98%
921
2 minutes
20
In mammals, transcription in the zygote begins after fertilization. This transcriptional wave is called zygotic gene activation (ZGA). During ZGA, epigenetic modifications, such as DNA methylation and histone modifications, are dynamically and drastically reconstructed in a sequence-specific manner. However, how such orchestrated gene upregulation is regulated remains unknown. Recently, using microinjection techniques, we have revealed that a class of long noncoding RNAs, named promoter-associated noncoding RNAs (pancRNAs), mediates specific gene upregulation through promoter DNA demethylation during ZGA. Here, we describe the experimental methods available to control the expression levels of pancRNAs and to evaluate epigenetic status after pancRNA manipulation.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/978-1-4939-6716-2_16 | DOI Listing |
Nat Struct Mol Biol
September 2025
Developmental Epigenetics, Department of Biochemistry, University of Oxford, Oxford, UK.
X-chromosome inactivation (XCI) in mammals is orchestrated by the noncoding RNA X-inactive-specific transcript (Xist) that, together with specific interacting proteins, functions in cis to silence an entire X chromosome. Defined sites on Xist RNA carry the N-methyladenosine (mA) modification and perturbation of the mA writer complex has been found to abrogate Xist-mediated gene silencing. However, the relative contribution of mA and its mechanism of action remain unclear.
View Article and Find Full Text PDFActa Pharmacol Sin
September 2025
Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
Chemotherapeutic resistance is a significant issue in the treatment of breast cancer, which is related to pyroptosis inhibition. Increasing evidence suggests that long non-coding RNAs (lncRNAs) contribute to tumorigenesis and drug resistance. In this study we investigated the role of the lncRNA STMN1P2 in doxorubicin resistance in breast cancer, as well as its correlation with pyroptosis inhibition.
View Article and Find Full Text PDFEMBO Rep
September 2025
Cell Biology and Epigenetics, Department of Biology, Technical University of Darmstadt, 64287, Darmstadt, Germany.
The flexibility of the spatio-temporal genome replication program during development and disease highlights the regulatory role of plastic epigenetic mechanisms over genetic determinants. Histone post-translational modifications are broadly implicated in replication timing control, yet the specific mechanisms through which individual histone marks influence replication dynamics, particularly in heterochromatin, remain unclear. Here, we demonstrate that H3K36me3 dynamically enriches at pericentromeric heterochromatin, composed of major satellite DNA repeats, prior to replication during mid S phase in mouse embryonic stem cells.
View Article and Find Full Text PDFCell Death Discov
September 2025
Department of Molecular Oncology, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia.
Ado-trastuzumab is considered a standard treatment for patients with HER2+ metastatic breast cancer (mBC). Current clinical practices do not reliably predict therapeutic outcomes for patients who are refractory to therapy. Long noncoding RNAs (lncRNAs) are emerging as critical regulators of gene expression and therapeutic resistance, and the use of lncRNAs as tumor biomarkers is becoming more common in other diseases.
View Article and Find Full Text PDFOpen Biol
September 2025
National Brain Research Centre, Manesar, Haryana, India.
E3 ubiquitin ligases regulate the cellular proteome proteasome-dependent protein degradation; however, there exist limited studies outlining their non-canonical functions. RNA-binding ubiquitin ligases (RBULs) represent a subset of E3 ligases that harbour RNA-binding domains, making them uniquely positioned to function as both RNA-binding proteins and E3 ligases. Our initial microarray screen for E3 ligases from mouse cortical neural progenitor cells identified MEX3B, a known RNA-binding ubiquitin ligase, to be differentially expressed.
View Article and Find Full Text PDF