The primary sequence of the genome is broadly constant and superimposed upon that constancy is the postreplicative modification of a small number of cytosine residues to 5-methylcytosine. The pattern of methylation is non-random; some sequence contexts are frequently methylated and some rarely methylated and some regions of the genome are highly methylated and some rarely methylated. Once established, methylation is not static: it can potentially change in response to developmental or environmental cues and this may result in correlated changes in gene expression. Changes can occur passively owing to a failure to maintain DNA methylation through rounds of DNA replication, or actively, through the action of enzymes with DNA glycosylase activity. Recent advances in genetic analyses and the generation of high resolution, genome-wide methylation maps are revealing in unprecedented detail the patterns and dynamic changes of DNA methylation in plants.
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http://dx.doi.org/10.1016/j.pbi.2010.11.004 | DOI Listing |
Mol Plant
January 2025
State Key Laboratory of Wheat Improvement, School of Advanced Agricultural Sciences, Peking University, Beijing 100871, China; Beijing Life Science Academy, Beijing 102299, China. Electronic address:
It has been hypothesized that DNA damage has the potential to induce DNA hypermethylation, contributing to carcinogenesis in mammals. However, there is no sufficient evidence to support that DNA damage can cause genome-wide DNA hypermethylation. Here, we demonstrated that DNA single-strand breaks with 3'-blocked ends (DNA 3'-blocks) can not only reinforce DNA methylation at normally methylated loci but also can induce DNA methylation at normally nonmethylated loci in plants.
View Article and Find Full Text PDFJ Pathol
January 2025
Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
DICER1-associated sarcoma is an emerging entity, defined by either somatic or germline dicer 1, ribonuclease III (DICER1) mutations and sharing characteristic morphologic features irrespective of the site of origin. In addition to the DICER1 driver mutation, concurrent genomic alterations, including tumor protein 53 (TP53) inactivation and RAS pathway activation, are frequently detected. Tumors that morphologically resemble malignant peripheral nerve sheath tumor (MPNST) have rarely been reported among DICER1 sarcomas and often pose diagnostic challenges.
View Article and Find Full Text PDFAnal Chim Acta
February 2025
Department of Archaeology and Anthropology, School of Humanities, University of Chinese Academy of Sciences, 100049, Beijing, China. Electronic address:
Background: Pottery lipid residue analysis has been extensively practiced worldwide as an important part of archaeometry studies, but in some cases, the complexity of archaeological residue cannot be fully revealed by one-dimensional gas chromatography (1D GC) separation. Although the development of comprehensive two-dimensional gas chromatography (GCxGC) has offered another way to achieve better separation and higher resolution, GCxGC separation has rarely been applied to pottery residue analysis. Clearly, GCxGC separation needs to be explored to examine and scrutinize the complexity of pottery lipid residue profile as well as rapid data treatment workflow.
View Article and Find Full Text PDFTumori
January 2025
IEO, European Institute of Oncology IRCCS, Division of Cancer Prevention and Genetics, Milan, Italy.
Lynch syndrome is a genetic condition predisposing to cancer, particularly colorectal cancer and endometrial cancer, due to germline mutations in MisMatch Repair genes. More rarely, Lynch syndrome is the result of a constitutional promoter methylation. This review summarizes the current knowledge about the role of this epigenetic mechanism in the Lynch syndrome.
View Article and Find Full Text PDFEpigenetics Chromatin
January 2025
Department of Maternal‑Fetal Biology, National Center for Child Health and Development, Tokyo, 157‑8535, Japan.
Background: DNA methylation plays a crucial role in mammalian development. While methylome changes acquired in the parental genomes are believed to be erased by epigenetic reprogramming, accumulating evidence suggests that methylome changes in sperm caused by environmental factors are involved in the disease phenotypes of the offspring. These findings imply that acquired sperm methylome changes are transferred to the embryo after epigenetic reprogramming.
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