant transformation. m6A reader YTHDF1 was overexpressed by copy number gain/amplification in majority of CRCs. YTHDF1 high expression and CNVs predict increased risk of CRC relapse. Transcriptome profiles of YTHDF1-high tumors exhibit highly metastatic features. YTHDF1 promoted CRC tumor cell and organoid proliferation and enhanced metastasis. Ythdf1 knockout dampened tumor growth in carcinogen-induced CRC model. Through multiomic integration, RhoA activator ARHGEF2 was characterized as the key functional YTHDF1 target based on its m6A and YTHDF1-binding signal, translation efficiency changes, protein correlations with YTHDF1 in clinical samples, and disrupted RhoA features by YTHDF1 knockdown. Moreover, YTHDF1-ARHGEF2 co-regulation was observed in YTHDF1-overexpressing metastatic sites and carcinogen-induced Ythdf1-null CRC tumors. ARHGEF2 overexpression significantly rescued RhoA signaling, tumor cell survival and invasiveness impaired by YTHDF1 knockdown both in vitro and in vivo, further confirming the essential function of ARHGEF2.

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FMRP phosphorylation modulates neuronal translation through YTHDF1

Project description:Translation activation of local synaptic mRNA is critical to learning and memory. Despite extensive studies on how phosphorylations of ribosome units and translation factors enable fast response to exogenous stimuli, our knowledge on molecular pathways utilized by RNA binding proteins (RBPs) to control translation of specific mRNAs remains incomplete. We have previously found that YTHDF1 regulates depolarization-induced protein synthesis by promoting translation of N6-methyladenosine (m6A)-modified transcripts. Here we report an unexpected mechanism that the stimuli-induced neuronal translation is mediated by phosphorylation of a YTHDF1-binding protein FMRP. Phosphorylation of FMRP serine 499 induced by neuronal depolarization alters the condensing behavior of prion-like protein YTHDF1. Unphosphorylated FMRP sequesters YTHDF1 away from the translation initiation complex, whereas the stimulation-induced FMRP phosphorylation releases YTHDF1 to form translational active condensates with the ribosome to activate translation of YTHDF1 target transcripts. In fragile X syndrome (FXS) models characterized with low FMRP expression, we observed YTHDF1-mediated hyperactive translation, which notably impacts FXS pathophysiology. Developmental defects in an FXS forebrain organoid model could be reversed by a selective small-molecule inhibitor of YTHDF1 which acts by suppressing its condensation in neurons. We characterized transcriptome-wide translation alterations with the inhibitor treatment in organoids and identified targets that explain alleviated FXS pathology. Our study thus reveals FMRP and its phosphorylation as an important regulator of the activity-dependent translation during neuronal development and stimulation, and identifies YTHDF1 as a potential therapeutic target for FXS in which developmental defects caused by FMRP depletion could be reversed through YTHDF1 inhibition.

2023-10-31 | GSE214882 | GEO

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