Quantitative predictions on auxin-induced polar distribution of PIN proteins during vein formation in leaves

The dynamic patterning of the plant hormone auxin and its efflux facilitator the PIN protein are the key regulator for the spatial and temporal organization of plant development. In particular auxin induces the polar localization of its own efflux facilitator. Due to this positive feedback auxin flow is directed and patterns of auxin and PIN arise. During the earliest stage of vein initiation in leaves auxin accumulates in a single cell in a rim of epidermal cells from which it flows into the ground meristem tissue of the leaf blade. There the localized auxin supply yields the successive polarization of PIN distribution along a strand of cells. We model the auxin and PIN dynamics within cells with a minimal canalization model. Solving the model analytically we uncover an excitable polarization front that triggers a polar distribution of PIN proteins in cells. As polarization fronts may extend to opposing directions from their initiation site we suggest a possible resolution to the puzzling occurrence of bipolar cells, such we offer an explanation for the development of closed, looped veins. Employing non-linear analysis we identify the role of the contributing microscopic processes during polarization. Furthermore, we deduce quantitative predictions on polarization fronts establishing a route to determine the up to now largely unknown kinetic rates of auxin and PIN dynamics.Comment: 9 pages, 4 figures, supplemental information included, accepted for publication in Eur. Phys. J.

Relation between the Polyakov loop and the chiral order parameter at strong coupling

We discuss the relation between the Polyakov loop and the chiral order parameter at finite temperature by using the Gocksch-Ogilvie model with fundamental or adjoint quarks. The model is based on the double expansion of strong coupling and large dimensionality on the lattice. In an analytic way with the mean field approximation employed, we show that the confined phase must be accompanied by the spontaneous breaking of the chiral symmetry for both fundamental and adjoint quarks. Then we proceed to numerical analysis to look into the coupled dynamics of the Polyakov loop and the chiral order parameter. In the case of fundamental quarks, the pseudo-critical temperature inferred from the Polyakov loop behavior turns out to coincide with the pseudo-critical temperature of the chiral phase transition. We discuss the physical implication of the coincidence of the pseudo-critical temperatures in two extreme cases; one is the deconfinement dominance and the other is the chiral dominance. As for adjoint quarks, the deconfinement transition of first order persists and the chiral phase transition occurs distinctly at higher temperature than the deconfinement transition does. The present model study gives us a plausible picture to understand the results from the lattice QCD and aQCD simulations.Comment: 19 pages, 9 figures, to appear in Phys.Rev.D. Appendix A is modified; references are adde

The CARMENES search for exoplanets around M dwarfs. First visual-channel radial-velocity measurements and orbital parameter updates of seven M-dwarf planetary systems

Stars and planetary system

Computational identification and experimental validation of microRNAs binding to the Alzheimer-related gene ADAM10.

BACKGROUND: MicroRNAs (miRNAs) are post-transcriptional regulators involved in numerous biological processes including the pathogenesis of Alzheimer's disease (AD). A key gene of AD, ADAM10, controls the proteolytic processing of APP and the formation of the amyloid plaques and is known to be regulated by miRNA in hepatic cancer cell lines. To predict miRNAs regulating ADAM10 expression concerning AD, we developed a computational approach. METHODS: MiRNA binding sites in the human ADAM10 3' untranslated region were predicted using the RNA22, RNAhybrid and miRanda programs and ranked by specific selection criteria with respect to AD such as differential regulation in AD patients and tissue-specific expression. Furthermore, target genes of miR-103, miR-107 and miR-1306 were derived from six publicly available miRNA target site prediction databases. Only target genes predicted in at least four out of six databases in the case of miR-103 and miR-107 were compared to genes listed in the AlzGene database including genes possibly involved in AD. In addition, the target genes were used for Gene Ontology analysis and literature mining. Finally, we used a luciferase assay to verify the potential effect of these three miRNAs on ADAM10 3' UTR in SH-SY5Y cells. RESULTS: Eleven miRNAs were selected, which have evolutionary conserved binding sites. Three of them (miR-103, miR-107, miR-1306) were further analysed as they are linked to AD and most strictly conserved between different species. Predicted target genes of miR-103 (p-value = 0.0065) and miR-107 (p-value = 0.0009) showed significant overlap with the AlzGene database except for miR-1306. Interactions between miR-103 and miR-107 to genes were revealed playing a role in processes leading to AD. ADAM10 expression in the reporter assay was reduced by miR-1306 (28%), miR-103 (45%) and miR-107 (52%). CONCLUSIONS: Our approach shows the requirement of incorporating specific, disease-associated selection criteria into the prediction process to reduce the amount of false positive predictions. In summary, our method identified three miRNAs strongly suggested to be involved in AD, which possibly regulate ADAM10 expression and hence offer possibilities for the development of therapeutic treatments of AD