1st ed. xii, 349 s., obr., grafy
Opuscula biologica
1. vyd. 263, [1] s.
- MeSH
- Organelle Biogenesis MeSH
- Cilia MeSH
- Endoplasmic Reticulum MeSH
- Lysosomes MeSH
- Mitochondria MeSH
- Organelles MeSH
- Peroxisomes MeSH
- Ribonucleoproteins MeSH
- Publication type
- Collected Work MeSH
- Conspectus
- Biologické vědy
- NML Fields
- biologie
- MeSH
- Organelle Biogenesis * MeSH
- Cycloheximide MeSH
- Cytochromes c MeSH
- Cytoplasm MeSH
- Erythromycin MeSH
- Eukaryotic Cells MeSH
- Genome, Mitochondrial MeSH
- RNA, Messenger biosynthesis MeSH
- DNA, Mitochondrial MeSH
- Mitochondria * genetics metabolism ultrastructure MeSH
- Proteins * metabolism ultrastructure MeSH
- Electron Transport Complex IV MeSH
- RNA, Ribosomal biosynthesis MeSH
- RNA, Transfer biosynthesis MeSH
- Statistics as Topic MeSH
- Models, Theoretical MeSH
- Publication type
- Research Support, Non-U.S. Gov't MeSH
In mammals, mature oocytes and early preimplantation embryos contain transcriptionally inactive structures termed nucleolus precursor bodies instead of the typical fibrillo-granular nucleoli. These nuclear organelles are essential and strictly of maternal origin. If they are removed from oocytes, the resulting embryos are unable to replace them and consequently fail to develop. Historically, nucleolus precursor bodies have been perceived as a passive repository site of nucleolar proteins that are required for embryos to form fully functional nucleoli. Recent results, however, contradict this long-standing dogma and show that these organelles are dispensable for nucleologenesis and ribosome biogenesis. In this article, we discuss the possible roles of nucleolus precursor bodies and propose how they might be involved in embryogenesis. Furthermore, we argue that these organelles are essential only shortly after fertilization and suggest that they might actively participate in centromeric chromatin establishment.
- MeSH
- Organelle Biogenesis * MeSH
- Cell Nucleolus physiology MeSH
- Embryo, Mammalian physiology MeSH
- Embryonic Development * MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
The biosynthesis of ribosomes is a complex process that requires the coordinated action of many factors and a huge energy investment from the cell. Ribosomes are essential for protein production, and thus for cellular survival, growth and proliferation. Ribosome biogenesis is initiated in the nucleolus and includes: the synthesis and processing of ribosomal RNAs, assembly of ribosomal proteins, transport to the cytoplasm and association of ribosomal subunits. The disruption of ribosome biogenesis at various steps, with either increased or decreased expression of different ribosomal components, can promote cell cycle arrest, senescence or apoptosis. Additionally, interference with ribosomal biogenesis is often associated with cancer, aging and age-related degenerative diseases. Here, we review current knowledge on impaired ribosome biogenesis, discuss the main factors involved in stress responses under such circumstances and focus on examples with clinical relevance.
- MeSH
- Organelle Biogenesis MeSH
- Humans MeSH
- Neoplasms metabolism MeSH
- Ribosomal Proteins metabolism MeSH
- Ribosomes metabolism MeSH
- Aging metabolism MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
Two experiments were carried out to examine the impacts of hydroxytyrosol (HT) on lipid metabolism and mitochondrial function in Megalobrama amblycephala. Triplicate groups of fish were fed four test diets: (1) low-fat diet (LFD, 5% fat), (2) high-fat diet (HFD, 15% fat), (3) LFD + 100 mg/kg HT (LFD + HT), and (4) HFD + 100 mg/kg HT (HFD + HT) (in vivo). Hepatocytes from the same batch were exposed to three media including L-15 medium (L15), oleic acid (OA) medium [L15 + 400 μM OA], and OA + HT medium [L15 + 400 μM OA + 10 μM HT] to explore the roles of HT in mitochondrial function (in vitro). Fish fed HFD had excessive fat deposition in the liver, and HT inclusion in the HFD decreased hepatic fat deposition. Transmission electron microscopy revealed that the HFD triggers loss of cristae and metrical density and hydropic changes in mitochondria and that HT supplementation attenuates the ultrastructural alterations of mitochondria. The in vitro test showed that HT decreases fat deposition in hepatocytes, suppresses the reactive oxygen species formation, and facilitates the expression of phospho-AMPK protein and the genes involved in mitochondria biogenesis (PGC-1, NRF-1, TFAM) and autophagy (PINK1, Mul1, Atg5). These findings suggest the lipid-lowering effect of HT mediated by activation of mitochondrial biogenesis and autophagy through the AMPK pathway.
- MeSH
- Autophagy * MeSH
- Organelle Biogenesis MeSH
- Cyprinidae genetics metabolism MeSH
- Dietary Fats metabolism MeSH
- Phenylethyl Alcohol analogs & derivatives metabolism MeSH
- Hepatocytes metabolism MeSH
- Liver cytology metabolism MeSH
- Animal Feed analysis MeSH
- Mitochondria metabolism MeSH
- AMP-Activated Protein Kinases genetics metabolism MeSH
- Fish Proteins genetics metabolism MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH