<HashMap><database>biostudies-arrayexpress</database><scores/><additional><submitter>Fabian Finger</submitter><organism>Mus musculus</organism><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-17333</full_dataset_link><description>Cardiolipin (CL) is a mitochondria-specific phospholipid essential for inner membrane architecture and respiratory chain function. To determine how loss of CL biosynthesis affects skeletal muscle transcriptional programs in a fiber-type-dependent manner, we generated skeletal muscle-specific Crls1 knockout mice (MUCKO) and performed bulk mRNA sequencing on two functionally distinct muscles: the oxidative Soleus and the glycolytic Extensor Digitorum Longus (EDL). RNA-seq was performed on MUCKO and littermate control mice for both muscle types, enabling comparison of CL-depletion-induced gene expression changes across oxidative and glycolytic fiber contexts. This dataset supports findings that cardiolipin loss drives fiber-type-specific transcriptional and metabolic adaptations, including differential regulation of proteostasis and lipid-handling pathways between oxidative and glycolytic muscle.</description><repository>biostudies-arrayexpress</repository><sample_protocol>Sample Collection - Skeletal muscle-specific Crls1 knockout (MUCKO) mice and littermate controls were used for this study. MUCKO mice carry a constitutive, skeletal muscle-specific knockout of Crls1; no tamoxifen or other inducible recombination scheme was used. Mice were sacrificed at 12 weeks of age by cervical dislocation. Soleus (oxidative) and extensor digitorum longus (EDL, glycolytic) muscles were dissected and immediately snap-frozen for downstream RNA extraction.</sample_protocol><sample_protocol>Sequencing - Libraries were sequenced as paired-end reads on the Illumina HiSeq 1500 platform.</sample_protocol><sample_protocol>Nucleic Acid Extraction - Total RNA was extracted from snap-frozen Soleus and EDL muscle tissue using TriReagent (Sigma-Aldrich), followed by isopropanol precipitation.</sample_protocol><sample_protocol>Library Construction - For generation of RNA-sequencing libraries, polyadenylated mRNA was isolated from total RNA by incubation with oligo-dT beads and libraries were prepared according to the manufacturer’s protocol (TruSeq 2, Illumina).</sample_protocol><figure_sub>Organization</figure_sub><figure_sub>MINSEQE Score</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>Processed Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><data_protocol>Data Transformation - Sequencing reads were mapped to the mouse reference genome (mm9) using STAR. Tag directories were generated using HOMER and exon reads were counted using iRNA-seq.</data_protocol><omics_type>Metabolomics</omics_type><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><instrument_platform>Illumina HiSeq 1500</instrument_platform><instrument_platform>not applicable</instrument_platform><study_type>RNA-seq of coding RNA</study_type><species>Mus musculus</species><pubmed_authors>Fabian Finger</pubmed_authors></additional><is_claimable>false</is_claimable><name>RNA-seq analysis of skeletal muscle-specific Crls1 knockout (MUCKO) mice reveals fiber-type-dependent transcriptional remodeling in Soleus and EDL</name><description>Cardiolipin (CL) is a mitochondria-specific phospholipid essential for inner membrane architecture and respiratory chain function. To determine how loss of CL biosynthesis affects skeletal muscle transcriptional programs in a fiber-type-dependent manner, we generated skeletal muscle-specific Crls1 knockout mice (MUCKO) and performed bulk mRNA sequencing on two functionally distinct muscles: the oxidative Soleus and the glycolytic Extensor Digitorum Longus (EDL). RNA-seq was performed on MUCKO and littermate control mice for both muscle types, enabling comparison of CL-depletion-induced gene expression changes across oxidative and glycolytic fiber contexts. This dataset supports findings that cardiolipin loss drives fiber-type-specific transcriptional and metabolic adaptations, including differential regulation of proteostasis and lipid-handling pathways between oxidative and glycolytic muscle.</description><dates><release>2026-08-08T00:00:00Z</release><modification>2026-08-08T01:01:03.258Z</modification><creation>2026-07-08T15:05:20.62Z</creation></dates><accession>E-MTAB-17333</accession><cross_references><ENA>ERP200909</ENA><EFO>EFO_0002944</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0003816</EFO><EFO>EFO_0003738</EFO><EFO>EFO_0004184</EFO></cross_references></HashMap>