Bacterial pathogens secrete effector proteins to manipulate host signaling proteins and cellular structures. In this issue of Cell Host & Microbe, Pagliuso et al. (2019) propose an effector mechanism in Listeria monocytogenes whereby an RNA-binding protein associates with bacterial RNA that stimulates RIG-I (retinoic acid inducible gene I)-based innate immunity in the host cytosol.
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http://dx.doi.org/10.1016/j.chom.2019.11.005 | DOI Listing |
Nucleic Acids Res
January 2025
Molecular Microbiology and Structural Biochemistry, MMSB-IBCP, CNRS UMR 5086 , Université Claude Bernard Lyon 1, F-69367 Lyon, France.
The nonsense-mediated mRNA decay (NMD) pathway triggers the degradation of defective mRNAs and governs the expression of mRNAs with specific characteristics. Current understanding indicates that NMD is often significantly suppressed during viral infections to protect the viral genome. In numerous viruses, this inhibition is achieved through direct or indirect interference with the RNA helicase UPF1, thereby promoting viral replication and enhancing pathogenesis.
View Article and Find Full Text PDFCell
January 2025
Laboratory of Cancer Epigenetics, Faculty of Medicine, ULB-Cancer Research Center (U-CRC), Université libre de Bruxelles (ULB), Institut Jules Bordet, Brussels, Belgium. Electronic address:
The marking of DNA, histones, and RNA is central to gene expression regulation in development and disease. Recent evidence links N6-methyladenosine (mA), installed on RNA by the METTL3-METTL14 methyltransferase complex, to histone modifications, but the link between mA and DNA methylation remains scarcely explored. This study shows that METTL3-METTL14 recruits the DNA methyltransferase DNMT1 to chromatin for gene-body methylation.
View Article and Find Full Text PDFGenes Dev
December 2024
Howard Hughes Medical Institute, Department of Biological Sciences, Columbia University, New York, New York 10025, USA.
The pan-neuronally expressed and phylogenetically conserved CUT homeobox gene orchestrates pan-neuronal gene expression throughout the nervous system of As in many other species, including humans, is encoded by a complex locus that also codes for a Golgi-localized protein, called CASP (Cux1 alternatively spliced product) in humans and CONE-1 ("CASP of nematodes") in How gene expression from this complex locus is controlled-and, in , directed to all cells of the nervous system-has not been investigated. We show here that pan-neuronal expression of CEH-44/CUX is controlled by a pan-neuronal RNA splicing factor, UNC-75, the homolog of vertebrate CELF proteins. During embryogenesis, the locus exclusively produces the Golgi-localized CONE-1/CASP protein in all tissues, but upon the onset of postmitotic terminal differentiation of neurons, UNC-75/CELF induces the production of the alternative CEH-44/CUX CUT homeobox gene-encoding transcript exclusively in the nervous system.
View Article and Find Full Text PDFFragile X Syndrome (FXS) is characterized by intellectual impairment caused by CGG repeat expansion in the FMR1 gene. When repeats exceed 200, they induce DNA methylation of the promoter and the repeat region, resulting in transcriptional silencing of the FMR1 gene and the subsequent loss of FMRP protein. In the past decade or so, research has focused on the role of FMRP as an RNA-binding protein involved in translation inhibition in the brain in FXS model mice, particularly by slowing or stalling ribosome translocation on mRNA.
View Article and Find Full Text PDFNucleic Acids Res
December 2024
Institute of Biochemistry, University of Kiel, Rudolf-Höber-Straße 1, Kiel 24118, Germany.
Transcripts produced by RNA polymerase II (RNAPII) are fundamental for cellular responses to environmental changes. It is therefore no surprise that there exist multiple avenues for the regulation of this process. To explore the regulation mediated by RNAPII-interacting proteins, we used a small interfering RNA (siRNA)-based screen to systematically evaluate their influence on RNA synthesis.
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