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Modulation of protein activity by small RNA base pairing internal to coding sequences

Molecular Cell 2025年第9期85卷 1824-1837.e7页

作者： Thongdee, Narumon Alaniz, Miranda M. Samatova, Ekaterina Zhong, Aoshu Esnault, Caroline Zhang, Hongen Dale, Ryan K. Rodnina, Marina V. Storz, Gisela Division of Molecular and Cellular Biology Eunice Kennedy Shriver National Institute of Child Health and Human Development Bethesda 20892 MD United States Max Planck Institute for Multidisciplinary Sciences Department of Physical Biochemistry Göttingen 37077 Germany Bioinformatics and Scientific Programming Core Eunice Kennedy Shriver National Institute of Child Health and Human Development Bethesda 20892 MD United States

Most characterized interactions between bacterial small RNAs (sRNAs) and their target mRNAs occur near ribosome binding sites, resulting in changes in translation initiation or target mRNA decay. To understand the consequences of sRNA pairing internal to coding sequences detected by global RNA-RNA interactome approaches, we examined the impact of sRNA overexpression on seven target proteins. Overexpression of the sRNA led to decreased target protein levels for two pairs, but there were no differences for the others. By further examining ArcZ-ligA and ArcZ-hemK, we discovered that ArcZ pairing with the mRNAs leads to translation pausing and increased protein activity. A ligA point mutation that eliminates sRNA pairing resulted in increased sensitivity to DNA damage, revealing the physiological consequences of the regulation. Thus, regulatory RNA pairing in coding sequences can locally slow translation elongation, likely impacting co-translational protein folding and allowing improved incorporation of co-factors or more optimal folding under specific conditions. © 2025

关键词： ArcZ co-factor incorperation DNA damage DNA ligase HemK Hfq protein folding regulatory RNAs translation elongation

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Deletion of a single CTCF motif at the boundary of a chromatin domain with three FGF genes disrupts gene expression and embryonic development

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Developmental Cell 2025年

作者： Chakraborty, Shreeta Wenzlitschke, Nina Anderson, Matthew J. Eraso, Ariel Baudic, Manon Thompson, Joyce J. Evans, Alicia A. Shatford-Adams, Lilly M. Chari, Raj Awasthi, Parirokh Dale, Ryan K. Lewandoski, Mark Petros, Timothy J. Rocha, Pedro P. Unit on Genome Structure and Regulation National Institute of Child Health and Human Development National Institutes of Health Bethesda 20892 MD United States Genetics of Vertebrate Development Section Cancer and Developmental Biology Laboratory National Cancer Institute National Institutes of Health Frederick 21702 MD United States Bioinformatics and Scientific Programming Core National Institute of Child Health and Human Development National Institutes of Health Bethesda 20892 MD United States Laboratory Animal Sciences Program Frederick National Laboratory for Cancer Research Frederick 21702 MD United States Unit on Cellular and Molecular Neurodevelopment National Institute of Child Health and Human Development National Institutes of Health Bethesda 20892 MD United States National Cancer Institute NIH Bethesda 20892 MD United States

Chromatin domains delimited by CTCF can restrict the range of enhancer action. However, disruption of some domain boundaries results in mild gene dysregulation and phenotypes. We tested whether perturbing a domain with multiple developmental regulators would lead to more severe outcomes. We chose a domain with three FGF ligand genes—Fgf3, Fgf4, and Fgf15—that control different murine developmental processes. Heterozygous deletion of a 23.9-kb boundary defined by four CTCF sites led to ectopic interactions of the FGF genes with enhancers active in the brain and induced FGF expression. This caused orofacial clefts, encephalocele, and fully penetrant perinatal lethality. Loss of the single CTCF motif oriented toward the enhancers—but not the three toward the FGF genes—recapitulated these phenotypes. Our works shows that small sequence variants at particular domain boundaries can have a surprisingly outsized effect and must be considered as potential sources of gene dysregulation in development and disease. © 2025

关键词： CTCF epigenetics FGF gene regulation nuclear organization

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The role of TMEM38B in OI osteoblasts differentiation and mineralization

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Bone Reports 2022年 16卷

作者： Milena Jovanovic Apratim Mitra Ryan K. Dale Joan C. Marini NICHD/NIH Heritable Disorders of Bone and Extracellular Matrix Bethesda United States NICHD/NIH Bioinformatics and Scientific Programming Core Bethesda United States

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Insight into the bone dysplasia mechanism of CRTAP-null osteoblasts

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Bone Reports 2022年 16卷

作者： Aileen Barnes Apratim Mitra Ryan Dale Joan Marini NICHD/NIH Section on Heritable Disorders of Bone and Extracellular Matrix Bethesda United States NICHD/NIH Bioinformatics & Scientific Programming Core Bethesda United States NICHD/NIH Computer Support Services Core Bethesda United States

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Studies of OI patient and murine osteoblasts to investigate phenotypic variability of dominant Osteogenesis Imperfecta

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Bone Reports 2021年 14卷

作者： Milena Jovanovic Apratim Mitra Chris Stephan Kenneth Kozloff Ryan Dale Joan C. Marini NICHD/NIH Heritable Disorders of Bone and Extracellular Matrix Bethesda United States NICHD/NIH Bioinformatics and Scientific Programming Core Bethesda United States University of Michigan Department of Orthopaedic Surgery Ann Arbor United States

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Author Correction: Anchoring cortical granules in the cortex ensures trafficking to the plasma membrane for post-fertilization exocytosis

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Nature communications 2019年第1期10卷 2926页

作者： Edgar-John Vogt Keizo Tokuhiro Min Guo Ryan Dale Guanghui Yang Seung-Wook Shin Maria Jimenez Movilla Hari Shroff Jurrien Dean Laboratory of Cellular and Developmental Biology NIDDK National Institutes of Health Bethesda MD 20892 USA. Charité - Universitätsmedizin Berlin Augustenburger Platz 1 13353 Berlin Germany. Department of Genome Editing Institute of Biomedical Science Kansai Medical University 2-5-1 Shinmachi Hirakata Osaka 573-1010 Japan. Section on High Resolution Optical Imaging NIBIB National Institutes of Health Bethesda MD 20892 USA. Bioinformatics and Scientific Programming Core Eunice Kennedy Shriver National Institute of Child Health and Human Development National Institutes of Health Bethesda MD 20892 USA. Department of Cell Biology and Histology Medical School University of Murcia IMIB 30100 Murcia Spain. Advanced Imaging and Microscopy Resource National Institutes of Health Bethesda MD 20892 USA. Laboratory of Cellular and Developmental Biology NIDDK National Institutes of Health Bethesda MD 20892 USA. jurrien.dean@nih.gov.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

关键词： Actin Exocytosis Super-resolution microscopy

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