Many reports have appeared describing a direct relationship between hypomethylated states of genes and gene activity. Even after the introduction of viral genomes, these new genes appear to be controlled by specific DNA methylations. A variety of other studies have shown chromatin structural changes being implicated in the activities of certain gene loci. Modifications of chromatin domains may also be initiated or under the control of methylation reactions. Embryonic genes may be controlled by particular methylations by virtue of a differential (hyper-) sensitivity to concentrations of active methyl groups, on a variety of chromatin domains thereby explaining the variation in S-adenosyl-L-methionine synthesis required in developing liver tissue. Also our finding of the ability to manipulate experimentally the activity of the alpha-fetoprotein gene by methyl group availability indicates some methyl-sensitive mechanism is operating with respect to embryonic genes.
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http://dx.doi.org/10.1016/0306-9877(87)90051-x | DOI Listing |
J Cell Sci
January 2025
Department of Biomedical Engineering, Northwestern University, Evanston, Illinois, 60208, USA.
Disrupted nuclear shape is associated with multiple pathological processes including premature aging disorders, cancer-relevant chromosomal rearrangements, and DNA damage. Nuclear blebs (i.e.
View Article and Find Full Text PDFNucleic Acids Res
January 2025
Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital of Guangzhou Medical University, 621 Gangwan Road, Huangpu District, Guangzhou, Guangdong, 510799, China.
Cell fate determination at the chromatin level is not fully comprehended. Here, we report that c-JUN acts on chromatin loci to limit mesoderm cell fate specification as cells exit pluripotency. Although c-JUN is widely expressed across various cell types in early embryogenesis, it is not essential for maintaining pluripotency.
View Article and Find Full Text PDFEMBO Rep
January 2025
Department of Biochemistry, University of Toronto, 1 King's College Circle, Toronto, ON, M5S 1A8, Canada.
Homologous recombination is a largely error-free DNA repair mechanism conserved across all domains of life and is essential for the maintenance of genome integrity. Not only are the mutations in homologous recombination repair genes probable cancer drivers, some also cause genetic disorders. In particular, mutations in the Bloom (BLM) helicase cause Bloom Syndrome, a rare autosomal recessive disorder characterized by increased sister chromatid exchanges and predisposition to a variety of cancers.
View Article and Find Full Text PDFGenes Dev
January 2025
Oncode Institute, Hubrecht Institute, Royal Netherlands Academy of Arts and Sciences (KNAW), University Medical Center Utrecht, Utrecht 3584 CT, the Netherlands;
Enhancers are tissue-specific regulatory DNA elements that can activate transcription of genes over distance. Their target genes most often are located in the same contact domain-chromosomal entities formed by cohesin DNA loop extrusion and typically flanked by CTCF-bound boundaries. Enhancers shared by multiple unrelated genes are underexplored but may be more common than anticipated.
View Article and Find Full Text PDFMicrobiol Spectr
January 2025
Institute of Bioinformatics and Applied Biotechnology, Bengaluru, Karnataka, India.
Alba domain-containing proteins are ubiquitously found in archaea and eukaryotes. By binding to either DNA, RNA, or DNA:RNA hybrids, these proteins function in genome stabilization, chromatin organization, gene regulation, and/or translational modulation. In the malaria parasite , six Alba domain proteins PfAlba1-6 have been described, of which PfAlba1 has emerged as a "master regulator" of translation during parasite intra-erythrocytic development (IED).
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