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Related Concept Videos

Regulation of Expression at Multiple Steps01:23

Regulation of Expression at Multiple Steps

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The gene expression in cells is regulated at different stages: (i) transcription, (ii) RNA processing, (iii) RNA localization, and (iv) translation. Transcriptional regulation is mediated by regulatory proteins such as transcription factors, activators, or repressors—these control gene expression by initiating or inhibiting the transcription of genes. Once a precursor or pre-mRNA is produced, it undergoes post-transcriptional modification, including 5' capping, splicing, and the...
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Regulation of Expression Occurs at Multiple Steps02:24

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Gene expression can be regulated at almost every step from gene to protein. Transcription is the step that is most commonly regulated. This involves the binding of proteins to short regulatory sequences on the DNA. This association can either promote or inhibit the transcription of a gene associated with the respective sequence.
Transcription results in the generation of precursor (pre-mRNA) that consists of both exons and introns, which needs further processing before being translated to a...
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Translational Regulation01:29

Translational Regulation

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Translational regulation in prokaryotes ensures efficient protein synthesis by controlling ribosome access to mRNA. This regulation is mediated by secondary RNA structures, including translational riboswitches, RNA thermometers, and small RNAs (sRNAs), which respond to intracellular and environmental signals to modulate gene expression.Translational RiboswitchesRiboswitches in the leader region of mRNAs can regulate translation by altering the accessibility of the Shine-Dalgarno (SD) sequence,...
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Translation01:31

Translation

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Translation is the process of synthesizing proteins from the genetic information carried by messenger RNA (mRNA). Following transcription, it constitutes the final step in the expression of genes. This process is carried out by ribosomes, complexes of protein and specialized RNA molecules. Ribosomes, transfer RNA (tRNA), and other proteins produce a chain of amino acids—the polypeptide—as the end product of translation.
Translation Produces the Building Blocks of Life
Proteins are...
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Phosphorylation01:02

Phosphorylation

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The addition or removal of phosphate groups from proteins is the most common chemical modification that regulates cellular processes. These modifications can affect the structure, activity, stability, and localization of proteins within cells as well as their interactions with other proteins.
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Nonsense-mediated mRNA Decay02:27

Nonsense-mediated mRNA Decay

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The Upf proteins that carry out nonsense-mediated decay (NMD) are found in all eukaryotic organisms, including humans. Each protein has an individual role, but they need to work in collaboration. Upf1 is an ATP-dependent RNA helicase that unwinds the RNA helix. Because Upf1 can unwind any RNA, Upf2 and Upf3 are required to help Upf1 discriminate between nonsense and normal mRNAs.
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Related Experiment Video

Updated: Jul 11, 2025

Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells
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FMRP phosphorylation modulates neuronal translation through YTHDF1.

Zhongyu Zou1, Jiangbo Wei1, Yantao Chen2

  • 1Department of Chemistry, The University of Chicago, Chicago, IL 60637, USA; Howard Hughes Medical Institute, The University of Chicago, Chicago, IL 60637, USA.

Molecular Cell
|November 10, 2023
PubMed
Summary

Fragile X syndrome defects in neurons are reversed by inhibiting YTHDF1. This occurs because FMRP phosphorylation releases YTHDF1, promoting translation and reversing developmental issues.

Keywords:
FMRPRNA-binding proteinsYTHDF1m(6)Aneuronal translation controlprotein condensates

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Related Experiment Videos

Last Updated: Jul 11, 2025

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • RNA-binding proteins (RBPs) are crucial for regulating messenger RNA (mRNA) fate in neurons.
  • Fragile X syndrome (FXS) is a developmental disorder linked to FMRP deficiency, impacting neuronal function.

Purpose of the Study:

  • To elucidate the mechanism of stimuli-induced neuronal translation regulation by FMRP.
  • To identify YTHDF1 as a potential therapeutic target for FXS.

Main Methods:

  • Investigated the interaction between FMRP, YTHDF1, and ribosomal proteins.
  • Utilized a small molecule inhibitor of YTHDF1 in an FXS organoid model.

Main Results:

  • Neuronal stimulation induces FMRP phosphorylation, releasing YTHDF1 to promote mRNA translation.
  • YTHDF1 inhibition reversed developmental defects in an FMRP-deficient FXS organoid model.
  • FMRP sequesters YTHDF1 away from ribosomes, inhibiting translation.

Conclusions:

  • FMRP phosphorylation is a key regulator of activity-dependent translation in neurons.
  • YTHDF1 inhibition offers a potential therapeutic strategy for reversing FXS developmental defects.