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PubMed1978

Membranes in lupin root nodules. I. The role of Golgi bodies in the biogenesis of infection threads and peribacteroid membranes.

The process of infection of lupin nodule cells by rhizobia was examined using thin-section and freeze-fracture electron-microscopic techniques to characterize the properties of different membranes and to establish relationships between them. The membranes of the Golgi bodies and the endoplasmic reticulum stained with zinc iodide-osmium tetroxide but not with phosphotungstic acid or silver. By contrast the infection thread membranes, peribacteroid membranes, plasma membranes and membranes of cytoplasmic vesicles did not stain with zinc iodide-osmium tetroxide but stained with phosphotungstic acid and silver. The peribacteroid membranes and plasma membranes are, however, different from each other since the particle density on the E face of freeze-fracture replicas of plasma membranes was twice that on the E face of the peribacteroid membranes. An examination of the tips of the infection threads in the cytoplasm of the plant cells, showed that the rhizobia bud off from the infection threads enclosed in the infection thread membranes. The rhizobia continue to divide still surrounded by membranes of plant origin, namely the peribacteroid membranes. Cytoplasmic vesicles are observed in both thin-section and freeze-fracture preparations of nodule tissue closely associated with, and apparently produced by, Golgi bodies. Formation of the walls and membranes of the infection threads and of the peribacteroid membranes involves fusion of the cytoplasmic vesicles with these membranes. It is proposed that the process of infection of plant cells in lupin nodules involves a change in the function of the Golgi body system for the biogenesis of plant cell walls and plasma membranes to include the synthesis of the walls and membranes of the infection threads and also the peribacteroid membranes.

Cell Membrane↗
PubMed1980

Human diploid fibroblast-like cells (CF-3) as a model system for the study of Golgi biogenesis.

Human diploid fibroblast-like cells were maintained in an arrested, essentially non-mitotic state for extended periods of time in culture by lowering the serum concentration in the medium from 10 to 0.5%. These arrested cells re-entered the proliferative state when subcultivated in medium containing 10% serum. The morphological distribution and enzyme activities associated with the Golgi complex were examined during growth, arrest, and recovery. Cells grown in medium containing 10% serum possessed a well-developed Golgi complex consisting of parallel arrays of membranes and associated vesicles. Galactosyl transferase activity was highest after 3 days growth (17.5 +/- 5.0 nmol galactose transferred/45 min/mg protein) and declined to 9.8 +/- 3.0 at day 7. When the serum concentration was reduced to 0.5%, Golgi complexes were rarely observed by electron microscopy and galactosyl transferase activity was further reduced into medium containing 10% serum recovered from the arrested state and ultrastructurally resembled cells continuously cultured at the higher serum level. Numerous Golgi complexes reappeared and galactosyl transferase activity increased to 13.0 +/- 3.34 days after subcultivation. These results indicate that the Golgi complex can be experimentally manipulated in human diploid fibroblast-like cells in a manner which may be useful for the study of the biogenesis of this organelle.

Cell Cycle↗
PubMed1976

[Study of amino acid composition and biosynthesis of protein components of the membrane system of corn plastids during biogenesis of chloroplasts].

The biosynthesis of membrane proteins in maize plastids at different stages of differentiation of the chloroplast lamellar system was studied. Prolamellar and lamellar system preparations were isolated from maize plastids, disintegrated by osmotic shock under hypotonic conditions. Changes in the amino acid composition of 14C membrane proteins were observed at all stages of chloroplast ultrastructure formation. The maximal level of the apolar amino acids was observed in the membrane fraction of chloroplasts. Washed membranes from maize proplastids and chloroplasts can be resolved into at least 14 protein bands on formic acid--urea polyacrylamide gel. It is pointed out that biogenesis process leads to the increase of lipophylic protein content in the chloroplast lamellae fraction.

Amino Acids↗
PubMed2000

Assembly of the cellular powerhouse: current issues in muscle mitochondrial biogenesis.

Mitochondrial biogenesis occurs in muscle in response to chronic exercise, resulting in fatigue resistance. The assembly of the organelle is initiated by contraction-induced signals, which lead to the transcriptional activation of nuclear genes. This is accompanied by alterations in mRNA stability, as well as increases in protein import and mitochondrial DNA copy number, leading to a greater muscle mitochondrial content.

Exercise↗
PubMed2001

Accessory proteins in the biogenesis of G protein-coupled receptors.

Intracellular accessory proteins can be critical for G protein-coupled receptor (GPCR) biogenesis, including aspects of GPCR trafficking. Recent discoveries include the identification of multiple membrane-associated proteins that dictate not only the intracellular sequestration and/or transport of GPCRs, but also modulate-quite dramatically-GPCR ligand specificity subsequent to delivery to the cell surface. These exciting discoveries have shifted earlier paradigms of GPCR functionality.

Animals↗
PubMed1994

Genetic evidence supporting the role of peroxisome assembly factor (PAF)-1 in peroxisome biogenesis. Polymerase chain reaction detection of a missense mutation in PAF-1 of Chinese hamster ovary cells.

The peroxisome/plasmalogen-deficient Chinese hamster ovary (CHO) mutant cell line ZR-78.1 contains a missense mutation in its cDNA-encoding peroxisome assembly factor-1 (PAF-1). Using a rapid polymerase chain reaction assay, we now demonstrate that the genome of ZR-78.1 contains only the mutant allele. When mutant ZR-78.1 is fused with wild-type karyoplasts, occasional "negative nuclear hybrids" are observed that lack peroxisomes (Allen, L.-A. H., Morand, O. H., and Raetz, C. R. H. (1989) Proc. Natl. Acad. Sci. U.S.A. 86, 7012-7016). Despite the fact that negative nuclear hybrids are tetraploid, they do not contain the wild-type PAF-1 gene, suggesting that a chromosome fragment bearing the wild-type copy of PAF-1 was lost. Negative nuclear hybrids reconstituted with wild-type cytoplasts do contain a wild-type PAF-1 gene, indicating that the cytoplasts somehow reintroduced the wild-type PAF-1 allele without increasing ploidy. These findings support the role of PAF-1 and exclude the hypothesis of an additional cytoplasmic requirement for reinitiation of peroxisome biogenesis in peroxisome-deficient CHO cells. The plasmalogen deficiency and some other biochemical properties of ZR-78.1 are partially corrected in 5-azacytidine-treated subclones. However, such pseudo-revertants do not contain peroxisomes, consistent with the fact that there is no wild-type PAF-1 gene to reactivate by demethylation.

Acyltransferases↗
PubMed1993

[Molecular biology of peroxisome biogenesis].

Molecular mechanisms of peroxisomal protein translocation and peroxisome assembly have been extensively studied these several years. One type of topogenic signals has been identified both in vivo and in vitro: the C-terminal -Ser-Lys-Leu-COOH (SKL) motif sequence. In patients with generalized peroxisomal disease such as autosomal recessive, cerebrohepatorenal Zellweger syndrome where peroxisomes are morphologically absent, all peroxisomal proteins appear to be normally synthesized but assembly of peroxisomes is impaired. We have isolated several somatic animal cell mutants defective in biogenesis of peroxisomes. By genetic complementation analysis following the transfection of cDNA library to a CHO cell mutant, Z65, we cloned a cNDA for 35-kDa peroxisome assembly factor-1 (PAF-1) essential for peroxisome assembly. Furthermore, we have recently delineated the primary defect in a Zellweger patient who belonged to the same complementation group as the Z65. The cause of this syndrome was a homozygous nonsense point mutation in the PAF-1 gene.

Amino Acid Sequence↗
PubMed2000

The location of pKi67 in the outer dense fibrillary compartment of the nucleolus points to a role in ribosome biogenesis during the cell division cycle.

Although widely used as a marker of cell proliferation, the biochemical properties and function of the Ki67 antigen remain poorly understood. Recent data indicate that it can interact with RNA, DNA, and a number of cellular proteins including elements of the ubiquitin proteolytic pathway and a novel kinase. The evidence for its expression only in cycling cells is extensive and it is not regulated by stress, apoptosis or DNA damage. It was reasoned that a detailed characterization of the localization of pKi67 and analysis of its spatial relationship to other nucleolar proteins may provide insights into its function. Using high-resolution laser scanning confocal microscopy with double and triple labelling, pKi67 expression in MCF7 cells has been defined in relation to the distribution of nucleolin, fibrillarin, p130 (human Nopp 140 homologue), p120 (Nol 1), RH-II/Gu helicase, and topoisomerase II beta. All of these molecules are perichromosomal during mitosis and all but fibrillarin and p130 show extra-nucleolar distribution in early G1. The majority of p120 (Nol 1) and RH-II/Gu helicase co-localize in the diffuse fibrillar centre (DFC) of nucleoli, while there is only partial overlap with nucleolin and fibrillarin. There is no co-localization between p130 and pKi67. These data refine current understanding of the distribution of pKi67 and its physical relationship with functional domains of the nucleolus and place pKi67 in a zone of the DFC associated with late rRNA processing. Taken together with recent biochemical data, these observations allow the proposal of a model of pKi67 function in which it acts as an 'efficiency factor' in ribosome biogenesis during the heavy metabolic demands placed on a cell during the cell division cycle.

Blood Proteins↗
PubMed1997

Biogenesis of peroxisomes in fetal liver.

Peroxisomes are single membrane-limited cell organelles that are involved in numerous metabolic functions. Peroxisomes do not contain DNA; the matrix and membrane proteins are encoded by the nuclear genome. It is assumed that new peroxisomes are formed by division of existing organelles. The present article gives an overview of microscopic studies and recent unpublished results dealing with peroxisome biogenesis in mammalian fetal liver and presents data on peroxisomes in oocytes. Cytochemical (catalase and D-aminoacid oxidase activity) and immunocytochemical data in rat and human liver (antigens of catalase, the three peroxisomal beta-oxidation enzymes, alanine: glyoxylate aminotransferase, peroxisomal membrane proteins with molecular weights of 42 and 70 kDa) indicate that during embryonic and fetal development the peroxisomal population undergoes a differentiation with respect to the composition of the matrix and to the size and number of the organelles. In the youngest stages, rare and small peroxisomes are present, into which the matrix components are imported in a sequential way. The import seems asynchronous in peroxisomes of the same hepatocyte. The size and number of the peroxisomes increase during liver development. In rat and human liver, no morphological or immunocytochemical evidence for an elaborate network of interconnected peroxisomes ("reticulum") was found. Instead, peroxisomes presented as individual organelles, which occasionally show membrane extensions. The importance of the metabolic functions of peroxisomes in human liver is emphasized by the peroxisomal disorders. In the liver of affected fetuses, the microscopic features associated with the defect can already be recognized; i.e., either catalase containing peroxisomes are absent and catalase is localized in the cytoplasm (in fetuses affected with Zellweger syndrome or with infantile Refsum disease) or peroxisomes are present but they are abnormally enlarged (e.g., a fetus affected with acyl-CoA oxidase deficiency). In the quail ovary, numerous peroxisomes are observed in the oocyte and in the granulosa cells during follicle maturation, but not in the full-grown egg. Thus, the mechanism of peroxisome inheritance remains unresolved.

Animals↗
PubMed2000

Protein localisation approaches for understanding yeast cell wall biogenesis.

Yeast cells are surrounded by the cell wall, a rigid but dynamic structure that is essential for their viability. The complexity and functionality of this structure suggest that a high number of proteins must be involved in the biogenesis of the cell wall architecture and, as a consequence, in the maintenance of cell integrity. Among them, a high percentage is assumed to be located at the cell surface, mostly as structural or enzymatic components of the cell wall. Therefore, the presence of a protein in the cell wall is suggestive of its cell wall-related function. Different techniques can be used to specifically detect the cell wall localisation of a given protein or to identify cell wall proteins in large-scale analyses. These include the detection of proteins in whole cells or specific cell wall fractions by immunological, biochemical, microscopic, or genetic approaches, as well as the emerging proteomic technology. The advantages, limitations, and usefulness of these techniques are discussed and illustrated with some examples.

Cell Wall↗
PubMed2000

Mitochondria-targeted green fluorescent proteins: convenient tools for the study of organelle biogenesis in Saccharomyces cerevisiae.

We describe the construction and characterization of a novel set of plasmids for expression of mitochondria-targeted green fluorescent protein (GFP) in Saccharomyces cerevisiae. The vectors include constructs with strong regulatable and constitutive promoters, four different auxotrophic markers for yeast transformation, and a green (S65T) and a blue-shifted (P4-3) variant of GFP. Mitochondria are brightly fluorescent in living yeast cells grown on different carbon sources and at different temperatures, with virtually no background staining. Specific staining of mitochondria is also shown for a respiratory-deficient mutant with abnormal mitochondrial morphology. The plasmids facilitate convenient analysis of mutants defective in mitochondrial morphology or inheritance and, at the same time, are suitable vectors for easy construction of different kinds of GFP fusion proteins to study various aspects of organelle biogenesis in living yeast cells.

Cloning, Molecular↗
PubMed2000

Phenotype-genotype relationships in PEX10-deficient peroxisome biogenesis disorder patients.

The peroxisome biogenesis disorders (PBD) are characterized by neural, hepatic, and renal deficiencies, severe mental retardation, and are often lethal. These disorders are genetically and phenotypically heterogeneous and are caused by defective peroxisomal protein import and decreased peroxisomal metabolic function. Mutations in PEX10 have been identified in patients from complementation group 7 (CG7) of the PBDs and we report here an analysis of the genotypes and phenotypes of PEX10-deficient patients. All four PEX10-deficient Zellweger Syndrome (ZS) patients were found to have nonsense, frameshift, or splice site mutations that remove large portions of the PEX10 coding region. In contrast, a more mildly affected PEX10-deficient neonatal adrenoleukodystrophy patient expressed a PEX10 allele with a missense mutation, H290Q, affecting the C-terminal zinc-binding domain of the PEX10 product. These results support the hypothesis that severe, loss-of-function mutations in PEX genes cause more severe clinical phenotypes, whereas mildly affected PBD patients have PEX gene mutations that retain residual function. To quantitate the effects of the PEX10 mutations identified here and elsewhere we employed a functional complementation assay. Surprisingly, we observed that nonsense and frameshift mutations predicted to delete the C-terminal 2/3 (R125X) or 1/3 (c.704insA) of the protein displayed nearly normal PEX10 activity. Even more surprising, we found that the unexpectedly high PEX10 activity displayed by these cDNAs could be eliminated by removing or mutating segments of the PEX10 cDNA downstream of the mutations. Although these results demonstrate serious flaws in the PEX10 functional complementation assay, they do suggest that the C-terminal zinc-binding domain is critical for PEX10 function.

Alleles↗
PubMed2000

A proteomic approach for the study of Saccharomyces cerevisiae cell wall biogenesis.

In fungi, cell shape is determined by the presence of a rigid cell wall which separates the cell from the extracellular medium. This highly dynamic structure is essential for the maintenance of cell integrity and is involved in several phenomena such as flocculation, adherence and pathogenicity. The composition of the fungal cell wall is well known, but issues such as the assembly and remodeling of its components remain poorly understood. In an attempt to study the de novo construction of the yeast cell wall, we have undertaken a large-scale proteomic approach to analyze the proteins secreted by regenerating protoplasts. Upon incubation of protoplasts in regenerating conditions, numerous proteins are secreted into the culture medium. These presumably include proteins destined for the cell wall, comprising both structural proteins as well as enzymes involved in cell wall biogenesis. This work reports the establishment of a reference map of proteins secreted by regenerating protoplasts by means of two-dimensional polyacrylamide gel electrophoresis (2-D PAGE) and their identification by mass spectrometry. Thirty-two different proteins have been identified, including known cell wall proteins, glycolytic enzymes, heat shock proteins, and proteins involved in several other processes. Using this approach, novel proteins possibly involved in cell wall construction have also been identified. This reference map will allow comparative analyses to be carried out on a selected collection of mutants affected in the cell wall.

Amino Acid Sequence↗
PubMed1985

Plasma membrane biogenesis in the avian salt gland: a biochemical and quantitative electron microscopic autoradiographic study.

The avian salt gland provides an ideal system for the study of plasma membrane (PM) biogenesis. Feeding ducklings 1% sodium chloride (salt stress) induces the secretory cells of the gland to synthesize large amounts of PM, which forms an extensive basolateral PM domain after 7-9 days of treatment. In the present study, the initial biosynthetic events following salt stress were investigated. In vivo studies using 3H-uridine indicated that increased rates of RNA synthesis could be detected by 2 hr after the beginning of salt stress and continued through at least 12 hr. Under in vitro conditions, increased rates of protein and glycoprotein synthesis (as monitored by 3H-leucine and 3H-fucose incorporation, respectively) were also detected after 2 hr and continued through 7-9 days. Increased levels of Na,K-ATPase, a specific secretory cell PM marker, were detected after 8 hr of treatment as monitored by specific activity and 3H-ouabain binding. Sodium dodecyl sulfate-polyacrylamide slab gel electrophoresis coupled with fluorography indicated that both 3H-leucine and 3H-fucose were incorporated into partially purified preparations of Na,K-ATPase isolated after 12 hr. Light microscopic autoradiographic analysis of pulse-chase experiments indicated that in secretory cells of 12-hr salt-stressed glands, 3H-leucine- and 3H-fucose-labelled products reached the cell periphery by 1-2 hr after the initial pulse. The incorporation of both tritiated precursors was predominantly associated with the secretory cells. Quantitative electron microscopic autoradiography indicated that 3H-leucine is initially taken up by elements of the rough endoplasmic reticulum (RER) and cytoplasm (5 min postpulse), subsequently transported to and concentrated within components of the Golgi apparatus (10 min of chase), and ultimately incorporated into all domains of the plasma membrane of secretory cells by 1-2 hr of chase. The data is consistent with a flow of newly synthesized membrane components from RER to Golgi to plasma membrane and is analogous to the pattern previously found for the synthesis and processing of PM proteins in a wide variety of cell types.

Animals↗
PubMed1987

Radioautographic tracing of 3H-proline in the endodermal cells of the parietal yolk sac as an indicator of the biogenesis of basement membrane components.

The biogenesis of basement-membrane components was investigated in the endodermal cells of the rat parietal yolk sac in 12.5-day pregnant rats; 3H-proline was injected into conceptuses. After various time intervals, the parietal yolk sac, including endodermal cells and the associated Reichert's membrane, was removed and processed for electron-microscopic radioautography. Silver grains were counted over endodermal cell organelles and Reichert's membrane. At 2 and 5 min after 3H-proline injection, endodermal cells showed heavy labeling in rough endoplasmic reticulum (rER). Silver grain density over the rER decreased from 2 to 20 min and then remained at a plateau. Grain density was moderate over the Golgi apparatus initially but rose to a peak at 2 hr and decreased by 4 hr and later. Grain density was negligible over secretory granules at 2 and 5 min and increased moderately with time to reach a maximum at 8 hr. Thus, radioautographic peaks occurred sequentially in rER, Golgi apparatus, and secretory granules. By 4 hr and later, silver grains accumulated over Reichert's membrane. These results indicated that endodermal cells incorporated labeled proline into substances which were processed from the rER through the Golgi apparatus, transported from there to the cell surface by secretory granules, and released for export to Reichert's membrane. To clarify the nature of the exported substances, the amount of label present in proline and hydroxyproline residues after 3H-proline injection was measured in Reichert's membrane with or without the associated endodermal cells. Within the cells, 61.8% of the labeled proteins were classified as "sedentary" and 38.2% as "exportable." Of the label exported to Reichert's membrane, 66.3% consisted of type IV collagen and the rest of other basement-membrane components. The results obtained with this model suggest that basement-membrane proteins, including type IV collagen, are elaborated by the associated cells through the classical pathway: rER-Golgi apparatus-secretory granules.

Animals↗
PubMed2004

Peroxisome biogenesis disorders with prolonged survival: phenotypic expression in a cohort of 31 patients.

The peroxisome biogenesis disorders (PBDs) with generalized peroxisomal dysfunction include Zellweger syndrome (ZS), neonatal adrenoleukodystrophy (NALD), and infantile Refsum disease (IRD). There is clinical, biochemical, and genetic overlap among the three phenotypes, also known as Zellweger spectrum disorders. Clinical distinctions between the phenotypes are not sharply defined. Only limited sources are available to serve as a background for prognosis in PBD, especially in case of prolonged survival. We delineated the natural history of 31 PBD patients (age 1.2-24 years) through systematic clinical and biochemical investigations. We excluded classical ZS from our study, and included all patients with a biochemically confirmed generalized peroxisomal disorder over 1 year of age, irrespective of the previously diagnosed phenotype. The initial clinical suspicion, age at diagnosis, growth, development, neurological symptoms, organ involvements, and survival are summarized. Common to all patients were cognitive and motor dysfunction, retinopathy, sensorineural hearing impairment, and hepatic involvement. Many patients showed postnatal growth failure, 10 patients displayed hyperoxaluria of whom 4 had renal stones. Motor skills ranged from sitting with support to normal gait. Speech development ranged from non-verbal expression to grammatical speech and comprehensive reading. The neurodevelopmental course was variable with stable course, rapid decline with leukodystrophy, spinocerebellar syndrome, and slow decline over a wide range of faculties as outcome profiles. At the molecular level, 21 patients had mutations in the PEX1 gene. The two most common PEX1 mutations were the G843D (c.2528G-->A) missense and the c.2097insT frameshift mutation. Patients having the G843D/G843D or the G843D/c.2097insT genotypes were compared. Patients homozygous for G843D generally had a better developmental outcome. However, one patient who was homozygous for the "mild" G843D mutation had an early lethal disease, whereas two other patients had a phenotype overlapping with the G843D/c.2097insT group. This indicates that next to the PEX1 genotype other yet unknown factors determine the ultimate phenotype.

ATPases Associated with Diverse Cellular Activitie↗
PubMed2006

Mitochondrial biogenesis in the anticonvulsant mechanism of the ketogenic diet.

OBJECTIVE: The full anticonvulsant effect of the ketogenic diet (KD) can require weeks to develop in rats, suggesting that altered gene expression is involved. The KD typically is used in pediatric epilepsies, but is effective also in adolescents and adults. Our goal was to use microarray and complementary technologies in adolescent rats to understand its anticonvulsant effect. METHODS: Microarrays were used to define patterns of gene expression in the hippocampus of rats fed a KD or control diet for 3 weeks. Hippocampi from control- and KD-fed rats were also compared for the number of mitochondrial profiles in electron micrographs, the levels of selected energy metabolites and enzyme activities, and the effect of low glucose on synaptic transmission. RESULTS: Most striking was a coordinated upregulation of all (n = 34) differentially regulated transcripts encoding energy metabolism enzymes and 39 of 42 transcripts encoding mitochondrial proteins, which was accompanied by an increased number of mitochondrial profiles, a higher phosphocreatine/creatine ratio, elevated glutamate levels, and decreased glycogen levels. Consistent with increased energy reserves, synaptic transmission in hippocampal slices from KD-fed animals was resistant to low glucose. INTERPRETATION: These data show that a calorie-restricted KD enhances brain metabolism. We propose an anticonvulsant mechanism of the KD involving mitochondrial biogenesis leading to enhanced alternative energy stores.

Animals↗