Showing papers by "University of Freiburg published in 1994"

Function and activation of NF-kappa B in the immune system.

Abstract: NF-kappa B is a ubiquitous transcription factor. Nevertheless, its properties seem to be most extensively exploited in cells of the immune system. Among these properties are NF-kappa B's rapid posttranslational activation in response to many pathogenic signals, its direct participation in cytoplasmic/nuclear signaling, and its potency to activate transcription of a great variety of genes encoding immunologically relevant proteins. In vertebrates, five distinct DNA binding subunits are currently known which might extensively heterodimerize, thereby forming complexes with distinct transcriptional activity, DNA sequence specificity, and cell type- and cell stage-specific distribution. The activity of DNA binding NF-kappa B dimers is tightly controlled by accessory proteins called I kappa B subunits of which there are also five different species currently known in vertebrates. I kappa B proteins inhibit DNA binding and prevent nuclear uptake of NF-kappa B complexes. An exception is the Bcl-3 protein which in addition can function as a transcription activating subunit in th nucleus. Other I kappa B proteins are rather involved in terminating NF-kappa B's activity in the nucleus. The intracellular events that lead to the inactivation of I kappa B, i.e. the activation of NF-kappa B, are complex. They involve phosphorylation and proteolytic reactions and seem to be controlled by the cells' redox status. Interference with the activation or activity of NF-kappa B may be beneficial in suppressing toxic/septic shock, graft-vs-host reactions, acute inflammatory reactions, acute phase response, and radiation damage. The inhibition of NF-kappa B activation by antioxidants and specific protease inhibitors may provide a pharmacological basis for interfering with these acute processes.

Climate change and social vulnerability: Toward a sociology and geography of food insecurity

Abstract: Coping with climatic variations or future climate change must be rooted in a full understanding of the complex structures and causes of present vulnerability, and how it may evolve over the coming decades. A theory of the social vulnerability of food insecurity draws upon explanations in human ecology, expanded entitlements and political economy to map the risk of exposure to harmful perturbations, ability to cope with crises, and potential for recovery. Vulnerable socio-economic groups in Zimbabwe and the potential effects of climate change illustrate some of the applications of the theory.

Relation between myocardial function and expression of sarcoplasmic reticulum Ca(2+)-ATPase in failing and nonfailing human myocardium.

Abstract: Expression of sarcoplasmic reticulum (SR) Ca(2+)-ATPase was shown to be reduced in failing human myocardium. The functional relevance of this finding, however, is not known. We investigated the relation between myocardial function and protein levels of SR Ca(2+)-ATPase in nonfailing human myocardium (8 muscle strips from 4 hearts) and in myocardium from end-stage failing hearts with dilated (10 muscle strips from 9 hearts) or ischemic (7 muscle strips from 5 hearts) cardiomyopathy. Myocardial function was evaluated by the force-frequency relation in isometrically contracting muscle strip preparations (37 degrees C, 30 to 180 min-1). In nonfailing myocardium, twitch tension rose with increasing rates of stimulation and was 76% higher at 120 min-1 compared with 30 min-1 (P < .02). In failing myocardium, there was no significant increase in average tension at stimulation rates above 30 min-1. At 120 min-1, twitch tension was decreased by 59% (P < .05) in dilated cardiomyopathy and 76% (P < .05) in ischemic cardiomyopathy compared with nonfailing myocardium. Protein levels of SR Ca(2+)-ATPase, normalized per total protein or per myosin, were reduced by 36% (P < .02) or 32% (P < .05), respectively, in failing compared with nonfailing myocardium. SR Ca(2+)-ATPase protein levels were closely related to SR Ca2+ uptake, measured in homogenates from the same hearts (r = .70, n = 16, and P < .005).(ABSTRACT TRUNCATED AT 250 WORDS)

A proteasome inhibitor prevents activation of NF-kappa B and stabilizes a newly phosphorylated form of I kappa B-alpha that is still bound to NF-kappa B.

Abstract: Activation of the inducible transcription factor NF-kappa B involves removal of the inhibitory subunit I kappa B-alpha from a latent cytoplasmic complex. It has been reported that I kappa B-alpha is subject to both phosphorylation and proteolysis in the process of NF-kappa B activation. In this study, we present evidence that the multicatalytic cytosolic protease (proteasome) is involved in the degradation of I kappa B-alpha. Micromolar amounts of the peptide Cbz-Ile-Glu(O-t-Bu)-Ala-leucinal (PSI), a specific inhibitor of the chymotrypsin-like activity of the proteasome, prevented activation of NF-kappa B in response to tumor necrosis factor-alpha (TNF) and okadaic acid (OA) through inhibition of I kappa B-alpha degradation. The m-calpain inhibitor Cbz-Leu-leucinal was ineffective. In the presence of PSI, a newly phosphorylated form of I kappa B-alpha accumulated in TNF- and OA-stimulated cells. However, the covalent modification of I kappa B-alpha was not sufficient for activation of NF-kappa B: no substantial NF-kappa B DNA binding activity appeared in cells because the newly phosphorylated form of I kappa B-alpha was still tightly bound to p65 NF-kappa B. Pyrrolidinedithiocarbamate, an antioxidant inhibitor of NF-kappa B activation which did not interfere with proteasome activities, prevented de novo phosphorylation of I kappa B-alpha as well as its subsequent degradation. This suggests that phosphorylation of I kappa B-alpha is equally necessary for the activation of NF-kappa B.(ABSTRACT TRUNCATED AT 250 WORDS)

New member of the winged-helix protein family disrupted in mouse and rat nude mutations

Abstract: Mutations at the nude locus of mice and rats disrupt normal hair growth and thymus development, causing nude mice and rats to be immune-deficient. The mouse nude locus has been localized on chromosome 11 (refs 3, 4) within a region of < 1 megabase. Here we show that one of the genes from this critical region, designated whn, encodes a new member of the winged-helix domain family of transcription factors, and that it is disrupted on mouse nu and rat rnuN alleles. Mutant transcripts do not encode the characteristic DNA-binding domain, strongly suggesting that the whn gene is the nude gene. Mutations in winged-helix domain genes cause homeotic transformations in Drosophila and distort cell-fate decisions during vulval development in Caenorhabditis elegans. The whn gene is thus the first member of this class of genes to be implicated in a specific developmental defect in vertebrates.

Specific mutations of the RET proto-oncogene are related to disease phenotype in MEN 2A and FMTC.

Abstract: We have analysed 118 families with inherited medullary thyroid carcinoma (MTC) for mutations of the RET proto-oncogene. These included cases of multiple endocrine neoplasia types 2A (MEN 2A) and 2B (MEN 2B) and familial MTC (FMTC). Mutations at one of 5 cysteines in the extracellular domain were found in 97% of patients with MEN 2A and 86% with FMTC but not in MEN 2B patients or normal controls. 84% of the MEN2A mutations affected codon 634. MEN 2A patients with a Cys634 to Arg substitution had a greater risk of developing parathyroid disease than those with other codon 634 mutations. Our data show a strong correlation between disease phenotype and the nature and position of the RET mutation, suggesting that a simple, constitutive activation of the RET tyrosine kinase is unlikely to explain the events leading to MEN 2A and FMTC.

Gene expression of the cardiac Na(+)-Ca2+ exchanger in end-stage human heart failure.

Abstract: The regulation of cytosolic Ca2+ concentration during excitation-contraction coupling is altered in the failing human heart. Previous studies have focused on disturbances in Ca2+ release and reuptake from the sarcoplasmic reticulum (SR), whereas functional studies of the cardiac Na(+)-Ca2+ exchanger, another important determinant of myocyte homeostasis, are lacking for the failing human heart. Using a cardiac Na(+)-Ca2+ exchanger cDNA recently cloned from a guinea pig cDNA library, we investigated the gene expression of the cardiac Na(+)-Ca2+ exchanger in relation to the SR Ca(2+)-ATPase. Expression of both genes was quantified in left ventricular myocardium from 24 failing human cardiac explants and 7 control heart samples in relation to beta-myosin heavy chain mRNA by slot blot analysis. Compared with patients with nonfailing hearts, patients with dilated cardiomyopathy (DCM, n = 13) showed a 55% increase in Na(+)-Ca2+ exchanger mRNA levels (P < .05 versus control value) and a 41% increase in patients with coronary artery disease (CAD, n = 11). In the same hearts, SR Ca(2+)-ATPase mRNA levels were decreased by 50% in DCM and by 45% in CAD (P < .05 for both versus control value). There was a positive correlation between Na(+)-Ca2+ exchanger and SR Ca(2+)-ATPase mRNA levels both in normal and failing human hearts, albeit with different slopes and intercepts of the regression line. The Na(+)-Ca2+ exchanger protein levels as assessed by Western blot analysis and normalized to beta-myosin heavy chain protein were increased in DCM and CAD (P < .05 and P < .01 versus control value, respectively), whereas SR Ca(2+)-ATPase protein levels were reduced (P < .05 for both groups versus control values). Thus, the Na(+)-Ca2+ exchanger gene expression is enhanced in failing human hearts and may, in part, compensate for the depressed SR function with regard to diastolic Ca2+ removal.

Mutant p53 potentiates protein kinase C induction of vascular endothelial growth factor expression.

Abstract: Many tumor cells produce vascular endothelial growth factor (VEGF), which is thought to be a pivotal mediator of tumor neoangiogenesis. Expression of the VEGF gene can be induced by tumor promoting phorbol esters, such as 12-O-tetradecanoylphorbol-13-acetate (TPA), which activate protein kinase C (PKC). Here we show that in transient transfection assays a mutated form of the murine p53 tumor suppressor gene (ala135-->val) induces expression of VEGF mRNA and potentiates TPA stimulated VEGF mRNA expression. In NIH 3T3 cells which stably overexpress the temperature sensitive p53 (ala135-->val), displaying mutant phenotype at 37 degrees C and wildtype phenotype at 32.5 degrees C, induction of VEGF mRNA and protein by activated PKC is strongly synergistic with mutant, but not wildtype p53. Mutant p53 specifically increases TPA induction of VEGF without affecting the expression of other TPA inducible genes. TPA dependent VEGF expression is also enhanced by human p53 mutated at amino acid 175. Thus, our data link PKC and p53, the gene most frequently altered in human tumors, with the regulation of tumor angiogenesis.

The Geography of Firm Births in Germany

Abstract: AUDRETSCH D. B. and FRITSCH M. (1994) The geography of firm births in Germany, Reg. Studies 28, 359–365. The linkages between the extent to which increasing returns to production exist within a spatial unit of observation and the tendency towards increased concentration of economic activity, measured in terms of the birth of new firms, is the focus of this paper. Based on 75 regions in west Germany, we find considerable evidence suggesting that birth rates are greater in regions exhibiting characteristics reflecting convexities in production. This provides support for the theory that the location of new economic activity tends to occur in the geographic space where such production convexities are the greatest. AUDRETSCH D. B. et FRITSCH M. (1994) La geographie de la naissance d'entreprises en Allemagne, Reg. Studies 28, 359–365. Cet article porte sur les liens entre l'importance des rendements croissants au sein d'une aire geographique delimitee et la tendance a la concentration accrue de l'activite econo...

Self-replication of complementary nucleotide-based oligomers

Abstract: The development of non-enzymatic self-replicating systems based on autocatalytic template-directed reactions is a current objective of bioorganic chemistry. Typically, a self-complementary template molecule AB is synthesized autocatalytically from two complementary template fragments A and B. Natural replication of nucleic acids, however, utilizes complementary rather than self-complementary strands. Here we report on a minimal implementation of this type of replication based on cross-catalytic template-directed syntheses of hexadeoxynucleotide derivatives from amino-trideoxynucleotides. In our experiments, two self-complementary and two complementary templates compete for their combinatorial synthesis from four common trimeric precursors. We provide kinetic evidence that cross-catalytic self-replication of complementary templates can proceed with an efficiency similar to that of autocatalytic self-replication of self-complementary templates. We observe selective stimulation of template synthesis, and thus information transfer, on seeding the reaction mixtures with one of four chemically labelled templates bearing the sequence of the reaction products. Our results bring a stage closer the development of schemes that might explain how replicating systems based on nucleic acids arose on the prebiotic Earth.

Constitutive NF-kappa B activity in neurons.

Abstract: NF-kappa B is inducible transcription factor present in many cell types in a latent cytoplasmic form. So far, only immune cells including mature B cells, thymocytes, and adherent macrophages have been reported to contain constitutively active forms of NF-kappa B in the nucleus. A recent study showed that the human immunodeficiency virus type 1 (HIV-1) promoter is highly active in several brain regions of transgenic mice (J. R. Corboy, J. M. Buzy, M. C. Zink, and J. E. Clements, Science 258:1804-1807, 1992). Since the activity of this viral enhancer is governed mainly by two binding sites for NF-kappa B, we were prompted to investigate the state of NF-kappa B activity in neurons. Primary neuronal cultures derived from rat hippocampus and cerebral cortex showed a high constitutive expression of an HIV-1 long terminal repeat-driven luciferase reporter gene, which was primarily dependent on intact NF-kappa B binding sites and was abolished upon coexpression of the NF-kappa B-specific inhibitor I kappa B-alpha. Indirect immunofluorescence and confocal laser microscopy showed that the activity of NF-kappa B correlated with the presence of the NF-kappa B subunits p50 and RelA (p65) in nuclei of cultured neurons. NF-kappa B was also constitutively active in neurons in vivo. As investigated by electrophoretic mobility shift assays, constitutive NF-kappa B DNA-binding activity was highly enriched in fractions containing neuronal nuclei prepared from rat cerebral cortex. Nuclear NF-kappa B-specific immunostaining was also seen in cryosections from mouse cerebral cortex and hippocampus. Only a subset of neurons was stained. Activated NF-kappa B in the brain is likely to participate in normal brain function and to reflect a distinct state of neuronal activity or differentiation. Furthermore, it may explain the high level of activity of the HIV-1 enhancer in neurons, an observation potentially relevant for the etiology of the AIDS dementia complex caused by HIV infection of the central nervous system.

Comparative effects of chronic angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor blockade on cardiac remodeling after myocardial infarction in the rat

Abstract: BACKGROUNDAfter myocardial infarction, the noninfarcted left ventricle develops reactive hypertrophy associated with a depressed coronary flow reserve, myocardial interstitial fibrosis, and reduced capillary density. The present study investigated the comparative cardiac effects of chronic angiotensin-converting enzyme (ACE) inhibition and selective angiotensin II type 1 receptor (AT1) blockade in the rat model of myocardial infarction and failure.METHODS AND RESULTSSeven days after coronary ligation (MI), rats were randomized to enalapril (n = 8; 500 micrograms.kg-1.d-1), losartan (n = 9; 3 mg.kg-1.d-1), or placebo (n = 8) and treated for 6 weeks. Sham-operated rats (n = 10) served as controls. Coronary blood flow was measured with radiolabeled microspheres during baseline and maximal coronary dilation induced by dipyridamole (2 mg.kg-1.min-1 over 10 minutes). Right and left ventricular (LV) weight was increased in infarcted rats compared with sham-operated animals and enalapril- and losartan-treated MI ...

Toeplitz quantization of Kähler manifolds ang gl(N), N→∞ limits

Abstract: For general compact Kahler manifolds it is shown that both Toeplitz quantization and geometric quantization lead to a well-defined (by operator norm estimates) classical limit. This generalizes earlier results of teh authors and Klimek and Lesniewski obtained for the tours and higher genus Riemann surfaces, respectively. We thereby arrive at an approximation of the Poisson algebra by a sequence of finitedimensional matrix algebrasgl(N), N→∞.

Apoplastic Peroxidases and Lignification in Needles of Norway Spruce (Picea abies L.).

Abstract: The objective of the present study was to investigate the correlation of soluble apoplastic peroxidase activity with lignification in needles of field-grown Norway spruce (Picea abies L.) trees. Apoplastic peroxidases (EC 1.11.1.7) were obtained by vacuum infiltration of needles. The lignin content of isolated cell walls was determined by the acetyl bromide method. Accumulation of lignin and seasonal variations of apoplastic peroxidase activities were studied in the first year of needle development. The major phase of lignification started after bud break and was terminated about 4 weeks later. This phase correlated with a transient increase in apoplastic guaiacol and coniferyl alcohol peroxidase activity. NADH oxidase activity, which is thought to sustain peroxidase activity by production of H2O2, peaked sharply after bud break and decreased during the lignification period. Histochemical localization of peroxidase with guaiacol indicated that high activities were present in lignifying cell walls. In mature needles, lignin was localized in walls of most needle tissues including mesophyll cells, and corresponded to 80 to 130 [mu]mol lignin monomers/g needle dry weight. Isoelectric focusing of apoplastic washing fluids and activity staining with guaiacol showed the presence of strongly alkaline peroxidases (isoelectric point [greater than or equal to] 9) in all developmental stages investigated. New isozymes with isoelectric points of 7.1 and 8.1 appeared during the major phase of lignification. These isozymes disappeared after lignification was terminated. A strong increase in peroxidase activity in autumn was associated with the appearance of acidic peroxidases (isoelectric point [less than or equal to] 3). These results suggest that soluble alkaline apoplastic peroxidases participate in lignin formation. Soluble acidic apoplastic peroxidases were apparently unrelated to developmentally regulated lignification in spruce needles.

Mitochondrial Hsp70/MIM44 complex facilitates protein import

Abstract: Protein translocation into mitochondria requires the mitochondria! protein Hsp70. This molecular chaperone of the mitochondrial matrix is recruited to the protein import machinery by MIM44, a component associated with the inner membrane of the mitochondria. Formation of the mt-Hsp70/MIM44 complex is regulated by ATP. MIM44 and mt-Hsp70 interact in a sequential manner with incoming segments of unfolded preproteins and thereby facilitate stepwise vectorial translocation of proteins across the mitochondrial membranes. The complex appears to act as a molecular ratchet which is energetically driven by the hydrolysis of ATP.

Amiodarone-associated Proarrhythmic Effects: A Review with Special Reference to Torsade de Pointes Tachycardia

Abstract: Purpose: To assess the incidence of amiodarone-mediated aggravation of ventricular tachyarrhythmias or the development of new arrhythmias, such as torsade de pointes, in patients with cardiac disea...

The shoulder-hand syndrome after stroke: a prospective clinical trial.

Abstract: Shoulder-hand syndrome developed in 36 (27%) of 132 hemiplegic patients in a prospective study. Subluxation, paresis of the shoulder girdle, moderate spasticity, and deficits in confrontation visual field testing were the major risk factors. In a placebo-controlled, nonblinded trial, 31 of the 36 patients became almost symptom free within 10 days' treatment with low doses of oral corticosteroids. Shoulder joint capsules taken at autopsy of 7 patients showed signs of previous trauma of the affected shoulder. In the second part of this study on another 86 patients, early awareness of potential injuries to shoulder joint structures reduced the frequency of shoulder-hand syndrome from 27 to 8%. These clinical findings suggest that shoulder-hand syndrome in hemiplegia is initiated by peripheral lesions. A self-perpetuating vicious cycle may be established, followed by the clinical picture of a "reflex sympathetic dystrophy." In the majority of stroke patients, this clinical phenomenon seems to be preventable by avoiding shoulder trauma.

Liquid crystal elastomers: Influence of the orientational distribution of the crosslinks on the phase behaviour and reorientation processes

Abstract: The influence of the crosslinking conditions on the phase behaviour and reorientation processes of nematic elastomers is investigated. Two series of elastomers with various network anisotropies crosslinked either in the nematic or in the isotropic state were investigated by means of IR-dichroism and stress-strain measurements. The experimental results clearly demonstrate that for nematic elastomers not only the coupling between the network anisotropy and the state of order has to be considered. It is shown that the influence of the crosslinks and their orientational distribution on the phase behaviour, the state of order as well as on director reorientation processes cannot be neglected.

Oxygen and the control of gene expression

Abstract: The respiration of oxygen, while essential to aerobic organisms for the generation of energy, leads to the formation of reactive oxygen intermediates (ROIs) as harmful byproducts. ROIs damage nucleic acids, lipids and proteins. Therefore, protective mechanisms against elevated intracellular ROI levels, referred to as oxidative stress, have evolved. These include the activation of transcription factors which elevate the expression of protective enzymes. Eukaryotic cells have also evolved the ability to specifically generate ROIs following stimulation with various agents. In these cases, ROIs are used as second messengers to activate gene expression. Here we will discuss both prokaryotic and eukaryotic transcription factors that respond to ROIs. In addition, transcription factors will be described that are activated by either exposure to antioxidants, which reduce the intracellular ROI concentration, or by hypoxia, the absence of oxygen.

Mapping of the Gene for Autosomal Recessive Polycystic Kidney-disease (arpkd) To Chromosome 6p21-cen

Abstract: Autosomal recessive polycystic kidney disease (ARPKD) is one of the major hereditary nephropathies in children predominantly presenting in early childhood. The clinical picture is variable but there is a fatal outcome in many cases. We have performed linkage analysis in 16 ARPKD families and localized the ARPKD gene to chromosomal region 6p21-cen with no evidence for genetic heterogeneity among different clinical phenotypes. Linkage was confirmed using six adjacent microsatellite markers and the highest lod score of 7.42 was obtained with D6S272 at theta = 0.00. Our findings should lead to more accurate forms of prenatal diagnosis than those currently available using ultrasound.

Diversity of cultivable and uncultivable oral spirochetes from a patient with severe destructive periodontitis.

Abstract: To determine the genetic diversity of cultivable and uncultivable spirochetes in the gingival crevice of a patient with severe periodontitis, partial 16S rRNA genes were cloned from PCR-amplified products of DNA and RNA extracted from a subgingival plaque sample. Approximately 500 bp were amplified in PCRs by using universally conserved primers with polylinker tails. Purified PCR products were cloned into Escherichia coli by using the plasmid vector pUC19. The resultant clone library was screened by colony hybridization with a radiolabeled, treponeme-specific oligonucleotide probe. The 16S rRNA inserts of 81 spirochetal clones were then sequenced by standard procedures. Sequences were compared with 16S rRNA sequences of 35 spirochetes, including the four known cultivable oral treponeme species. The analysis revealed an unexpected diversity of oral treponemes from a single patient. When 98% or greater sequence similarity was used as the definition of a species-level cluster, the clone sequences were found to represent 23 species. When 92% similarity was used as the definition, the clones fell into eight major groups, only two of which contained named species, Treponema vincentii and Treponema denticola, while Treponema pectinovorum and Treponema socranskii were not represented in any cluster. Seven of the 81 spirochetal clones were found to contain chimeric 16S rRNA sequences. In situ fluorescence hybridization with a fluorescein isothiocyanate-labeled oligonucleotide probe specific for one of the new species representing cluster 19 was used to identify cells of the target species directly in clinical samples.

Observation of a fast response in functional MR.

Abstract: A spectroscopic MR technique was used to investigate the time course of the MR signal following a single visual stimulus. Gated experiments demonstrate there is an early response (500 ms after stimulus) leading to a reduction of the MR signal by -0.25% (P = 0.02), whereas a slower response (> 1500 ms after stimulus) results in a signal increase of +0.59% (P = 0.01). The fast negative response may be attributed to increased oxygen consumption, followed by a slower vascular response with overcompensation in blood oxygenation. This explanation would be in agreement with the blood oxygenation level dependent (BOLD) contrast mechanism considered the basis of functional MR. However, other physiological events might also be responsible for the signal drop observed.

A quantitative assessment of presynaptic inhibition of Ia afferents in spastics. Differences in hemiplegics and paraplegics.

Abstract: Soleus H-reflex facilitation evoked by a supramaximal conditioning stimulation to the femoral nerve was investigated in 28 healthy control subjects and 35 spastic patients of whom 17 were paraplegics with bilateral spinal cord lesion and 18 were hemiplegics with unilateral cerebral lesion. Heteronymous facilitation from quadriceps to soleus was measured 0.4 ms after onset, while the monosynaptic la excitation is still uncontaminated by any non-monosynaptic effect and can be used to assess ongoing presynaptic inhibition on la terminals to soleus motor neurons. In paraplegics, this heteronymous la facilitation was significantly larger than in control subjects (all individual results in these patients being above the mean observed in controls). This must reflect a decrease in presynaptic inhibition of la terminals in the paraplegics explored here. There was no correlation between this decreased presynaptic inhibition of la terminals and the degree of spasticity measured by Ashworth's scale. Surprisingly, the amount of heteronymous la facilitation in hemiplegics was the same as in normal subjects. This indicates that presynaptic inhibition of la terminals is unchanged in these patients and disagrees with the usual interpretation of reduced vibratory inhibition of the soleus H-reflex in hemiplegics. It is argued that this disagreement is due to the fact that vibratory inhibition of the reflex also depends on post-activation depression following repetitive synaptic transmission.

Phylogenetic Positions of Novel Aerobic, Bacteriochlorophyll a-Containing Bacteria and Description of Roseococcus thiosulfatophilus gen. nov., sp. nov., Erythromicrobium ramosum gen. nov., sp. nov., and Erythrobacter litoralis sp. nov.

Abstract: We analyzed the 16S ribosomal DNAs of three obligately aerobic, bacteriochlorophyll a-containing bacteria, “Roseococcus thiosulfatophilus,” “Erythromicrobium ramosum,” and new isolate T4T (T = type strain), which was obtained from a marine cyanobacterial mat. “Roseococcus thiosulfatophilus” is a member of the α-1 subclass of the Proteobacteria and is moderately related to Rhodopila globiformis, Thiobacillus acidophilus, and Acidiphilium cryptum (level of sequence similarity, 90%). “Erythromicrobium ramosum” and isolate T4T are closely related to Erythrobacter longus and Porphyrobacter neustonensis (level of sequence similarity, 95%). These organisms are members of the α-4 subclass of the Proteobacteria. Strain T4T is a motile, red or orange bacterium. The major carotenoids are bacteriorubixanthinal and erythroxanthin sulfate. In vivo measurements revealed bacteriochlorophyll absorption maxima at 377, 590, 800, and 868 nm. Strain T4T grows in the presence of 5 to 96%‰ salinity and uses glucose, fructose, acetate, pyruvate, glutamate, succinate, and lactate as substrates. On the basis of its distinct phylogenetic position and phenotypic characteristics which are different from those of Erythrobacter longus, we propose that strain T4T should be placed in a new species of the genus Erythrobacter, Erythrobacter litoralis. The descriptions of “Roseococcus thiosulfatophilus” and “Erythromicrobium ramosum” are emended.