Natural selection on cork oak: allele frequency reveals divergent selection in cork oak populations along a temperature cline

A recent study of population divergence at neutral markers and adaptive traits in cork oak has observed an association between genetic distances at locus QpZAG46 and genetic distances for leaf size and growth. In that study it was proposed that certain loci could be linked to genes encoding for adaptive traits in cork oak and, thus, could be used in adaptation studies. In order to investigate this hypothesis, here we (1) looked for associations between molecular markers and a set of adaptive traits in cork oak, and (2) explored the effects of the climate on among-population patterns in adaptive traits and molecular markers. For this purpose, we chose 9-year-old plants originating from thirteen populations spanning a broad range of climatic conditions. Plants established in a common garden site were genotyped at six nuclear microsatellites and phenotypically characterized for six functional traits potentially related to plant performance. Our results supported the proposed linkage between locus QpZAG46 and genes encoding for leaf size and growth. Temperature caused adaptive population divergence in leaf size and growth, which was expressed as differences in the frequencies of the alleles at locus QpZAG46

Phosphorylation of Nrf2 at Multiple Sites by MAP Kinases Has a Limited Contribution in Modulating the Nrf2-Dependent Antioxidant Response

The bZIP transcription factor Nrf2 has emerged as a pivotal regulator of intracellular redox homeostasis by controlling the expression of many endogenous antioxidants and phase II detoxification enzymes. Upon oxidative stress, Nrf2 is induced at protein levels through redox-sensitive modifications on cysteine residues of Keap1, a component of the E3 ubiquitin ligase that targets Nrf2 for ubiquitin-dependent degradation. The mitogen activated protein kinases (MAPKs) have previously been proposed to regulate Nrf2 in response to oxidative stress. However, the exact role of MAPKs and the underlying molecular mechanism remain poorly defined. Here we report the first evidence that Nrf2 is phosphorylated in vivo by MAPKs. We have identified multiple serine/threonine residues as major targets of MAPK-mediated phosphorylation. Combined alanine substitution on those residues leads to a moderate decrease in the transcriptional activity of Nrf2, most likely due to a slight reduction in its nuclear accumulation. More importantly, Nrf2 protein stability, primarily controlled by Keap1, is not altered by Nrf2 phosphorylation in vivo. These data indicate that direct phosphorylation of Nrf2 by MAPKs has limited contribution in modulating Nrf2 activity. We suggest that MAPKs regulate the Nrf2 signaling pathway mainly through indirect mechanisms

DEFECT SELECTIVE ETCHING OF THICK AlN LAYERS GROWN ON 6H-SIC SEEDS – A TRANSMISSION ELECTRON MICROSCOPY STUDY

In the present study, the type and densities of defects in AlN crystals grown on 6H-SiC seeds by the sublimation-recombination method were assessed. The positions of the defects in AlN were first identified by defect selective etching (DSE) in molten NaOH-KOH at 400 °C for 2 minutes. Etching produced pits of three different sizes: 1.8, 2.4, and 2.9 μm. The etch pits were either aligned together forming a sub-grain boundary or randomly distributed. The smaller etch pits were either isolated or associated with larger etch pits. After preparing cross-sections of the pits by the focused ion beam (FIB) technique, transmission electron microscopy (TEM) was performed to determine the dislocation type (edge, mixed or screw) associated with a specific etch pit size. Preliminary TEM bright field and dark field imaging using different zone axes and diffraction vectors indicates an edge dislocation with a Burgers vector 1/3[1120] is associated with the smallest etch pit size