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M Schlicht

Publications and source records attributed to M Schlicht.

12 recordsLinked to original sources
PubMed2005

Cell wall pectins and xyloglucans are internalized into dividing root cells and accumulate within cell plates during cytokinesis.

Recently, we have reported that cell wall pectins are internalized into apical meristem root cells. In cells exposed to the fungal metabolite brefeldin A, all secretory pathways were inhibited, while endocytic pathways remained intact, resulting in accumulation of internalized cell wall pectins within brefeldin A-induced compartments. Here we report that, in addition to the already published cell wall epitopes, rhamnogalacturonan I and xyloglucans also undergo large-scale internalization into dividing root cells. Interestingly, multilamellar endosomes were identified as compartments internalizing arabinan cell wall pectins reactive to the 6D7 antibody, while large vacuole-like endosomes internalized homogalacturonans reactive to the 2F4 antibody. As all endosomes belong topographically to the exocellular space, cell wall pectins deposited in these "cell wall islands", enclosed by the plasma-membrane-derived membrane, are ideally suited to act as temporary stores for rapid formation of cell wall and generation of new plasma membrane. In accordance with this notion, we report that all cell wall pectins and xyloglucans that internalize into endosomes are highly enriched within cytokinetic cell plates and accumulate within brefeldin A compartments. On the other hand, only small amounts of the pectins reactive to the JIM7 antibody, which are produced in the Golgi apparatus, localize to cell plates and they do not accumulate within brefeldin A compartments. In conclusion, meristematic root cells have developed pathways for internalization and recycling of cell wall molecules which are relevant for plant-specific cytokinesis.

Antibodies, Monoclonal↗
PubMed2001

Corynebacterium diphtheriae: a PTS view to the genome.

We have surveyed the publicly available genome sequence of Corynebacterium diphtheriae (www.sanger.ac.uk) to identify components of the phosphotransferase system (PTS), which plays a central role in carbon metabolism in many bacteria. Three gene loci were found to contain putative pts genes. These comprise: (i) the genes of the general phosphotransferases enzyme I (ptsI) and HPr (ptsH), a fructose-specific enzyme IIABC permease (fruA), and a fructose 1-phosphate kinase (fruK); (ii) a gene that encodes an enzyme IIAB of the fructose/mannitol family, and a novel HPr-like gene, ptsF, that encodes an HPr domain fused to a domain of unknown function; (iii) and a gene for a glucose-specific enzyme IIBCA (ptsG). A search for genes that may be putative PTS-targets or that may operate in general carbon regulation revealed a possible regulatory gene encoding an antiterminator protein downstream from ptsG. Furthermore, genes were detected encoding glycerol kinase, glucose kinase, and a homologue of the global activator of carbon catabolite repression in Escherichia coli, CAP. The possible significance of these observations in carbon metabolism and the novel features of the detected genes are discussed.

Bacterial Proteins↗
PubMed1995

A multidisciplinary approach to toxicological screening: I. Systemic toxicity.

The toxicity of 10 chemicals, including pesticides (carbaryl, chlordane, heptachlor, and triadimefon), solvents (carbon tetrachloride, dichloromethane, tetrachloroethylene, and trichloroethylene), and industrial chemicals [diethylhexylphthalate (DEHP) and phenol] was examined in the liver, kidneys, spleen, thymus, and adrenals of female F344 rats after 1 or 14 d of oral dosing. For each chemical, 4 doses were based on fractions of the acute LD50, which was estimated using an abbreviated (up-and-down) method. A multivariate analysis (MANOVA) was conducted for each organ using selected measures of toxicity. A post hoc contrast analysis was also conducted for significant MANOVA results in order to determine effective and ineffective doses. A single dose of heptachlor resulted in necrotic lymphocytes in the spleen and thymus at doses > or = 23 mg/kg. Triadimefon altered liver and spleen weights; this effect has not been described previously. Dichloromethane (> or = 337 mg/kg/d for 14 d) increased the incidence of necrosis of individual centrilobular hepatocytes. Trichloroethylene-induced hepatotoxicity was obtained at doses an order of magnitude lower than those reported in the literature. Acute DEHP (150 mg/kg) increased mitotic figures in hepatocytes, which were replaced by hepatocellular cytomegaly after 14 d of dosing at the same level. Following phenol exposure, there was an increased incidence in hepatocellular necrosis at 1 d, and an increased incidence of kidney lesions at 1 and 14 d; these findings were considered to be the result of vascular stasis. Overall, the algorithm used to select doses was effective for both 1- or 14-d dosing regimens. For all chemicals except carbon tetrachloride, the lowest effective dose for systemic toxicity was within the range of 3-56% of the LD50 for acute dosing, and 1-30% of the LD50 for repeated administration.

Administration, Oral↗
PubMed1995

A multidisciplinary approach to toxicological screening: IV. Comparison of results.

Toxicity data collected under standardized test conditions may be of the utmost importance in health risk assessment, in which human exposure limits are often derived from laboratory experiments. A standardized approach to data collection is also important for evaluating the sensitivity and specificity of test methods used to determine toxic potential. Several experiments were undertaken to determine the effects of chemical exposures using a multidisciplinary screening battery, which included tests for systemic, neurological and developmental toxicity. The effects of 1- and 14-d exposures to 10 chemicals on systemic and neurological indices of toxicity were determined in female F344 rats using standardized test batteries. Parallel experiments determined chemical effects on prenatal and postnatal development following exposure of the dams for 14 d. The chemicals included four pesticides (carbaryl, triadimefon, chlordane, and heptachlor), four solvents (trichloroethylene, tetrachloroethylene, carbon tetrachloride, and dichloromethane), and two industrial compounds (phenol and diethylhexyl phthalate). The results showed that the chemicals produced markedly different qualitative patterns of effect on systemic, neurological, and developmental indices of toxicity. Differences in the pattern of systemic and neurological effects were also obtained that depended on dosing duration. Quantitative analyses indicated that the highest ineffective dose as well as the lowest effective dose could vary by as much as two orders of magnitude across the different indices of toxicity. These results clearly show that a test battery focused on a single endpoint of toxicity cannot be used to accurately predict either qualitatively or quantitatively a chemical's systemic, neurological, and developmental toxicity profile.

Analysis of Variance↗
PubMed1980

[MBCK and infarct size (author's transl)].

In 128 patients (20 f., 98 m., age between 26 and 88 years, mean age 59 years) with acute myocardial infarction, infarct size was calculated from CK and MBCK serum activity using the individual fractional decay rate kD. Only a moderate correlation could be found between infarct size calculated from CK-serum curves (CK-IG) and from MBCK (MBCK-IG) (r = 0.65). Only little improvement was achieved by excluding those patients who had been resuscitated (n = 13, r = 0.69). In 20% of the patients there was a good correlation (+/- 5 g eq) between CK-IG and MBCK-IG. In 14% MBCK-IG was larger and in 66% smaller than CK-IG. Calculation of MBCK-IG is based on a constant MBCK percentage of CK in myocardium, namely 14%, and assumes that the distribution volume and amount of enzyme released into the serum is the same for CK and MBCK. Thus the percentage of MBCK in serum compared to CK should also be 14%. We found an average value approaching this (13.6%), but with a wide range between 4.7 and 21.2%. It is this variation which is responsible for the poor correlation between both IGs.

Adult↗
PubMed1978

Escherichia coli dnaB protein. Affinity chromatography on immobilized nucleotides.

The purification of the Escherichia coli dnaB protein by affinity chromatography on nucleotides bound to agarose is described. The dnaB protein, which contains an associated ribonucleoside triphosphatase activity (Wickner, S., Wright, M., and Hurwitz, J. (1974) Proc. Natl. Acad. Sci. U. S. A. 71, 783-787) binds to immobilized ATP, ADP, and UDP, but not to AMP. The type of linkage of ATP to agarose influences the adsorption, elution, and purification of the enzyme. Optimal purification is achieved using ATP bound to agarose via its oxidized ribose moiety. By this means, the dnaB protein can be obtained at least 95% electrophoretically pure after only three purification steps. The enzyme can be eluted from immobilized nucleoside-5'-di- and -triphosphates by ATP, ADP, and pyrophosphate, but not by AMP or orthophosphate. ADP and pyrophosphate, as well as the substrate ATP in high concentration are at the same time inhibitors of the ribonucleoside triphosphatase. The dnaB complementing and ribonucleoside triphosphatase activities could not be separated from each other by affinity chromatography, supporting the finding of others that they both reside on the same protein complex, namely a dnaB multimer. The results indicate that the dnaB protein binds to immobilized nucleotides by means of its ribonucleoside triphosphatase, and that at least the pyrophosphate moiety is essential for adsorption as well as elution of the enzyme.

Bacterial Proteins↗
PubMed1977

DNA synthesis in an Escherichia coli dna B dnaC mutant.

An Escherichia coli K12 dnaB dnaC mutant was constructed by P1 transduction of the dnaC allele into a dnaB recipient stain. dnaB dnaC transductant were discriminated from dnaB mutants by their inability to grow at 40 degree C after lysogenization with phage P1bac. The dnaB dnaC mutant character was verified by 1. P1 transduction, and 2. by in vitro complementation with dnaB and dnaC wild type protein fractions. DNA synthesis was studied in strains containing dnaB, dnaB dnaC alleles in an otherwise uniform genetic background with the dnaB character either unsuppressed or suppressed by P1bac prophage. Degradation at 42 degree C of [3H]-thymidine pulse-labeled DNA in dnaB and dnaB dnaC mutants is suppressed by P1bac. However, unlike the dnaC mutant, the P1bac lysogen of the dnaB dnaC mutant exhibits an abrupt cessation of DNA synthesis and less residual cell divisions at 42 degree C indicating an inhibition of DNA chain elongation rather than a defect in DNA initiation. It is suggested that denaturation of the dnaB protein effects the dnaC function.

Coliphages↗
PubMed1974

Mutants of Escherichia coli B-r defective in deoxyribonucleic acid initiation: dnaI, a new gene for replication.

Mutagenized E. coli B/r cells were subjected to a procedure designed to select mutants temperature-sensitive for initiation of deoxyribonucleic acid (DNA) replication. Seventeen mutants exhibiting limited residual DNA synthesis at 42 C were obtained and the dna(-) sites were mapped genetically. Sixteen of the sites map near dnaA, dnaB, and dnaC. One mutant (dna-208) maps in a new location between the trp and his genes. We propose to call this mutant dnaI208. In complementation experiments dnaC(+) and dnaI(+) were dominant to dnaC(-) and dnaI(-) alleles, respectively. However, dnaA(-) was dominant to the wild-type allele dnaA(+). All dnaA mutants and four out of six dnaC mutants could be suppressed by F factor integration. The pattern of suppression was specific for each mutant.

Bacterial Proteins↗
PubMed1973

Prophage induction by high temperature in thermosensitive dna mutants lysogenic for bacteriophage lambda.

High-temperature treatment of thermosensitive dna mutants lysogenic for phage lambda leads to prophage induction and release of phage (at the permissive temperature) in elongation-defective mutants of the genotypes dnaB, dnaE, and dnaG. In initiation-defective mutants no prophage induction occurs at 42 C in mutants of the genotype dnaA, whereas with a dnaC mutant as well as with strain HfrH 252 (map position not yet known) phages are released at 42 C. DNA degradation at the replication fork at 42 C is observed in all dnaB(lambda) mutants tested, but not in mutants of the genotypes dnaE(lambda) and dnaG(lambda). Therefore, degradation of replication fork DNA is not a prerequisite for prophage induction.

Coliphages↗