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Drosophila Models Reveal Properties of Mutant Lamins That Give Rise to Distinct Diseases
Journal article   Open access   Peer reviewed

Drosophila Models Reveal Properties of Mutant Lamins That Give Rise to Distinct Diseases

Sydney G. Walker, Christopher J. Langland, Jill Viles, Laura A. Hecker and Lori L. Wallrath
Cells (Basel, Switzerland), Vol.12(8), 1142
04/12/2023
DOI: 10.3390/cells12081142
PMCID: PMC10136830
PMID: 37190051
url
https://doi.org/10.3390/cells12081142View
Published (Version of record) Open Access

Abstract

Mutations in the LMNA gene cause a collection of diseases known as laminopathies, including muscular dystrophies, lipodystrophies, and early-onset aging syndromes. The LMNA gene encodes A-type lamins, lamins A/C, intermediate filaments that form a meshwork underlying the inner nuclear membrane. Lamins have a conserved domain structure consisting of a head, coiled-coil rod, and C-terminal tail domain possessing an Ig-like fold. This study identified differences between two mutant lamins that cause distinct clinical diseases. One of the LMNA mutations encodes lamin A/C p.R527P and the other codes lamin A/C p.R482W, which are typically associated with muscular dystrophy and lipodystrophy, respectively. To determine how these mutations differentially affect muscle, we generated the equivalent mutations in the Drosophila Lamin C (LamC) gene, an orthologue of human LMNA . The muscle-specific expression of the R527P equivalent showed cytoplasmic aggregation of LamC, a reduced larval muscle size, decreased larval motility, and cardiac defects resulting in a reduced adult lifespan. By contrast, the muscle-specific expression of the R482W equivalent caused an abnormal nuclear shape without a change in larval muscle size, larval motility, and adult lifespan compared to controls. Collectively, these studies identified fundamental differences in the properties of mutant lamins that cause clinically distinct phenotypes, providing insights into disease mechanisms.
Cardiomyopathy Drosophila Dunnigan type Emery–Dreifuss muscular dystrophy familial partial lipodystrophy intermediate filaments laminopathy lamins nuclear envelope nuclear pore

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