Transcriptional silencing is an essential mechanism for controlling the expression of genes, transgenes and heterochromatic repeats through specific epigenetic marks on chromatin that are maintained during DNA replication. In Arabidopsis, silenced transgenes and heterochromatic sequences are typically associated with high levels of DNA methylation, while silenced genes are enriched in H3K27me3. Reactivation of these loci is often correlated with decreased levels of these repressive epigenetic marks. Here, we report that the DNA helicase REGULATOR OF TELOMERE ELONGATION 1 (RTEL1) is required for transcriptional silencing. RTEL1 deficiency causes upregulation of many genes enriched in H3K27me3 accompanied by a moderate decrease in this mark, but no loss of DNA methylation at reactivated heterochromatic loci. Instead, heterochromatin exhibits DNA hypermethylation and increased H3K27me3 in rtel1. We further find that loss of RTEL1 suppresses the release of heterochromatin silencing caused by the absence of the MOM1 silencing factor. RTEL1 is conserved among eukaryotes and plays a key role in resolving DNA secondary structures during DNA replication. Inducing such aberrant DNA structures using DNA cross-linking agents also results in a loss of transcriptional silencing. These findings uncover unappreciated roles for RTEL1 in transcriptional silencing and in stabilizing DNA methylation and H3K27me3 patterns.
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http://dx.doi.org/10.1093/nar/gkad610 | DOI Listing |
Plant Signal Behav
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School of Medical Technology, Chongqing Three Gorges Medical College, Chongqing, China.
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Department of Gastroenterology, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou, Jiangsu 213003, China.
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View Article and Find Full Text PDFFront Genet
December 2024
Dino Ferrari Center, Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy.
Myotonia congenita, both in a dominant (Thomsen disease) and recessive form (Becker disease), is caused by molecular defects in that encodes the major skeletal muscle chloride channel, ClC-1. This channel is important for the normal repolarization of muscle action potentials and consequent relaxation of the muscle, and its dysfunction leads to impaired muscle relaxation after voluntary or evoked contraction and muscle stiffness. More than 300 pathogenic variants have been found in association with congenital myotonia, inherited as recessive or dominant traits (with complete or incomplete penetrance).
View Article and Find Full Text PDFBiotechnol J
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Department of Gastrointestinal Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China.
With a high mortality rate, colon cancer (CC) is the third most common malignant tumor worldwide. The primary causes are thought to be the high invasiveness and migration of CC cells. The functions of Golgi phosphoprotein 3 (GOLPH3), stress-induced phosphoprotein 1 (STIP1), and the signal transducer and activator of transcription 3 (STAT3) signaling pathway in the invasion and migration of CC cells were examined in this study.
View Article and Find Full Text PDFClin Teach
February 2025
Pediatrics, Yale School of Medicine, New Haven, Connecticut, USA.
Background: Physicians perform many difficult skills, but notifying loved ones about the death of a family member is a particularly challenging skill that requires specific training. Descriptions of such training are lacking in the literature. We developed a formative standardised patient encounter on death notification over the telephone for fourth-year medical students and evaluated their qualitative perspectives, including emotional safety.
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