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Navigating MARRVEL, a Web-Based Tool that Integrates Human Genomics and Model Organism Genetics Information

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A new hypothesis to explain disease dominance.

Brian Juvik¹, Lara Falcucci¹, Pia R Lundegaard²

¹Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Hessen, 61231, Germany; German Centre for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Bad Nauheim, Hessen, 61231, Germany.

Trends in Genetics : TIG

|January 9, 2025

Summary

Transcriptional adaptation (TA) is a new response to mRNA decay that contributes to dominant diseases. This process, involving adapting genes, can cause genetic compensation or worsen disease phenotypes.

Keywords:

Brugada syndrome frontotemporal lobar degeneration gain-of-function hypertrophic cardiomyopathy loss-of-function nonsense-mediated mRNA decay transcriptional adaptation

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Published on: January 16, 2019

Area of Science:

Genetics
Molecular Biology
Disease Mechanisms

Background:

Dominant diseases are typically attributed to haploinsufficiency or dominant-negative effects.
Recent research questions these established mechanisms for diseases like Brugada syndrome, hypertrophic cardiomyopathy, and frontotemporal lobar degeneration.

Purpose of the Study:

To propose transcriptional adaptation (TA) as an additional mechanism underlying dominant diseases.
To investigate the role of TA in modulating gene expression in response to mRNA decay.

Main Methods:

The study focuses on the conceptual framework of transcriptional adaptation.
It reviews recent findings challenging existing models of dominant disease etiology.

Main Results:

Transcriptional adaptation (TA) is identified as a response to mRNA decay.
TA influences the expression of adapting genes, potentially through mRNA decay products.
This modulation can lead to either genetic compensation or exacerbation of disease phenotypes.

Conclusions:

Transcriptional adaptation (TA) offers a new perspective on the pathogenesis of dominant diseases.
For dominant diseases linked to mRNA decay, TA-mediated gene dysregulation may significantly contribute to the observed phenotype.