Characterization of Microbial Mats from a Desert Wadi Ecosystem in the Sultanate of Oman

Desert wadis are widespread in the Arabian Peninsula and play a vital role in the ecology of the region; nevertheless, these ecosystems are among the least studied. Various types of microbial mats are predominant in wadis, but information on their bacterial diversity and spatial distribution is very scarce. We investigated bacterial diversity, pigments and lipid composition of ten mats located at the down-, mid- and upstream of a desert wadi in Oman. Direct microscopy revealed the existence of different unicellular and filamentous cyanobacteria, with the dominance of the heterocystous genera Calothrix and Scytonema. The majority of MiSeq 16S rRNA sequences (44-76%) were affiliated to Cyanobacteria and Proteobacteria. While Alphaproteobacteria was the most dominant proteobacterial class (10 to 48% of total sequences), Gamma- and Deltaproteobacteria were subdominant. Cluster analysis showed that the mats’ bacterial communities at the different locations along the wadi were different and shared less than 60% of their operational taxonomic units (OTUs). Chlorophyll a and scytonemin were the most predominant pigments in all mats. Different saturated, branched and mono- and poly-unsaturated fatty acids were detected in all mats, with C₁₆ and C₁₈ compounds as most dominant. The detected pigments and fatty acids indicate a major role of cyanobacteria in the wadi mats and the adaptation of microorganisms therein to the harsh wadi environment. Detection of diadinoxanthin and fucoxanthin confirmed the presence of diatoms. We conclude that microbial mats are important elements in wadi ecosystems and exist in a great variety of structure and community composition.     

Nitrogen fixation and diversity of benthic cyanobacterial mats on coral reefs in Curaçao

Coral Reefs - Benthic cyanobacterial mats (BCMs) have increased in abundance on coral reefs worldwide. However, their species diversity and role in nitrogen fixation are poorly understood. We...     

Post‐translational methylations of the archaeal Mre11:Rad50 complex throughout the DNA damage response

The Mre11:Rad50 complex is central to DNA double strand break repair in the Archaea and Eukarya, and acts through mechanical and nuclease activities regulated by conformational changes induced by ATP binding and hydrolysis. Despite the widespread use of Mre11 and Rad50 from hyperthermophilic archaea for structural studies, little is known in the regulation of these proteins in the Archaea. Using purification and mass spectrometry approaches allowing nearly full sequence coverage of both proteins from the species Sulfolobus acidocaldarius, we show for the first time post‐translational methylation of the archaeal Mre11:Rad50 complex. Under basal growth conditions, extensive lysine methylations were identified in Mre11 and Rad50 dynamic domains, as well as methylation of a few aspartates and glutamates, including a key Mre11 aspartate involved in nuclease activity. Upon γ‐irradiation induced DNA damage, additional methylated residues were identified in Rad50, notably methylation of Walker B aspartate and glutamate residues involved in ATP hydrolysis. These findings strongly suggest a key role for post‐translational methylation in the regulation of the archaeal Mre11:Rad50 complex and in the DNA damage response.     

Plant ABC proteins--a unified nomenclature and updated inventory

The ABC superfamily comprises both membrane-bound transporters and soluble proteins involved in a broad range of processes, many of which are of considerable agricultural, biotechnological and medical potential. Completion of the Arabidopsis and rice genome sequences has revealed a particularly large and diverse complement of plant ABC proteins in comparison with other organisms. Forward and reverse genetics, together with heterologous expression, have uncovered many novel roles for plant ABC proteins, but this progress has been accompanied by a confusing proliferation of names for plant ABC genes and their products. A consolidated nomenclature will provide much-needed clarity and a framework for future research.     

Differentiation of <Emphasis Type="Italic">Aspergillus niger</Emphasis> by random amplification of polymorphic DNA

The randomly amplified polymorphic DNA (RAPD) patterns of whole-cell lysates from five Aspergillus niger isolates, including one reference strain, two isolated from deep freeze, and two environmental strains from soil and plant infections, were investigated. PCR-RAPD analysis of genomic DNA was performed using eight primers (Tube-A1, Tube-A6, Tube-A17, Tube-B8, Tube-B11, Tube-B15, Tube-C5, Tube-C6). The RAPD assay discriminated between all strains. Comparison of deep freeze isolates showed identical RAPD patterns in some of the reference and environmental isolates. The data indicates that the RAPD technique is useful for fingerprinting A. niger.     

Antipyretic effect of ibuprofen in Gabonese children with uncomplicated falciparum malaria: a randomized, double-blind, placebo-controlled trial

Background

The protection afforded by human erythrocyte polymorphisms against the malaria parasite, Plasmodium falciparum, has been proposed to be due to reduced ability of the parasite to invade or develop in erythrocytes. If this were the case, variable levels of parasitaemia and rates of seroconversion to infected-erythrocyte variant surface antigens (VSA) should be seen in different host genotypes.

Methods

To test this hypothesis, P. falciparum parasitaemia and anti-VSA antibody levels were measured in a cohort of 555 asymptomatic children from an area of intense malaria transmission in Papua New Guinea. Linear mixed models were used to investigate the effect of α⁺-thalassaemia, complement receptor-1 and south-east Asian ovalocytosis, as well as glucose-6-phosphate dehydrogenase deficiency and ABO blood group on parasitaemia and age-specific seroconversion to VSA.

Results

No host polymorphism showed a significant association with both parasite prevalence/density and age-specific seroconversion to VSA.

Conclusion

Host erythrocyte polymorphisms commonly found in Papua New Guinea do not effect exposure to blood stage P. falciparum infection. This contrasts with data for sickle cell trait and highlights that the above-mentioned polymorphisms may confer protection against malaria via distinct mechanisms.     

Lifetime prevalence of mental disorders in Lebanon: first onset, treatment, and exposure to war

Background

There are no published data on national lifetime prevalence and treatment of mental disorders in the Arab region. Furthermore, the effect of war on first onset of disorders has not been addressed previously on a national level, especially in the Arab region. Thus, the current study aims at investigating the lifetime prevalence, treatment, age of onset of mental disorders, and their relationship to war in Lebanon.

Methods and Findings

The Lebanese Evaluation of the Burden of Ailments and Needs Of the Nation study was carried out on a nationally representative sample of the Lebanese population (n = 2,857 adults). Respondents were interviewed using the fully structured WHO Composite International Diagnostic Interview 3.0. Lifetime prevalence of any Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) disorder was 25.8%. Anxiety (16.7%) and mood (12.6%) were more common than impulse control (4.4%) and substance (2.2%) disorders. Only a minority of people with any mental disorder ever received professional treatment, with substantial delays (6 to 28 y) between the onset of disorders and onset of treatment. War exposure increased the risk of first onset of anxiety (odds ratio [OR] 5.92, 95% confidence interval [CI] 2.5–14.1), mood (OR 3.32, 95% CI 2.0–5.6), and impulse control disorders (OR 12.72, 95% CI 4.5–35.7).

Conclusions

About one-fourth of the sample (25.8%) met criteria for at least one of the DSM-IV disorders at some point in their lives. There is a substantial unmet need for early identification and treatment. Exposure to war events increases the odds of first onset of mental disorders.     

The effects of recombination rate on the distribution and abundance of transposable elements

Transposable elements (TEs) often accumulate in regions of the genome with suppressed recombination. But it is unclear whether this pattern reflects a reduction in the efficacy of selection against deleterious insertions or a relaxation of ectopic recombination. Discriminating between these two hypotheses has been difficult, because no formal model has investigated the effects of recombination under the deleterious insertion model. Here we take a simulation-based approach to analyze this scenario and determine the conditions under which element accumulation is expected in low recombination regions. We show that TEs become fixed as a result of Hill-Robertson effects in the form of Muller's ratchet, but only in regions of extremely low recombination when excision is effectively absent and synergism between elements is weak. These results have important implications for differentiating between the leading models of how selection acts on TEs and should help to interpret emerging population genetic and genomic data.     

The mechanism of specific binding of free cholesterol by the steroidogenic acute regulatory protein: evidence for a role of the C-terminal alpha-helix in the gating of the binding site

Steroidogenesis depends on the delivery of free cholesterol to the inner mitochondrial membrane by StAR (steroidogenic acute regulatory protein). Mutations in the StAR gene leads to proteins with limited cholesterol-binding capacity. This gives rise to the accumulation of cytoplasmic cholesterol, a deficit in steroid hormone production and to the medical condition of lipoid congenital adrenal hyperplasia. A detailed understanding of the mechanism of the specific binding of free cholesterol by StAR would be a critical asset in understanding the molecular origin of this disease. Previous studies have led to the proposal that the C-terminal alpha-helix 4 of StAR was undergoing a folding/unfolding transition. This transition is thought to gate the cholesterol-binding site. Moreover, a conserved salt bridge (Glu169-Arg188) in the cholesterol-binding site is also proposed to be critical to the binding process. Interestingly, some of the documented clinical mutations occur at this salt bridge (E169G, E169K and R188C) and in the C-terminal alpha-helix 4 (L275P). In the present study, using rationalized mutagenesis, activity assays, CD, thermodynamic studies and molecular modelling, we characterized the alpha-helix 4 mutations L271N and L275P, as well as the salt bridge double mutant E169M/R188M. The results provide experimental validation for the gating mechanism of the cholesterol-binding site by the C-terminal alpha-helix and the importance of the salt bridge in the binding mechanism. Altogether, our results offer a molecular framework for understanding the impact of clinical mutations on the reduction of the binding affinity of StAR for free cholesterol.