Project description:To get insight into the genetic characteristics of hyper active mutant line of rat, SPORTS, and the effect of exercise on gene expression, we compared gene expression profiles of exercised SPORTS rat, sedentary SPORTS rat, and sedentary wild type rat. Using RNA extracted from the muscle of these rats, we performed microarray analysis. Subsequent GO analyses revealed that genes belonging to muscle development and glycolysis were upregulated in exercised SPORTS rat compared to sedentary SPORTS rat, and genes related to coagulation were upreguated in sedentary SPORTS rat compared to wild type rat. These results were consistent with phenotypes, such as hyper activity and thrombotic tendency, which were reported for SPORTS rat.
Project description:Expression profiles of polg mutant cells reveal that many genes encoding proteins involved in cell wall biogenesis and stress response are induced, suggesting that polg mutant cells attempt to maintain growth potential and undergo extensive oxidative metabolism. Conversely, many genes encoding proteins involved in ribosome biogenesis and respiration are repressed, indicating that cells depleted of mtDNA are adapted to grow slowly in absence of mitochondrial function. We analyzed 5 arrays of polyg mutant cells vs wild type cells.
Project description:To identify and analyze mtDNA mutation-responsive genes, a comparison of gastrocnemius muscle tissues from WT (control) and D257A mice was conducted. We examined changes in gene expression in the muscle associated with mtDNA mutations. 1) Types of experiments: a) Effect of mitochondrial DNA (mtDNA) mutations b) Effect of aging c) WT (13 month-old Polg+/+ mice) vs. D257A (13 month-old PolgD257A/D257A) mice 2) Experimental factors: a) Type of gene: PolgD257A/D257A b) Time (age) 3) Number of hybridizations in the study: ~10 4) A common reference RNA was not used. 5) Quality control measures were not used. No replicates were done. Dye swap was not used.
Project description:Expression profiles of polg mutant cells reveal that many genes encoding proteins involved in cell wall biogenesis and stress response are induced, suggesting that polg mutant cells attempt to maintain growth potential and undergo extensive oxidative metabolism. Conversely, many genes encoding proteins involved in ribosome biogenesis and respiration are repressed, indicating that cells depleted of mtDNA are adapted to grow slowly in absence of mitochondrial function. Keywords: Schizosaccharomyces pombe ployg mutant cells vs wild type cells.
Project description:Exercise reduces tumor growth in certain models but the mechanisms driving this is unknown. Tumors from sedentary or exercised mice were removed and processed for single cell sequencing to explore transcriptional changes in the tumor microenvironment induced by exercise.
Project description:Consequence of physical exercise in skeletal muscle was investigated in C57BL/6 mice after 4 weeks of exercise training and compared to sedentary controls. Exercised mice received four 4 weeks of regular exercise training on a motorized treadmill and were compared to sedentary controls. 6 mice of each Treatment were used to extract RNA from the quadriceps muscle three hours after the last training bout
Project description:We have previosuly shown that our Polg(D181A) show spontaneous depressive episodes as a result of mtDNA mutations, but we do not know the cellular mechanisms that link mtDNA mutations to behavioural changes. We hypothesized that mtDNA mutation-induced mitochondrial dysfunction in PVT causes a dysregulation of epigenetics, causing a transcriptional response which ffects neuronal function and ultimately causes the depressive phenotype. We assessed this using a combination of RNA-seq, H3K27Ac ChIP-seq, and ATAC-seq and compared our H3K27Ac results to other brain regions.
Project description:This is a custom Affymetrix resequencing array for DNA sequencing of the entire coding region and exon-splice sites of 39 human genes (452 exons; 106,337 bases). These nuclear genes encode proteins localized to mitochondria and include known disease genes (i.e. POLG, C10orf2) and new candidate genes for mtDNA maintenance disorders. We sequenced 27 patient (P) and 13 control (C) samples using this array.
Project description:Pathogenic mutations in the catalytic DNA polymerase gamma (POLG1) gene result in the accumulation of mtDNA mutations, deletions and/or decrease of mtDNA copy number. These features interfere with proper functioning of the electron transport chain, mostly affecting metabolically active tissues such as the brain, the heart and the liver. So far, mechanisms underlying POLG pathogenesis are not fully understood. To identify general pathways influenced by mutant polymerase gamma, skeletal muscle gene expression profiles of six POLG1 patients and twelve controls were compared. Patient and control subject from three age categories (<10; 11-49; >50) were selected. RNA was extracted from skeletal muscle biopsies and hybridized on Affymetrix microarrays.
