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RNA Splicing

RNA Splicing

Splicing is the process by which eukaryotic RNA is edited before its translation into protein. The RNA strand transcribed from eukaryotic DNA is called the primary transcript. The primary transcripts that become mRNAs are called precursor messenger RNAs (pre-mRNAs). Eukaryotic pre-mRNA contains alternating sequences of exons and introns. Exons are nucleotide sequences that code for proteins, whereas introns are the non-coding regions. In RNA splicing, introns are removed and exons are bonded...

RNA Splicing

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Alternative RNA Splicing

Alternative RNA Splicing

Alternative RNA splicing is the regulated splicing of exons and introns to produce different mature mRNAs from a single pre-mRNA. Unlike in constitutive splicing where a single gene produces a single type of mRNA, alternative splicing allows an organism to produce multiple proteins from a single gene and plays an important role in protein diversity.
There are five types of alternative RNA splicing that vary in the ways the pre-mRNA segments are removed or retained in the mature mRNA. The first...

Alternative RNA Splicing

Alternative RNA Splicing

Negative Regulator Molecules

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.

Chromatin Structure Regulates pre-mRNA Processing

Chromatin Structure Regulates pre-mRNA Processing

In eukaryotic cells, nascent mRNA transcripts need to undergo many post-transcriptional modifications to reach the cell cytoplasm and translate into functional proteins. For a long time, transcription and pre-mRNA processing were considered two independent events that occur sequentially in the cell. However, it has now been well established that transcription and pre-mRNA processing are two simultaneous processes that are precisely regulated inside the cell.
The chromatin structure, especially...

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Related Experiment Video

Updated: Apr 19, 2026

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition

Published on: October 9, 2014

ERRβ splice variants differentially regulate cell cycle progression.

Mary Mazzotta Heckler¹, Rebecca B Riggins

¹a Lombardi Comprehensive Cancer Center; the Department of Oncology ; Georgetown University School of Medicine ; Washington , DC USA.

Cell Cycle (Georgetown, Tex.)

|December 16, 2014

Summary

This summary is machine-generated.

Estrogen-related receptors (ERRs) have distinct roles in cell cycle control. ERRβ splice variants, ERRβsf and ERRβ2, differentially regulate cell cycle checkpoints and senescence, revealing novel splice variant interactions.

Keywords:

ERRbeta ESRRB alternative splicing cell cycle nuclear receptor p53 senescence

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Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells

Published on: April 26, 2017

Area of Science:

Molecular Biology
Cell Biology
Endocrinology

Background:

Nuclear receptors are crucial regulators of gene expression.
Estrogen-related receptors (ERRs) are orphan nuclear receptors with unique functions.
ERRβ has splice variants with potentially distinct biological roles.

Purpose of the Study:

To investigate the differential roles of ERRβ splice variants, ERRβsf and ERRβ2, in cell cycle regulation.
To elucidate the mechanisms by which these variants influence cell cycle checkpoints and senescence.
To explore the interaction between ERRβ splice variants.

Main Methods:

Utilized DY131, a synthetic ERRβ agonist.
Employed splice-variant selective shRNA for gene knockdown.
Used exogenous ERRβsf and ERRβ2 cDNAs for overexpression studies.
Analyzed cell cycle progression and senescence markers.

Main Results:

ERRβsf mediates a G1 checkpoint through p21 and is essential for DY131-induced senescence.
ERRβ2 mediates a G2/M arrest in response to DY131.
Absence of ERRβ2 leads to reversal of G2/M arrest, p21 induction, and a G1 arrest.

Conclusions:

Estrogen-related receptor beta (ERRβ) splice variants exhibit distinct functions in cell cycle control.
ERRβsf promotes G1 arrest and senescence, while ERRβ2 induces G2/M arrest.
Evidence suggests interplay between ERRβ splice variants in regulating cellular responses.