Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA388762 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5638570_1.fastq.gz | Fastqsanger.gz | |||
| SRR5638570_2.fastq.gz | Fastqsanger.gz | |||
| SRR5638571_1.fastq.gz | Fastqsanger.gz | |||
| SRR5638571_2.fastq.gz | Fastqsanger.gz | |||
| SRR5638572_1.fastq.gz | Fastqsanger.gz |
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Project description:Histone variants, which can be expressed outside of S-phase and deposited DNA synthesis-independently, provide long-term histone replacement in postmitotic cells, including neurons. Beyond replenishment, histone variants also play active roles in gene regulation by modulating chromatin states or enabling nucleosome turnover. Here, we uncover crucial roles for the histone H3 variant H3.3 in neuronal development. We find that newborn cortical excitatory neurons, which have only just completed replication-coupled deposition of canonical H3.1 and H3.2, substantially accumulate H3.3 immediately post mitosis. Co-deletion of H3.3-encoding genes H3f3a and H3f3b from newly postmitotic neurons abrogates H3.3 accumulation, markedly alters the histone posttranslational modification (PTM) landscape, and causes widespread disruptions to the establishment of the neuronal transcriptome. These changes coincide with developmental phenotypes in neuronal identities and axon projections. Thus, preexisting, replication-dependent histones are insufficient for establishing neuronal chromatin and transcriptome; de novo H3.3 is required. Stage-dependent deletion of H3f3a and H3f3b from (1) cycling neural progenitor cells, (2) neurons immediately post mitosis, or (3) several days later, reveals the first postmitotic days to be a critical window for de novo H3.3. After H3.3 accumulation within this developmental window, co-deletion of H3f3a and H3f3b does not lead to immediate H3.3 loss, but causes progressive H3.3 depletion over several months without widespread transcriptional disruptions or cellular phenotypes. Our study thus uncovers key developmental roles for de novo H3.3 in establishing neuronal chromatin, transcriptome, identity, and connectivity immediately post mitosis that are distinct from its role in maintaining total histone H3 levels over the neuronal lifespan.
2022-07-27 | GSE181331 | GEO
Project description:The distinct contributions of replication-dependent (RD) and replication-independent (RI) histones to development and genome function remain unclear. We investigate how the RI expression and distinct protein identities of the histone H3.2 and H3.3 subtypes influence Drosophila development and gene regulation. Replacing RI H3.3 genes with RD H3.2 revealed that RI H3.3 is essential for fertility, adult locomotor behavior, and normal lifespan. However, development to adulthood does not depend on which RI H3 subtype is expressed. RI H3 is dispensable for establishing or maintaining global chromatin accessibility or gene expression in the adult brain. H3.2 expression becomes essential in post-mitotic cells lacking RI H3.3, and the HIRA histone chaperone complex in critical for preserving genome function when RI H3.3 is deleted. We conclude that an available pool of H3 is more critical than the specific identity of H3 in the pool.
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Project description:The distinct contributions of replication-dependent (RD) and replication-independent (RI) histones to development and genome function remain unclear. We investigate how the RI expression and distinct protein identities of the histone H3.2 and H3.3 subtypes influence Drosophila development and gene regulation. Replacing RI H3.3 genes with RD H3.2 revealed that RI H3.3 is essential for fertility, adult locomotor behavior, and normal lifespan. However, development to adulthood does not depend on which RI H3 subtype is expressed. RI H3 is dispensable for establishing or maintaining global chromatin accessibility or gene expression in the adult brain. H3.2 expression becomes essential in post-mitotic cells lacking RI H3.3, and the HIRA histone chaperone complex in critical for preserving genome function when RI H3.3 is deleted. We conclude that an available pool of H3 is more critical than the specific identity of H3 in the pool.
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Project description:Histone H3.3 is a highly conserved histone H3 replacement variant in metazoans, and has been implicated in many important biological processes including cell differentiation and reprogramming. Germline and somatic mutations in H3.3 genomic incorporation pathway components, or in H3.3 encoding genes, have been associated with human congenital diseases and cancers, respectively. However, the role of H3.3 in mammalian development remains unclear. To address this question, we generated H3.3 null mouse models through classical genetic approaches. We found H3.3 plays an essential role in mouse development. Complete depletion of H3.3 leads to developmental retardation and early embryonic lethality. At the cellular level, H3.3 loss triggers cell cycle suppression and cell death. Surprisingly, H3.3 depletion does not dramatically disrupt gene regulation in the developing embryo. Instead, H3.3 depletion causes dysfunction of heterochromatin structures at telomeres, centromeres and pericentromeric regions of chromosomes leading to mitotic defects. The resulting karyotypical abnormalities and DNA damage lead to p53 pathway activation. In summary, our results reveal that an important function of H3.3 is to support chromosomal heterochromatic structures, thus maintaining genome integrity during mammalian development. RNA-seq in embryos at E10.5 comparing 3 samples with the following genotype Trp53-/-; H3f3afl/-; H3f3bfl/-; Sox2-CreTg/0 to three samples with the following genotype Trp53-/-; H3f3afl/+; H3f3bfl/+; Sox2-CreTg/0
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Project description:The Role of Tet1 During Somatic Cell Reprogramming
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Project description:Mature oocyte cytoplasm can reprogram somatic cell nuclei to the pluripotent state through a series of sequential events including protein exchange between the donor nucleus and ooplasm, chromatin remodeling, and pluripotency gene reactivation. Maternal factors that are responsible for this reprogramming process remain largely unidentified. Here, we demonstrate that knockdown of histone variant H3.3 in mouse oocytes results in compromised reprogramming and down-regulation of key pluripotency genes; and this compromised reprogramming both for developmental potentials and transcription of pluripotency genes can be rescued by injecting exogenous H3.3 mRNA, but not H3.2 mRNA into oocytes in somatic cell nuclear transfer (SCNT) embryos. We show that maternal H3.3, and not H3.3 in the donor nucleus, is essential for successful reprogramming of somatic cell nucleus into the pluripotent state. Furthermore, H3.3 is involved in this reprogramming process by remodeling the donor nuclear chromatin through replacement of donor nucleus-derived H3 with de novo synthesized maternal H3.3 protein. Our study shows that H3.3 is a crucial maternal factor for oocyte reprogramming and provides a practical model to directly dissect the oocyte for its reprogramming capacity. Transcriptome sequencing of 4-cell NT embryos, Luciferase 4-cell SCNT embryos, 4-cell NT embryos_H3.3KD, 4-cell NT embryos_H3.3KD+H3.3mRNA, H3.3 KD + H3.2 mRNA SCNT embryos
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