All critical developmental and physiological events in a plant's life cycle depend on the proper activation and repression of specific gene sets, and this often involves epigenetic mechanisms. Some mutants with disorders of the epigenetic machinery exhibit pleiotropic defects, including incurved leaves and early flowering, due to the ectopic and heterochronic derepression of developmental regulators. Here, we studied one such mutant class, the () loss-of-function mutants. We have identified as the founding member of a small gene family that we have named (). This family is part of the 2-oxoglutarate/Fe(II)-dependent dioxygenase superfamily. and its closest paralog, have unequally redundant functions: although mutants are phenotypically wild type, double mutants skip vegetative development and flower upon germination. This phenotype is reminiscent of loss-of-function mutants of the Polycomb-group genes () and Double mutants harboring alleles and loss-of-function alleles of genes encoding components of the epigenetic machinery exhibit synergistic, severe phenotypes, and some are similar to those of mutants. Hundreds of genes are misexpressed in plants, including (), and derepression of causes the leaf phenotype of ICU11 and CP2 are nucleoplasmic proteins that act as epigenetic repressors through an unknown mechanism involving histone modification, but not DNA methylation.
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http://dx.doi.org/10.1105/tpc.18.00300 | DOI Listing |
Cancer Lett
December 2024
Shanghai Center for Systems Biomedicine, Key Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Jiao Tong University, Shanghai, 200240, China. Electronic address:
Lipid metabolism reprogramming is critical for the initiation and progression of hepatocellular carcinoma (HCC). However, how the dysregulation of lipid metabolism contributes to HCC development remains largely unknown. Here, we report that the mA reader YTHDC1-mediated epigenetic regulation of the long noncoding RNA NEAT1 activates stearoyl-CoA desaturase (SCD)-associated lipid metabolic processes during HCC progression.
View Article and Find Full Text PDFA major challenge in epigenetics is uncovering the dynamic distribution of nucleosomes and other DNA-binding proteins, which plays a crucial role in regulating cellular functions. Established approaches such as ATAC-seq, ChIP-seq, and CUT&RUN provide valuable insights but are limited by the ensemble nature of their data, masking the cellular and molecular heterogeneity that is often functionally significant. Recently, long-read sequencing technologies, particularly Single Molecule, Real-Time (SMRT/PacBio) sequencing, have introduced transformative capabilities, such as N6-methyladenine (6mA) footprinting.
View Article and Find Full Text PDFUnlabelled: Epigenetic complexes tightly regulate gene expression and colocalize with RNA splicing machinery; however, the consequences of these interactions are uncertain. Here, we identify unique interactions of the CoREST repressor complex with RNA splicing factors and their functional consequences in tumorigenesis. Using mass spectrometry, in vivo binding assays, and cryo-EM we find that CoREST complex-splicing factor interactions are direct and perturbed by the CoREST complex inhibitor, corin, leading to extensive changes in RNA splicing in melanoma and other malignancies.
View Article and Find Full Text PDFMed Sci (Paris)
December 2024
Université Paris Cité, CNRS UMR7216, Épigénétique et destin cellulaire, Paris, France.
The development of sequencing technologies and their increased accessibility in clinical services and genetic laboratories have considerably accelerated the identification of genetic variants associated with rare diseases (RDs). Among these, Mendelian disorders of the epigenetic machinery (MDEM) are rare monogenic diseases characterized by the presence of mutations in genes encoding epigenetic regulators that play a key role in organismal development and cellular functions. Loss of function of these regulators is expected to lead to epigenetic modifications that profoundly affect genome expression and cellular identity.
View Article and Find Full Text PDFFASEB J
December 2024
State Key Laboratory of Microbial Technology, Shandong University-Qingdao Campus, Qingdao, P.R. China.
Mammalian spermatogenesis is a tightly controlled cellular process including spermatogonial development and differentiation, meiosis of spermatocyte, and the morphological specification of haploid spermatozoa, during which the post-transcriptional gene regulations are vital but poorly understood. Nonsense-mediated mRNA decay (NMD), a highly conserved post-transcriptional regulatory mechanism of gene expression in eukaryotes, recently emerges as a licensing mechanism in cell fate transition, including stem cell differentiation and organogenesis. The function of NMD in spermatogonial development remains elusive.
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