Diversity of a cytokinin dehydrogenase gene in wild and cultivated barley

The cytokinin dehydrogenase gene HvCKX2.1 is the regulatory target for the most abundant heterochromatic small RNAs in drought-stressed barley caryopses. We investigated the diversity of HvCKX2.1 in 228 barley landraces and 216 wild accessions and identified 14 haplotypes, five of these with ten or more members, coding for four different protein variants. The third largest haplotype was abundant in wild accessions (51 members), but absent from the landrace collection. Protein structure predictions indicated that the amino acid substitution specific to haplotype 3 could result in a change in the functional properties of the HvCKX2.1 protein. Haplotypes 1–3 have overlapping geographical distributions in the wild population, but the average rainfall amounts at the collection sites for haplotype 3 plants are significantly higher during November to February compared to the equivalent data for plants of haplotypes 1 and 2. We argue that the likelihood that haplotype 3 plants were excluded from landraces by sampling bias that occurred when the first wild barley plants were taken into cultivation is low, and that it is reasonable to suggest that plants with haplotype 3 are absent from the crop because these plants were less suited to the artificial conditions associated with cultivation. Although the cytokinin signalling pathway influences many aspects of plant development, the identified role of HvCKX2.1 in the drought response raises the possibility that the particular aspect of cultivation that mitigated against haplotype 3 relates in some way to water utilization. Our results therefore highlight the possibility that water utilization properties should be looked on as a possible component of the suite of physiological adaptations accompanying the domestication and subsequent evolution of cultivated barley

Evolution of Salmonella enterica Virulence via Point Mutations in the Fimbrial Adhesin

Whereas the majority of pathogenic Salmonella serovars are capable of infecting many different animal species, typically producing a self-limited gastroenteritis, serovars with narrow host-specificity exhibit increased virulence and their infections frequently result in fatal systemic diseases. In our study, a genetic and functional analysis of the mannose-specific type 1 fimbrial adhesin FimH from a variety of serovars of Salmonella enterica revealed that specific mutant variants of FimH are common in host-adapted (systemically invasive) serovars. We have found that while the low-binding shear-dependent phenotype of the adhesin is preserved in broad host-range (usually systemically non-invasive) Salmonella, the majority of host-adapted serovars express FimH variants with one of two alternative phenotypes: a significantly increased binding to mannose (as in S. Typhi, S. Paratyphi C, S. Dublin and some isolates of S. Choleraesuis), or complete loss of the mannose-binding activity (as in S. Paratyphi B, S. Choleraesuis and S. Gallinarum). The functional diversification of FimH in host-adapted Salmonella results from recently acquired structural mutations. Many of the mutations are of a convergent nature indicative of strong positive selection. The high-binding phenotype of FimH that leads to increased bacterial adhesiveness to and invasiveness of epithelial cells and macrophages usually precedes acquisition of the non-binding phenotype. Collectively these observations suggest that activation or inactivation of mannose-specific adhesive properties in different systemically invasive serovars of Salmonella reflects their dynamic trajectories of adaptation to a life style in specific hosts. In conclusion, our study demonstrates that point mutations are the target of positive selection and, in addition to horizontal gene transfer and genome degradation events, can contribute to the differential pathoadaptive evolution of Salmonella

Where less may be more: how the rare biosphere pulls ecosystems strings

Rare species are increasingly recognized as crucial, yet vulnerable components of Earth’s ecosystems. This is also true for microbial communities, which are typically composed of a high number of relatively rare species. Recent studies have demonstrated that rare species can have an over-proportional role in biogeochemical cycles and may be a hidden driver of microbiome function. In this review, we provide an ecological overview of the rare microbial biosphere, including causes of rarity and the impacts of rare species on ecosystem functioning. We discuss how rare species can have a preponderant role for local biodiversity and species turnover with rarity potentially bound to phylogenetically conserved features. Rare microbes may therefore be overlooked keystone species regulating the functioning of host-associated, terrestrial and aquatic environments. We conclude this review with recommendations to guide scientists interested in investigating this rapidly emerging research area

Systemic sclerosis (scleroderma). A case of recovery of cardiomyopathy after vitamin E treatment.

A 60-year-old woman with systemic sclerosis, systemic hypertension, and chronic renal failure, presented with clinical manifestations of heart failure. An echocardiogram showed a mildly dilated left ventricle and global hypokinesis. A six-month treatment including reduced sodium intake, furosemide, and nifedipine did not change the clinical and instrumental findings. Casually, vitamin E (600 mg daily) was added. After 6 months, clinical manifestations of heart failure were disappeared and the echocardiogram showed a normally-sized left ventricle with normal wall motion

Expression of innate immunity receptors in an experimental model of Parkinson’s like disease

The innate immunity receptors CD14 ant toll like receptor 4 (TLR4), that function as lipopolysaccharide (LPS) receptor and LPS signal transmitter into the cell respectively, have been recently related to neuroinflammation processes. Parkinson's disease (PD) is a progressive neurodegenerative disorder in which loss of dopaminergic neurons of substantia nigra (SN) occurs, leading to a drastic reduction of dopamine levels in the striatum. Recently it has been found that, both in patients and in experimental animal models of PD, neuroinflammation appears to be an ubiquitous finding. Upregulation of inflammatory response in the brain is associated with a number of neurodegenerative diseases; moreover recently have been found evidences that systemic infections and inflammation can cause exacerbation of symptoms and drive the progression of neurodegeneration in chronic neurodegenerative diseases. Therefore, the aim of this work was to study a possible role of LPS receptor complex in the pathogenesis of 1-methyl-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced parkinsonism. In particular, we investigated the expression of CD14 and TLR4 in SN and striatum in brains obtained from MPTP treated mice, the most commonly used toxic model of PD in mouse. In particular, the analysis of the gene transcripts and protein expression of CD14 and TLR4 showed an augmented expression of both receptors in the SN of MPTP treated mice in comparison to untreated ones. No significant differences were found in the mRNA and protein levels of both CD14 and TLR4 in the striatum of MPTP treated animals if compared with controls. Overall, these results show that innate immunity receptors CD14 and TLR4 are over expressed in distinct anatomical areas of the brain from mice with MPTP induced Parkinson’s-like disease