Transcriptome analysis of IFM-specific actin and myosin nulls in Drosophila melanogaster unravels lesion-specific expression blueprints across muscle mutations

A Madan, D Thimmaiya, A Franco-Cea, M Aiyaz… - Gene, 2017 - Elsevier
A Madan, D Thimmaiya, A Franco-Cea, M Aiyaz, P Kumar, JC Sparrow, U Nongthomba
Gene, 2017Elsevier
Muscle contraction is a highly fine-tuned process that requires the precise and timely
construction of large protein sub-assemblies to form sarcomeres. Mutations in many genes
encoding constituent proteins of this macromolecular machine result in defective functioning
of the muscle tissue. However, the pathways underlying muscle degeneration, and
manifestation of myopathy phenotypes are not well understood. In this study, we explored
transcriptional alterations that ensue from the absence of the two major muscle proteins …
Abstract
Muscle contraction is a highly fine-tuned process that requires the precise and timely construction of large protein sub-assemblies to form sarcomeres. Mutations in many genes encoding constituent proteins of this macromolecular machine result in defective functioning of the muscle tissue. However, the pathways underlying muscle degeneration, and manifestation of myopathy phenotypes are not well understood. In this study, we explored transcriptional alterations that ensue from the absence of the two major muscle proteins – myosin and actin - using the Drosophila indirect flight muscles. Our aim was to understand how the muscle tissue responds as a whole to the absence of either of the major scaffold proteins, whether the responses are generic to the tissue; or unique to the thick versus thin filament systems. Our results indicated that muscles respond by altering gene transcriptional levels in multiple systems active in muscle remodelling, protein degradation and heat shock responses. However, there were some responses that were filament-specific signatures of muscle degeneration, like immune responses, metabolic alterations and alterations in expression of muscle structural genes and mitochondrial ribosomal genes. These general and filament-specific changes in gene expression may be of relevance to human myopathies.
Elsevier
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