Gradient Photonic Materials Based on One‐Dimensional Polymer Photonic Crystals

In nature, animals such as chameleons are well‐known for the complex color patterns of their skin and the ability to adapt and change the color by manipulating sophisticated photonic crystal systems. Artificial gradient photonic materials are inspired by these color patterns. A concept for the preparation of such materials and their function as tunable mechanochromic materials is presented in this work. The system consists of a 1D polymer photonic crystal on a centimeter scale on top of an elastic poly(dimethylsiloxane) substrate with a gradient in stiffness. In the unstrained state, this system reveals a uniform red reflectance over the entire sample. Upon deformation, a gradient in local strain of the substrate is formed and transferred to the photonic crystal. Depending on the magnitude of this local strain, the thickness of the photonic crystal decreases continuously, resulting in a position‐dependent blue shift of the reflectance peak and hence the color in a rainbow‐like fashion. Using more sophisticated hard‐soft‐hard‐soft‐hard gradient elastomers enables the realization of stripe‐like reflectance patterns. Thus, this approach allows for the tunable formation of reflectance gradients and complex reflectance patterns. Envisioned applications are in the field of mechanochromic sensors, telemedicine, smart materials, and metamaterials

The WTX/AMER1 gene family: evolution, signature and function

<p>Abstract</p> <p>Background</p> <p><it>WTX </it>is a novel gene mutated in a proportion of Wilms' tumors and in patients suffering from sclerosing bone dysplasia. On the molecular level WTX has been shown to act as an antagonist of canonical <it>Wnt/β-catenin </it>signaling in fish and mammals thus linking it to an essential pathway involved in normal development and cancer formation. Interestingly, WTX seems to also localize to an intranuclear component called paraspeckles. In spite of the growing interest of molecular biologists in <it>WTX</it>, little is known about its paralogs and its phylogenetic history.</p> <p>Results</p> <p>Using the amino-acid sequence of <it>WTX/AMER1 </it>as a tool for the assignment of orthology and paralogy, we here identify two novel proteins, <it>AMER2 </it>and <it>AMER3</it>, as "<it>WTX</it>" related. This <it>Amer </it>gene family is present in all currently available vertebrate genome sequences, but not invertebrate genomes and is characterized by six conserved blocks of sequences. The phylogenetic analysis suggests that the <it>protoAmer </it>gene originated early in the vertebrate lineage and was then duplicated due to whole genome duplications (WGD) giving rise to the three different <it>Amer </it>genes.</p> <p>Conclusion</p> <p>Our study represents the first phylogenetic analysis of <it>Amer </it>genes and reveals a new vertebrate specific gene family that is likely to have played an important role in the evolution of this subphylum. Divergent and conserved molecular functions of <it>Wtx/Amer1</it>, <it>Amer2 </it>and <it>Amer3 </it>are discussed.</p

Conditional Sox9 ablation reduces chondroitin sulfate proteoglycan levels and improves motor function following spinal cord injury

Chondroitin sulfate proteoglycans (CSPGs) found in perineuronal nets and in the glial scar after spinal cord injury have been shown to inhibit axonal growth and plasticity. Since we have previously identified SOX9 as a transcription factor that upregulates the expression of a battery of genes associated with glial scar formation in primary astrocyte cultures, we predicted that conditional Sox9 ablation would result in reduced CSPG expression after spinal cord injury and that this would lead to increased neuroplasticity and improved locomotor recovery. Control and Sox9 conditional knock-out mice were subject to a 70 kdyne contusion spinal cord injury at thoracic level 9. One week after injury, Sox9 conditional knock-out mice expressed reduced levels of CSPG biosynthetic enzymes (Xt-1 and C4st), CSPG core proteins (brevican, neurocan, and aggrecan), collagens 2a1 and 4a1, and Gfap, a marker of astrocyte activation, in the injured spinal cord compared with controls. These changes in gene expression were accompanied by improved hind limb function and locomotor recovery as evaluated by the Basso Mouse Scale (BMS) and rodent activity boxes. Histological assessments confirmed reduced CSPG deposition and collagenous scarring at the lesion of Sox9 conditional knock-out mice, and demonstrated increased neurofilament-positive fibers in the lesion penumbra and increased serotonin immunoreactivity caudal to the site of injury. These results suggest that SOX9 inhibition is a potential strategy for the treatment of SCI. © 2012 Wiley Periodicals, Inc

Tree species richness differentially affects the chemical composition of leaves, roots and root exudates in four subtropical tree species

Plants produce thousands of compounds, collectively called the metabolome, which mediate interactions with other organisms. The metabolome of an individual plant may change according to the number and nature of these interactions. We tested the hypothesis that tree diversity level affects the metabolome of four subtropical tree species in a biodiversity–ecosystem functioning experiment, BEF‐China. We postulated that the chemical diversity of leaves, roots and root exudates increases with tree diversity. We expected that the strength of this diversity effect differs among leaf, root and root exudates samples. Considering their role in plant competition, we expected to find the strongest effects in root exudates. Roots, root exudates and leaves of four tree species ( Cinnamomum camphora , Cyclobalanopsis glauca , Daphniphyllum oldhamii and Schima superba ) were sampled from selected plots in BEF‐China. The exudate metabolomes were normalized over their non‐purgeable organic carbon level. Multivariate analyses were applied to identify the effect of both neighbouring (local) trees and plot diversity on tree metabolomes. The species‐ and sample‐specific metabolites were assigned to major compound classes using the ClassyFire tool, whereas potential metabolites related to diversity effects were annotated manually. Individual tree species showed distinct leaf, root and root exudate metabolomes. The main compound class in leaves was the flavonoids, whereas carboxylic acids, prenol lipids and specific alkaloids were most prominent in root exudates and roots. Overall, plot diversity had a stronger effect on metabolome profiles than the local diversity. Leaf metabolomes responded more often to tree diversity level than exudates, whereas root metabolomes varied the least. We found no uniform or general pattern of alterations in metabolite richness or diversity in response to variation in tree diversity. The response differed among species and tissues. Synthesis . Classification of metabolites supported initial ecological interpretation of differences among species and organs. Particularly, the metabolomes of leaves and root exudates respond to differences in tree diversity. These responses were neither linear nor uniform and individual metabolites showed different dynamics. More controlled interaction experiments are needed to dissect the causes and consequences of the observed shifts in plant metabolomes

Myocardial-specific R-spondin3 drives proliferation of the coronary stems primarily through the Leucine Rich Repeat G Protein coupled receptor LGR4

Coronary artery anomalies are common congenital disorders with serious consequences in adult life. Coronary circulation begins when the coronary stems form connections between the aorta and the developing vascular plexus. We recently identified the WNT signaling modulator R-spondin 3 (Rspo3), as a crucial regulator of coronary stem proliferation. Using expression analysis and tissue-specific deletion we now demonstrate that Rspo3 is primarily produced by cardiomyocytes. Moreover, we have employed CRISPR/Cas9 technology to generate novel Lgr4-null alleles that showed a significant decrease in coronary stem proliferation and thus phenocopied the coronary artery defects seen in Rspo3 mutants. Interestingly, Lgr4 mutants displayed slightly hypomorphic right ventricles, an observation also made after myocardial specific deletion of Rspo3. These results shed new light on the role of Rspo3 in heart development and demonstrate that LGR4 is the principal Rspondin 3 receptor in the heart

A mosaic of induced and non-induced branches promotes variation in leaf traits, predation and insect herbivore assemblages in canopy trees

Forest canopies are complex and highly diverse environments. Their diversity is affected by pronounced gradients in abiotic and biotic conditions, including variation in leaf chemistry. We hypothesised that branch-localised defence induction and vertical stratification in mature oaks constitute sources of chemical variation that extend across trophic levels. To test this, we combined manipulation of plant defences, predation monitoring, food-choice trials with herbivores and sampling of herbivore assemblages. Both induction and vertical stratification affected branch chemistry, but the effect of induction was stronger. Induction increased predation in the canopy and reduced herbivory in bioassays. The effects of increased predation affected herbivore assemblages by decreasing their abundance, and indirectly, their richness. In turn, we show that there are multiple factors contributing to variation across canopies. Branch-localised induction, variation between tree individuals and predation may be the ones with particularly strong effects on diverse assemblages of insects in temperate forests

Crosstalk between androgen receptor and WNT/β-catenin signaling causes sex-specific adrenocortical hyperplasia in mice

Female bias is highly prevalent in conditions such as adrenal cortex hyperplasia and neoplasia, but the reasons behind this phenomenon are poorly understood. In this study, we show that overexpression of the secreted WNT agonist R-spondin 1 (RSPO1) leads to ectopic activation of WNT/β-catenin signaling and causes sex-specific adrenocortical hyperplasia in mice. Although female adrenals show ectopic proliferation, male adrenals display excessive immune system activation and cortical thinning. Using a combination of genetic manipulations and hormonal treatment, we show that gonadal androgens suppress ectopic proliferation in the adrenal cortex and determine the selective regulation of the WNT-related genes Axin2 and Wnt4. Notably, genetic removal of androgen receptor (AR) from adrenocortical cells restores the mitogenic effect of WNT/β-catenin signaling. This is the first demonstration that AR activity in the adrenal cortex determines susceptibility to canonical WNT signaling-induced hyperplasia.</p

The adrenal capsule is a signaling center controlling cell renewal and zonation through <i>Rspo3</i>

Adrenal glands are zonated endocrine organs that are essential in controlling body homeostasis. How zonation is induced and maintained and how renewal of the adrenal cortex is ensured remain a mystery. Here we show that capsular RSPO3 signals to the underlying steroidogenic compartment to induce β-catenin signaling and imprint glomerulosa cell fate. Deletion of RSPO3 leads to loss of SHH signaling and impaired organ growth. Importantly, Rspo3 function remains essential in adult life to ensure replenishment of lost cells and maintain the properties of the zona glomerulosa. Thus, the adrenal capsule acts as a central signaling center that ensures replacement of damaged cells and is required to maintain zonation throughout life

Pituitary stem cells produce paracrine WNT signals to control the expansion of their descendant progenitor cells

In response to physiological demand, the pituitary gland generates new hormonesecreting cells from committed progenitor cells throughout life. It remains unclear to what extent pituitary stem cells (PSCs), which uniquely express SOX2, contribute to pituitary growth and renewal. Moreover, neither the signals that drive proliferation nor their sources have been elucidated. We have used genetic approaches in the mouse, showing that the WNT pathway is essential for proliferation of all lineages in the gland. We reveal that SOX2+ stem cells are a key source of WNT ligands. By blocking secretion of WNTs from SOX2+ PSCs in vivo, we demonstrate that proliferation of neighbouring committed progenitor cells declines, demonstrating that progenitor multiplication depends on the paracrine WNT secretion from SOX2+ PSCs. Our results indicate that stem cells can hold additional roles in tissue expansion and homeostasis, acting as paracrine signalling centres to coordinate the proliferation of neighbouring cells

Crosstalk between androgen receptor and WNT/β-catenin signaling causes sex-specific adrenocortical hyperplasia in mice

Female bias is highly prevalent in conditions such as adrenal cortex hyperplasia and neoplasia, but the reasons behind this phenomenon are poorly understood. In this study, we show that overexpression of the secreted WNT agonist R-spondin 1 (RSPO1) leads to ectopic activation of WNT/β-catenin signaling and causes sex-specific adrenocortical hyperplasia in mice. Although female adrenals show ectopic proliferation, male adrenals display excessive immune system activation and cortical thinning. Using a combination of genetic manipulations and hormonal treatment, we show that gonadal androgens suppress ectopic proliferation in the adrenal cortex and determine the selective regulation of the WNT-related genes Axin2 and Wnt4. Notably, genetic removal of androgen receptor (AR) from adrenocortical cells restores the mitogenic effect of WNT/β-catenin signaling. This is the first demonstration that AR activity in the adrenal cortex determines susceptibility to canonical WNT signaling-induced hyperplasia