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Data-driven model reveals increased stability of CAG-expanded huntingtin RNA due to MID1 binding
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Data-driven model reveals increased stability of CAG-expanded huntingtin RNA due to MID1 binding
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Journal Article
Data-driven model reveals increased stability of CAG-expanded huntingtin RNA due to MID1 binding
2026
Overview
RNA-binding proteins (RBP) are important regulators of RNA metabolism. In neurodegenerative disorders such as Huntington's Disease (HD), disrupted RBP-RNA interactions contribute to neuronal dysfunction. One such RBP, Midline 1 (MID1), has been shown to aberrantly associate with mutant huntingtin (Htt) RNA, enhancing its translation, yet the mechanism driving this effect remains unknown. Here, we develop a computational model to understand the role of MID1. Based on previously published data, our model predicts that MID1 increases the stability of the Htt RNA. We experimentally validate this prediction, showing that overexpression of MID1 significantly prolongs the half-life of mutant Htt RNA. Furthermore, we evaluate model refinements, including clustering of MID1-bound RNA, which allow capturing all key observations in the data. Together, we provide a data-driven framework that underlines the importance of RBP-RNA interaction in post-transcriptional regulation. This framework also shows how individual molecular reactions jointly determine RNA stability and protein levels in HD.
Publisher
PLOS,Public Library of Science (PLoS)
Subject
/ Humans
/ Huntingtin Protein - genetics
/ Huntingtin Protein - metabolism
/ Huntington Disease - genetics
/ Huntington Disease - metabolism
/ Medicine and Health Sciences
/ Nerve Tissue Proteins - genetics
/ Nerve Tissue Proteins - metabolism
/ Research and Analysis Methods
/ RNA-Binding Proteins - genetics
/ RNA-Binding Proteins - metabolism
/ Transcription Factors - genetics
