Structures of Microbial Communities in Alpine Soils: Seasonal and Elevational Effects

Microbial communities in alpine environments are exposed to several environmental factors related to elevation and local site conditions and to extreme seasonal variations. However, little is known on the combined impact of such factors on microbial community structure. We assessed the effects of seasonal variations on soil fungal and bacterial communities along an elevational gradient (from alpine meadows to a glacier forefield, 1930–2519 m a.s.l.) over 14 months. Samples were taken during all four seasons, even under the winter snowpack and at snowmelt. Microbial community structures and abundances were investigated using Terminal Restriction Fragment Length Polymorphism (T-RFLP) and quantitative PCR (qPCR) of the 16S and 18S rRNA genes. Illumina sequencing was performed to identify key bacterial groups in selected samples. We found that the soil properties varied significantly with the seasons and along the elevational gradient. For example, concentrations of soluble nutrients (e.g., NH+4-N, SO2−4-S, PO3−4-P) significantly increased in October but decreased drastically under the winter snowpack. At all times, the alpine meadows showed higher soluble nutrient concentrations than the glacier forefield. Microbial community structures at the different sites were strongly affected by seasonal variations. Under winter snowpack, bacterial communities were dominated by ubiquitous groups (i.e., beta-Proteobacteria, which made up to 25.7% of the total reads in the glacier forefield). In the snow-free seasons, other groups (i.e., Cyanobacteria) became more abundant (from 1% under winter snow in the glacier forefield samples to 8.1% in summer). In summary, elevation had a significant effect on soil properties, whereas season influenced soil properties as well as microbial community structure. Vegetation had a minor impact on microbial communities. At every elevation analyzed, bacterial, and fungal community structures exhibited a pronounced annual cycle

TLR2 genotypes and Borrelia infection of bank voles

TLR2 genotypes and Borrelia infection of bank voles from different locations in the Swiss Alp

Data from: Small-scale spatial variation in infection risk shapes the evolution of a Borrelia resistance gene in wild rodents

Spatial variation in pathogen-mediated selection is predicted to influence the evolutionary trajectory of host populations and lead to spatial variation in their immunogenetic composition. However, to date few studies have been able to directly link small-scale spatial variation in infection risk to host immune gene evolution in natural, non-human populations. Here we use a natural rodent-Borrelia system to test for associations between landscape-level spatial variation in Borrelia infection risk along replicated elevational gradients in the Swiss Alps and Toll-like receptor 2 (TLR2) evolution, a candidate gene for Borrelia resistance, across bank vole (Myodes glareolus) populations. We found that Borrelia infection risk (i.e. the product of Borrelia prevalence in questing ticks and the average tick load of voles at a sampling site) was spatially variable and significantly negatively associated with elevation. Across sampling sites, Borrelia prevalence in bank voles was significantly positively associated with Borrelia infection risk along the elevational clines. We observed a significant association between naturally occurring TLR2 polymorphisms in hosts and their Borrelia infection status. The TLR2 variant associated with a reduced likelihood of Borrelia infection was most common in rodent populations at lower elevations that face a high Borrelia infection risk, and its frequency changed in accordance with the change in Borrelia infection risk along the elevational clines. These results suggest that small-scale spatial variation in parasite-mediated selection affects the immunogenetic composition of natural host populations, providing a striking example that the microbial environment shapes the evolution of the host’s immune system in the wild

Higher genetic diversity on mountain tops: the role of historical and contemporary processes in shaping genetic variation in the bank vole

Glacial phases during the Pleistocene caused remarkable changes in species range distributions, with inevitable genetic consequences. Specifically, during interglacial phases, when the ice melted and new habitats became suitable again, species could recolonize regions that were previously covered by ice, such as high latitudes and elevations. Based on theoretical models and empirical data, a decrease in genetic variation is predicted along recolonization routes as a result of the consecutive founder effects that characterize the recolonization process. In the present study, we assessed the relative importance of historical and contemporary processes in shaping genetic diversity and differentiation of bank vole (Myodes glareolus) populations at different elevations in the Swiss Alps. By contrast to expectations, we found that genetic variation increased with elevation. Estimates of recent migration rates and a contrasting pattern of genetic differentiation observed at the mitochondrial cytochrome b gene and nuclear microsatellites support the hypothesis that higher genetic diversity at high elevation results from contemporary gene flow. Although historical recolonization processes can have marked effects on the genetic structure of populations, the present study provides an example where contemporary processes along an environmental gradient can reverse predicted patterns of genetic variation

Higher genetic diversity on mountain tops: the role of historical and contemporary processes in shaping genetic variation in the bank vole

Glacial phases during the Pleistocene caused remarkable changes in species range distributions, with inevitable genetic consequences. Specifically, during interglacial phases, when the ice melted and new habitats became suitable again, species could recolonize regions that were previously covered by ice, such as high latitudes and elevations. Based on theoretical models and empirical data, a decrease in genetic variation is predicted along recolonization routes as a result of the consecutive founder effects that characterize the recolonization process. In the present study, we assessed the relative importance of historical and contemporary processes in shaping genetic diversity and differentiation of bank vole (Myodes glareolus) populations at different elevations in the Swiss Alps. By contrast to expectations, we found that genetic variation increased with elevation. Estimates of recent migration rates and a contrasting pattern of genetic differentiation observed at the mitochondrial cytochrome b gene and nuclear microsatellites support the hypothesis that higher genetic diversity at high elevation results from contemporary gene flow. Although historical recolonization processes can have marked effects on the genetic structure of populations, the present study provides an example where contemporary processes along an environmental gradient can reverse predicted patterns of genetic variation

The LRRK2 signaling network converges on a centriolar phospho-Rab10/RILPL1 complex to cause deficits in centrosome cohesion and cell polarization.

The Parkinson's-disease-associated LRRK2 kinase phosphorylates multiple Rab GTPases including Rab8 and Rab10, which enhances their binding to RILPL1 and RILPL2. The nascent interaction between phospho-Rab10 and RILPL1 blocks ciliogenesis in vitro and in the intact brain, and interferes with the cohesion of duplicated centrosomes in dividing cells. We show here that regulators of the LRRK2 signaling pathway including vps35 and PPM1H converge upon causing centrosomal deficits. The cohesion alterations do not require the presence of other LRRK2 kinase substrates including Rab12, Rab35 and Rab43 or the presence of RILPL2. Rather, they depend on the RILPL1-mediated centrosomal accumulation of phosphorylated Rab10. RILPL1 localizes to the subdistal appendage of the mother centriole, followed by recruitment of the LRRK2-phosphorylated Rab proteins to cause the centrosomal defects. The centrosomal alterations impair cell polarization as monitored by scratch wound assays which is reverted by LRRK2 kinase inhibition. These data reveal a common molecular pathway by which enhanced LRRK2 kinase activity impacts upon centrosome-related events to alter the normal biology of a cell.This work was supported by The Michael J. Fox Foundation for Parkinson's research (to S.H.), the Spanish Ministry of Economy and Competitiveness [SAF2017-89402-R to S.H.], intramural funds from Rutgers University (to S.H.), the Spanish Ministry of Education, Culture and Sport [FPU15/05233 to A.J.L.O.], the Spanish Ministry of Science, Innovation and Universities [EST18/00412 to A.J.L.O.], the National Institute of Health [R01GM086197 to D.B.], Branfman Family Foundation (to D.B.), and the National Center for Microscopy and Imaging Research [P41 GM103412]. Open Access funding provided by Rutgers New Jersey Medical School. Deposited in PMC for immediate release

The LRRK2 signaling network converges on a centriolar phospho-Rab10/RILPL1 complex to cause deficits in centrosome cohesion and cell polarization

The Parkinson's-disease-associated LRRK2 kinase phosphorylates multiple Rab GTPases including Rab8 and Rab10, which enhances their binding to RILPL1 and RILPL2. The nascent interaction between phospho-Rab10 and RILPL1 blocks ciliogenesis in vitro and in the intact brain, and interferes with the cohesion of duplicated centrosomes in dividing cells. We show here that regulators of the LRRK2 signaling pathway including vps35 and PPM1H converge upon causing centrosomal deficits. The cohesion alterations do not require the presence of other LRRK2 kinase substrates including Rab12, Rab35 and Rab43 or the presence of RILPL2. Rather, they depend on the RILPL1-mediated centrosomal accumulation of phosphorylated Rab10. RILPL1 localizes to the subdistal appendage of the mother centriole, followed by recruitment of the LRRK2-phosphorylated Rab proteins to cause the centrosomal defects. The centrosomal alterations impair cell polarization as monitored by scratch wound assays which is reverted by LRRK2 kinase inhibition. These data reveal a common molecular pathway by which enhanced LRRK2 kinase activity impacts upon centrosome-related events to alter the normal biology of a cell

Epitaxial growth of β -Ga 2 O 3 by hot-wall MOCVD

The hot-wall metalorganic chemical vapor deposition (MOCVD) concept, previously shown to enable superior material quality and highperformance devices based on wide bandgap semiconductors, such as Ga(Al)N and SiC, has been applied to the epitaxial growth ofβ-Ga2O3. Epitaxial β-Ga2O3 layers at high growth rates (above 1 μm/h), at low reagent flows, and at reduced growth temperatures(740 ○C) are demonstrated. A high crystalline quality epitaxial material on a c-plane sapphire substrate is attained as corroborated by a combination of x-ray diffraction, high-resolution scanning transmission electron microscopy, and spectroscopic ellipsometry measurements. Thehot-wall MOCVD process is transferred to homoepitaxy, and single-crystalline homoepitaxial β-Ga2O3 layers are demonstrated with a 201 ¯rocking curve width of 118 arc sec, which is comparable to those of the edge-defined film-fed grown (201) ¯ β-Ga2O3 substrates, indicative ofsimilar dislocation densities for epilayers and substrates. Hence, hot-wall MOCVD is proposed as a prospective growth method to be furtherexplored for the fabrication of β-Ga2O

Renal expression of FGF23 and peripheral resistance to elevated FGF23 in rodent models of polycystic kidney disease

Fibroblast growth factor 23 (FGF23) regulates phosphate homeostasis and is linked to cardiovascular disease and all-cause mortality in chronic kidney disease. FGF23 rises in patients with CKD stages 2-3, but in patients with autosomal dominant polycystic kidney disease, the increase of FGF23 precedes the first measurable decline in renal function. The mechanisms governing FGF23 production and effects in kidney disease are largely unknown. Here we studied the relation between FGF23 and mineral homeostasis in two animal models of PKD. Plasma FGF23 levels were increased 10-fold in 4-week-old cy/+ Han:SPRD rats, whereas plasma urea and creatinine concentrations were similar to controls. Plasma calcium and phosphate levels as well as TmP/GFR were similar in PKD and control rats at all time points examined. Expression and activity of renal phosphate transporters, the vitamin D3-metabolizing enzymes, and the FGF23 co-ligand Klotho in the kidney were similar in PKD and control rats through 8 weeks of age, indicating resistance to FGF23, although phosphorylation of the FGF receptor substrate 2α protein was enhanced. In the kidneys of rats with PKD, FGF23 mRNA was highly expressed and FGF23 protein was detected in cells lining renal cysts. FGF23 expression in bone and spleen was similar in control rats and rats with PKD. Similarly, in an inducible Pkd1 knockout mouse model, plasma FGF23 levels were elevated, FGF23 was expressed in kidneys, but renal phosphate excretion was normal. Thus, the polycystic kidney produces FGF23 but is resistant to its action.Kidney International advance online publication, 8 January 2014; doi:10.1038/ki.2013.526