Authigenic iron oxide proxies for marine zinc over geological time and implications for eukaryotic metallome evolution.

Here, we explore enrichments in paleomarine Zn as recorded by authigenic iron oxides including Precambrian iron formations, ironstones, and Phanerozoic hydrothermal exhalites. This compilation of new and literature-based iron formation analyses track dissolved Zn abundances and constrain the magnitude of the marine reservoir over geological time. Overall, the iron formation record is characterized by a fairly static range in Zn/Fe ratios throughout the Precambrian, consistent with the shale record (Scott et al., 2013, Nature Geoscience, 6, 125-128). When hypothetical partitioning scenarios are applied to this record, paleomarine Zn concentrations within about an order of magnitude of modern are indicated. We couple this examination with new chemical speciation models to interpret the iron formation record. We present two scenarios: first, under all but the most sulfidic conditions and with Zn-binding organic ligand concentrations similar to modern oceans, the amount of bioavailable Zn remained relatively unchanged through time. Late proliferation of Zn in eukaryotic metallomes has previously been linked to marine Zn biolimitation, but under this scenario the expansion in eukaryotic Zn metallomes may be better linked to biologically intrinsic evolutionary factors. In this case, zinc's geochemical and biological evolution may be decoupled and viewed as a function of increasing need for genome regulation and diversification of Zn-binding transcription factors. In the second scenario, we consider Archean organic ligand complexation in such excess that it may render Zn bioavailability low. However, this is dependent on Zn-organic ligand complexes not being bioavailable, which remains unclear. In this case, although bioavailability may be low, sphalerite precipitation is prevented, thereby maintaining a constant Zn inventory throughout both ferruginous and euxinic conditions. These results provide new perspectives and constraints on potential couplings between the trajectory of biological and marine geochemical coevolution.

Draft Genome Sequence of a Single Cell of SAR86 Clade Subgroup IIIa.

SAR86 denotes a 16S clade of gammaproteobacteria that are ubiquitous in ocean surface waters. So far, SAR86 is resistant to cultivation; thus, little is known about the genome contents or physiology of this clade. Recently, four partial genome sequences for SAR86 subclades I and II were published. Here, we present the draft genome sequence of a single cell from SAR86 subgroup IIIa isolated from coastal waters in San Diego, CA.

Genetic identification of a high-affinity Ni transporter and the transcriptional response to Ni deprivation in Synechococcus sp. strain WH8102.

One biological need for Ni in marine cyanobacteria stems from the utilization of the Ni metalloenzyme urease for the assimilation of urea as a nitrogen source. In many of the same cyanobacteria, including Synechococcus sp. strain WH8102, an additional and obligate nutrient requirement for Ni results from usage of a Ni superoxide dismutase (Ni-SOD), which is encoded by sodN. To better understand the effects of Ni deprivation on WH8102, parallel microarray-based analysis of gene expression and gene knockout experiments were conducted. The global transcriptional response to Ni deprivation depends upon the nitrogen source provided for growth; fewer than 1% of differentially expressed genes for Ni deprivation on ammonium or urea were concordantly expressed. Surprisingly, genes for putative Ni transporters, including one colocalized on the genome with sodN, sodT, were not induced despite an increase in Ni transport. Knockouts of the putative Ni transporter gene sodT appeared to be lethal in WH8102, so the genes for sodT and sodN in WH8102 were interrupted with the gene for Fe-SOD, sodB, and its promoter from Synechococcus sp. strain WH7803. The sodT::sodB exconjugants were unable to grow at low Ni concentrations, confirming that SodT is a Ni transporter. The sodN::sodB exconjugants displayed higher growth rates at low Ni concentrations than did the wild type, presumably due to a relaxed competition between urease and Ni-SOD for Ni. Both sodT::sodB and sodN::sodB lines exhibited an impaired ability to grow at low Fe concentrations. We propose a posttranslational allosteric SodT regulation involving the binding of Ni to a histidine-rich intracellular protein loop.

The dddP gene, encoding a novel enzyme that converts dimethylsulfoniopropionate into dimethyl sulfide, is widespread in ocean metagenomes and marine bacteria and also occurs in some Ascomycete fungi.

The marine alphaproteobacterium Roseovarius nubinhibens ISM can produce the gas dimethyl sulfide (DMS) from dimethylsulfoniopropionate (DMSP), a widespread secondary metabolite that occurs in many phytoplankton. Roseovarius possesses a novel gene, termed dddP, which when cloned, confers on Escherichia coli the ability to produce DMS. The DddP polypeptide is in the large family of M24 metallopeptidases and is wholly different from two other enzymes, DddD and DddL, which were previously shown to generate DMS from dimethylsulfoniopropionate. Close homologues of DddP occur in other alphaproteobacteria and more surprisingly, in some Ascomycete fungi. These were the biotechnologically important Aspergillus oryzae and the plant pathogen, Fusarium graminearum. The dddP gene is abundant in the bacterial metagenomic sequences in the Global Ocean Sampling Expedition. Thus, dddP has several novel features and is widely dispersed, both taxonomically and geographically.

Diversity, function and evolution of genes coding for putative Ni-containing superoxide dismutases.

We examined the phylogenetic distribution, functionality and evolution of the sodN gene family, which has been shown to code for a unique Ni-containing isoform of superoxide dismutase (Ni-SOD) in Streptomyces. Many of the putative sodN sequences retrieved from public domain genomic and metagenomic databases are quite divergent from structurally and functionally characterized Ni-SOD. Structural bioinformatics studies verified that the divergent members of the sodN protein family code for similar three-dimensional structures and identified evolutionarily conserved amino acid residues. Structural and biochemical studies of the N-terminus 'Ni-hook' motif coded for by the putative sodN sequences confirmed both Ni (II) ligating and superoxide dismutase activity. Both environmental and organismal genomes expanded the previously noted phylogenetic distribution of sodN, and the sequences form four well-separated clusters, with multiple subclusters. The phylogenetic distribution of sodN suggests that the gene has been acquired via horizontal gene transfer by numerous organisms of diverse phylogenetic background, including both Eukaryotes and Prokaryotes. The presence of sodN correlates with the genomic absence of the gene coding for Fe-SOD, a structurally and evolutionarily distinct isoform of SOD. Given the low levels of Fe found in the marine environment from where many sequences were attained, we suggest that the replacement of Fe-SOD with Ni-SOD may be an evolutionary adaptation to reduce iron requirements.

Blood manganese levels in children with convulsive disorder.

Manganese deficiency syndromes have been well described in animals and include among a wide variety of metabolic aberrations the heightened susceptibility to convulsions induced by electroshock or drugs. We have measured manganese blood levels in two populations of children: (1) a reference group of 120 ambulatory patients without neurologic disease, (2) 197 patients with convulsive disorder. Blood manganese was found to be age related in infants under 1 year of age. Highly significant was the lower mean blood manganese found in the convulsive disorder group as compared to the reference group. There was also a slight trend in the convulsive group for blood manganese to decrease from 1 to 22 years of age. No significant differences in manganese levels were found related to sex, type of seizure disorder, type of anticonvulsant drug therapy, or serum level of drug. Although this study does not demonstrate a causal relation between manganese and seizure disorder, and cannot be used as the basis for altering current approaches to therapy, it provides insight into the potentially important role of previously unrecognized factors in the pathophysiology of this syndrome.

[Uricolytic therapy. Value of urate oxidase in the treatment of hyperuricemias]. / La thérapeutique uricolytique. Intérêt de l'urate oxydase dans le traitement des hyperuricémies

In addition to uricosuric agents and purine synthesis inhibitors, Urate Oxydase may be used in the treatment of hyperuricaemia. This substance breaks down uric acid to allantoin which is soluble and easily excreted. Use of the medication in 14 cases of major gout with tophi and 9 cases of hyperuricaemia secondary to renal insufficiency showed the good tolerance of the substance and it's clinical and biological effectiveness.

The LaBrosse VMA spot test revisited.

The LaBrosse spot test, in our experience, is not very useful as a screening procedure since the majority of specimens give an intermediate reaction, representing a heterogeneous group which may include many patients with abnormal 24-hour VMA excretion. The test is helpful only if either "positive" or "negative" in the individual patient who presents symptoms or signs compatible with abnormal catecholamine excretion. It is also of value in following patients with catecholamine-secreting tumors. The clinician should be aware of the limitations of VMA screening tests as they exist to date, and should assure himself, as well, that a specific quantitative assay is used to confirm doubtful or positive screening test results.