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Autoregulation of RPL7B by inhibition of a structural splicing enhancer
David Granas1, Ishan Gammadde Hewa2, Michael A White2
1Department of Genetics and Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St Louis, MO 63110, United States.
Nucleic Acids Research
|July 31, 2025
Summary
Yeast ribosomal protein RPL7B gene expression is controlled by splicing regulation. When Rpl7 protein is abundant, it binds an intron structure, blocking splicing and preventing further gene expression.
Area of Science:
- Molecular Biology
- Gene Regulation
- Yeast Genetics
Background:
- The ribosomal protein gene RPL7B in yeast is subject to autoregulation.
- Efficient splicing of the RPL7B pre-mRNA is crucial for gene expression.
- The first intron contains a nonconsensus branch point sequence (UGCUAAC).
Purpose of the Study:
- To investigate the mechanism of RPL7B autoregulation by splicing inhibition.
- To elucidate the role of the first intron's structure in regulating RPL7B gene expression.
Main Methods:
- Analysis of intron secondary structures.
- Splicing assays in yeast.
- RNA-protein binding studies.
Main Results:
- The first intron possesses a "zipper stem" enhancer structure that facilitates splicing by positioning the 5' splice site near the branch point.
- An alternative, conserved structure within the intron acts as a binding site for the Rpl7 protein.
- Rpl7 protein binding to this alternative structure disrupts the enhancer, repressing splicing and autoregulating gene expression.
Conclusions:
- Yeast ribosomal protein RPL7B is autoregulated through a splicing inhibition mechanism.
- The interplay between intron structure, Rpl7 protein binding, and splicing efficiency controls RPL7B gene expression.
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