Browsing by Subject "mitochondria"

Now showing 1 - 4 of 4
  • Thumbnail Image
    ItemOpen Access
    A Mitochondrial Progesterone Receptor Increases Cardiac Beta-Oxidation and Remodeling.
    (Journal of the Endocrine Society, 2019-02) Dai, Qunsheng; Likes, Creighton E; Luz, Anthony L; Mao, Lan; Yeh, Jason S; Wei, Zhengzheng; Kuchibhatla, Maragatha; Ilkayeva, Olga R; Koves, Timothy R; Price, Thomas M; Price, Thomas M
    Progesterone is primarily a pregnancy-related hormone, produced in substantial quantities after ovulation and during gestation. Traditionally known to function via nuclear receptors for transcriptional regulation, there is also evidence of nonnuclear action. A previously identified mitochondrial progesterone receptor (PR-M) increases cellular respiration in cell models. In these studies, we demonstrated that expression of PR-M in rat H9c2 cardiomyocytes resulted in a ligand-dependent increase in oxidative cellular respiration and beta-oxidation. Cardiac expression in a TET-On transgenic mouse resulted in gene expression of myofibril proteins for remodeling and proteins involved in oxidative phosphorylation and fatty acid metabolism. In a model of increased afterload from constant transverse aortic constriction, mice expressing PR-M showed a ligand-dependent preservation of cardiac function. From these observations, we propose that PR-M is responsible for progesterone-induced increases in cellular energy production and cardiac remodeling to meet the physiological demands of pregnancy.
  • Thumbnail Image
    ItemOpen Access
    An Exploration into Fern Genome Space.
    (Genome Biol Evol, 2015-08-26) Wolf, PG; Sessa, EB; Marchant, DB; Li, F; Rothfels, CJ; Sigel, EM; Gitzendanner, MA; Visger, CJ; Banks, JA; Soltis, DE
    Ferns are one of the few remaining major clades of land plants for which a complete genome sequence is lacking. Knowledge of genome space in ferns will enable broad-scale comparative analyses of land plant genes and genomes, provide insights into genome evolution across green plants, and shed light on genetic and genomic features that characterize ferns, such as their high chromosome numbers and large genome sizes. As part of an initial exploration into fern genome space, we used a whole genome shotgun sequencing approach to obtain low-density coverage (∼0.4X to 2X) for six fern species from the Polypodiales (Ceratopteris, Pteridium, Polypodium, Cystopteris), Cyatheales (Plagiogyria), and Gleicheniales (Dipteris). We explore these data to characterize the proportion of the nuclear genome represented by repetitive sequences (including DNA transposons, retrotransposons, ribosomal DNA, and simple repeats) and protein-coding genes, and to extract chloroplast and mitochondrial genome sequences. Such initial sweeps of fern genomes can provide information useful for selecting a promising candidate fern species for whole genome sequencing. We also describe variation of genomic traits across our sample and highlight some differences and similarities in repeat structure between ferns and seed plants.
  • Thumbnail Image
    ItemOpen Access
    Redox mechanisms of cardiomyocyte mitochondrial protection.
    (Front Physiol, 2015) Bartz, Raquel R; Suliman, Hagir B; Piantadosi, Claude A
    Oxidative and nitrosative stress are primary contributors to the loss of myocardial tissue in insults ranging from ischemia/reperfusion injury from coronary artery disease and heart transplantation to sepsis-induced myocardial dysfunction and drug-induced myocardial damage. This cell damage caused by oxidative and nitrosative stress leads to mitochondrial protein, DNA, and lipid modifications, which inhibits energy production and contractile function, potentially leading to cell necrosis and/or apoptosis. However, cardiomyocytes have evolved an elegant set of redox-sensitive mechanisms that respond to and contain oxidative and nitrosative damage. These responses include the rapid induction of antioxidant enzymes, mitochondrial DNA repair mechanisms, selective mitochondrial autophagy (mitophagy), and mitochondrial biogenesis. Coordinated cytoplasmic to nuclear cell-signaling and mitochondrial transcriptional responses to the presence of elevated cytoplasmic oxidant production, e.g., H2O2, allows nuclear translocation of the Nfe2l2 transcription factor and up-regulation of downstream cytoprotective genes such as heme oxygenase-1 which generates physiologic signals, such as CO that up-regulates Nfe212 gene transcription. Simultaneously, a number of other DNA binding transcription factors are expressed and/or activated under redox control, such as Nuclear Respiratory Factor-1 (NRF-1), and lead to the induction of genes involved in both intracellular and mitochondria-specific repair mechanisms. The same insults, particularly those related to vascular stress and inflammation also produce elevated levels of nitric oxide, which also has mitochondrial protein thiol-protective functions and induces mitochondrial biogenesis through cyclic GMP-dependent and perhaps other pathways. This brief review provides an overview of these pathways and interconnected cardiac repair mechanisms.
  • Thumbnail Image
    ItemEmbargo
    The role of protein translation and mitochondrial specialization in anchor cell invasion through basement membranes in C. elegans
    (2024) Kenny-Ganzert, Isabel Winefred

    Basement membranes (BM) are dense layers of cross-linked extracellular matrix (ECM) proteins that provide structure for tissues, as well as serving as a barrier that prevents cell movement between tissues. Despite formidable barrier properties, specialized cells have acquired the ability to invade BM during development and physiological homeostasis. Furthermore, dysregulation of invasive behavior is the root of many diseases and disorders. Cell invasion is a robust process that requires extensive signaling, cytoskeletal, and proteolytic proteins to coordinate the physical and chemical removal of BM. Therefore, it is crucial to understand how cells construct, support, and fuel machinery required for invasion. Here, I use the C. elegans anchor cell (AC), an experimentally tractable and visually accessible in vivo model for cell invasion through the BM, to investigate ribosome biogenesis, endomembrane expansion, and mitochondrial specialization in cell invasion through BM. In Chapter 1, I review AC invasion as a model of cell invasion. In Chapter 2, I identified new invasion regulators, an enrichment of ribosomal proteins, and key roles for ribosome biogenesis and endomembrane expansion to meet the heightened protein-translation demands of the cell during invasion through BM. In Chapter 3, I discover that AC basal mitochondria have a specialized electron transport chain (ETC) to produce rapid amounts of ATP to fuel cell invasion and that mitochondrial specialization is dependent on mitochondrial protein import machinery enrichment, cristae remodeling, and mitochondria-endoplasmic reticulum contact sites (MERCS). In Chapter 4, I discuss the implications of these finding on our understanding of how cells construct, support, and fuel machinery required for invasion.