98%
921
2 minutes
20
() is essential for stem cell maintenance and radial patterning in Arabidopsis () roots, but how its expression is regulated is unknown. Here, we report that the Elongator complex, which consists of six subunits (ELP1 to ELP6), regulates the transcription of Depletion of Elongator drastically reduced expression and led to defective root stem cell maintenance and radial patterning. The importance of the nuclear localization of Elongator for its functioning, together with the insensitivity of the mutant to the transcription elongation inhibitor 6-azauracil, and the direct interaction of the ELP4 subunit with the carboxyl-terminal domain of RNA polymerase II, support the notion that Elongator plays important roles in transcription elongation. Indeed, we found that ELP3 associates with the premessenger RNA of and that mutation of Elongator reduces the enrichment of RNA polymerase II on the gene body. Moreover, Elongator interacted in vivo with SUPPRESSOR OF Ty4, a well-established transcription elongation factor that is recruited to the locus. Together, these results demonstrate that Elongator acts in concert with SUPPRESSOR OF Ty4 to regulate the transcription of .
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6324240 | PMC |
http://dx.doi.org/10.1104/pp.18.00534 | DOI Listing |
Stem Cell Res
September 2025
Department of General Pediatrics, Neonatology, and Pediatric Cardiology, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine-University, Düsseldorf 40225, Germany. Electronic address:
Pathogenic variants in the gene COQ4 cause primary coenzyme Q deficiency, which is associated with symptoms ranging from early epileptic encephalopathy up to adult-onset ataxia-spasticity spectrum disease. We genetically modified commercially available wild-type iPS cells by using a CRISPR/Cas9 approach to create heterozygous and homozygous isogenic cell lines carrying the disease-causing COQ4 variants c.458C > T, p.
View Article and Find Full Text PDFAnnu Rev Pathol
September 2025
3Department of Pathology, Stanford University, Stanford, California, USA;
Clonal hematopoiesis, originally identified as a precursor to hematologic malignancies, has emerged as a significant factor in various nonmalignant diseases. Recent research highlights how somatic mutations in hematopoietic stem cells lead to the expansion of circulating mutated immune cells that exert profound effects on organ function and disease progression. These mutated clones display altered inflammatory profiles and tissue-specific functional consequences, contributing to various diseases including atherosclerotic cardiovascular disease, osteoporosis, heart failure, and neurodegenerative conditions.
View Article and Find Full Text PDFCells
September 2025
Department of Medical, Oral and Biotechnological Sciences, University of Chieti-Pescara, Via dei Vestini 29, 66100 Chieti, Italy.
The journal retracts the article titled "Multipotent Stromal Cells from Subcutaneous Adipose Tissue of Normal Weight and Obese Subjects: Modulation of Their Adipogenic Differentiation by Adenosine A Receptor Ligands" [...
View Article and Find Full Text PDFBraz Oral Res
September 2025
Universidade de São Paulo - USP, School of Dentistry of Ribeirão Preto, Department of Pediatric Dentistry, Ribeirão Preto, SP, Brazil.
Tumor necrosis factor-alpha (TNF-α) is a cytokine involved in the immune-inflammatory response. It can induce an odontoblastic phenotype and enhance biomineralization in dental pulp mesenchymal stem cells but does not have the same effect on osteoblasts. The reasons for this differential response, despite the shared lineage of these cell types, are not yet clear.
View Article and Find Full Text PDFPLoS One
September 2025
Cancer Research Institute, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Crosstalk between leukemic cells and their surrounding mesenchymal stromal cells (MSCs) in the bone marrow microenvironment is crucial for the pathogenesis of myelodysplastic syndromes (MDS) and is mediated by extracellular vesicles (EVs). The EV-specific miRNAs derived from MDS-MSCs remain poorly explored. EVs isolated from HS-5, an immortalized stromal cell line, promoted the proliferation and 5-azacytidine (AZA) resistance of SKM-1 cells.
View Article and Find Full Text PDF