bioRxiv Science⌕ Search

Biology subjects

Volkers, M.

Publications and source records attributed to Volkers, M..

3 recordsLinked to original sources

Muscle LIM Protein is a Non-Canonical RNA-Binding Protein that Engages in RNA-Dependent Cytoskeletal Assemblies

Muscle LIM Protein (MLP) is a key component of the cardiomyocyte Z disc that is essential for sarcomere integrity and cardiac homeostasis. Accordingly, loss of MLP function results in (cardio)myopathy phenotypes in animal models and human patients. In this study, we present the first RNA-binding proteome (RBPome) of human cardiomyocytes using enhanced RNA interactome capture (eRIC). Data integration with existing RBPome datasets identified MLP as an evolutionary conserved and previously unrecognized non-canonical RNA-binding protein (RBP) in cardiomyocytes. Using complementary biochemical approaches, we confirmed direct RNA association of MLP. Moreover, RNA integrity was required for MLP interactions with cytoskeletal proteins and for the formation of higher-order MLP-containing assemblies, revealed by co-immunoprecipitation and RNA-dependent sedimentation profiling. Subcellular fractionation and imaging analyses indicated that MLPs association with cytoskeletal complexes may be weaker and more dynamic compared to core sarcomere proteins like -actinin. Domain mapping identified two glycine-rich regions within MLP as RNA contact sites, and RNA-binding-deficient MLP mutants showed impaired association with cytoskeletal complexes. Together, our findings suggest RNA binding as a regulated property of MLP and uncover an RNA-dependent layer of cytoskeletal organization in cardiomyocytes.

molecular biology↗

Comprehensive analysis of nonsense-mediated mRNA decay targets and activity in cardiomyocytes

Nonsense-mediated mRNA decay (NMD) serves as a mechanism to suppress the expression of mutant alleles containing premature termination codons, limit the expression of aberrantly spliced transcript isoforms, and control the expression of numerous regular genes. While the principles by which NMD recognizes target transcripts are well understood, much less is known about the range of mRNAs subject to NMD in tissues and specialized cell types. Here we describe the landscape of genes whose expression is controlled by NMD in cardiomyocytes derived from human induced pluripotent stem cells (iPSC-CM), using small read RNA sequencing in combination with a potent inhibitor of SMG1, a kinase essential for NMD. We find that NMD targets are highly conserved between iPSC-CM lines derived from two healthy individuals. Beyond gene level analysis, we identify individual exon and intron RNA sequences that strongly accumulate upon SMG1 inhibition. Using the cardiac NMD targets identified at gene, exon and intron level, we then demonstrate reduced NMD efficiency upon knockdown of two essential NMD factors, UPF1 and UPF2, in iPSC-CM. Our analysis demonstrates that quantifying the transcriptome-wide response to SMG1 inhibition represents a highly sensitive approach to assess global activity of the NMD pathway.

molecular biology↗

A cross-species multimodal database of gene expression in cardiac hypertrophy

Changes in gene expression determine the pathophysiological response of the heart during increased workload and biomechanical stress.1,2 Understanding the complex gene expression regulation during physiological and pathological stress provides insight into mechanisms that mediate the transition from cardiac hypertrophy to heart failure. We curated and generated a multi-omics database of cardiac hypertrophy and heart failure and exemplified its usage by evaluating the regulation of UCK2, a gene that belongs to a conserved cardiomyocyte hypertrophy gene expression signature with unknown function in heart disease. To provide the community with simple access to the database, we developed CHEERIO (Cardiac HypErtrophy gEne expRessIOn Database), a free and easy-to-use interactive web application to explore rodent and human gene expression during early, late, physiological and pathological cardiac hypertrophy, as well as heart failure at transcriptome, translatome, proteome, bulk and single-cell resolution. CHEERIO is freely available at https://voelkerslab.shinyapps.io/CHEERIO/.

physiology↗