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NFIB Is a Pioneer Factor for DNA Replication by Acting as a Genome Organizer [Micro-C]

ABSTRACT: Micro-C performed on U2OS cells without or with NFIB depletion at G1/S phase and S phase to investigate the effect of NFIB on higher-order chromatin structure during DNA replication.

ORGANISM(S): Homo sapiens

PROVIDER: GSE201864 | GEO | 2023/08/22

REPOSITORIES: GEO

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NFIB Is a Pioneer Factor for DNA Replication by Acting as a Genome Organizer [CUT&TAG]

Project description:Genome-wide binding profile of NFIB and ORC1 in G1 phase of U2OS cells without or with NFIB depletion were profiled using cleavage under targets and tagmentation sequencing (CUT&Tag-seq).

2023-08-22 | GSE201863 | GEO

NFIB Is a Pioneer Factor for DNA Replication by Acting as a Genome Organizer [H3K9me3 CUT&Tag]

Project description:Genome-wide profiling of histone H3K9me3 of G1 or S phase U2OS cells without or with NFIB depletion.

2023-08-22 | GSE223440 | GEO

NFIB Is a Pioneer Factor for DNA Replication by Acting as a Genome Organizer [H3K4me3 CUT&Tag]

Project description:Genome-wide profiling of histone H3K4me3 of G1 or S phase U2OS cells without or with NFIB depletion.

2023-08-22 | GSE223438 | GEO

NFIB Is a Pioneer Factor for DNA Replication by Acting as a Genome Organizer [ATAC-seq]

Project description:Chromatin accessibility of G1 phase of U2OS cells without or with NFIB depletion were profiled using transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) to identify potential regulatory elements.

2023-08-22 | GSE201861 | GEO

NFIB Is a Pioneer Factor for DNA Replication by Acting as a Genome Organizer [ATAC-seq II]

Project description:Chromatin accessibility of G1 or S phase of U2OS cells without or with NFIB depletion were profiled using transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) to identify potential regulatory elements.

2023-08-22 | GSE223437 | GEO

NFIB Is a Pioneer Factor for DNA Replication by Acting as a Genome Organizer [Repli-seq]

Project description:Genome-wide DNA replication profiles of U2OS cells without or with NFIB depletion.

2023-08-22 | GSE223441 | GEO

NFIB Is a Pioneer Factor for DNA Replication by Acting as a Genome Organizer [NS-seq]

Project description:Nascent strand sequencing (NS-seq) in U2OS cells without or with NFIB depletion to identify de facto activated replication origins.

2023-08-22 | GSE201865 | GEO

NFIB Is a Pioneer Factor for DNA Replication by Acting as a Genome Organizer [WGS]

Project description:Whole genome sequencing (WGS) of MCF-10A cells without or with NFIB overexpression cultured at 30 or 75 days and 5-fluoracil-resistant or oxaliplatin-resistant MCF-10A cells with NFIB overexpression cultured at 75 days to investigate whether the oncogenic potential of NFIB is linked to its function in replication initiation.

2023-08-22 | GSE201866 | GEO

NFIB Is a Pioneer Factor for DNA Replication by Acting as a Genome Organizer [Micro-C]

Project description:NFIB Is a Pioneer Factor for DNA Replication by Acting as a Genome Organizer [Micro-C]

| PRJNA833341 | ENA

NFIB facilitates replication licensing by acting as a genome organizer.

Project description:The chromatin-based rule governing the selection and activation of replication origins in metazoans remains to be investigated. Here we report that NFIB, a member of Nuclear Factor I (NFI) family that was initially purified in host cells to promote adenoviral DNA replication but has since mainly been investigated in transcription regulation, is physically associated with the pre-replication complex (pre-RC) in mammalian cells. Genomic analyses reveal that NFIB facilitates the assembly of the pre-RC by increasing chromatin accessibility. Nucleosome binding and single-molecule magnetic tweezers shows that NFIB binds to and opens up nucleosomes. Transmission electron microscopy indicates that NFIB promotes nucleosome eviction on parental chromatin. NFIB deficiency leads to alterations of chromosome contacts/compartments in both G1 and S phase and affects the firing of a subset of origins at early-replication domains. Significantly, cancer-associated NFIB overexpression provokes gene duplication and genomic alterations recapitulating the genetic aberrance in clinical breast cancer and empowering cancer cells to dynamically evolve growth advantage and drug resistance. Together, these results point a role for NFIB in facilitating replication licensing by acting as a genome organizer, shedding new lights on the biological function of NFIB and on the replication origin selection in eukaryotes.

| S-EPMC10442334 | biostudies-literature

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