Recent origin,active speciation and dispersal for the lichen genus Nephroma (Peltigerales) in Macaronesia

Aim We reconstructed the phylogeny of the lichen genus Nephroma (Peltigerales) to assess the relationships of species endemic to Macaronesia. We estimated dates of divergences to test the hypothesis that the species arose in Macaronesia (neo‐endemism) versus the oceanic archipelagos serving as refugia for formerly widespread taxa (palaeo‐endemism). Location Cosmopolitan with a special focus on the archipelagos of the Azores, Madeira and the Canary Islands. Methods DNA sequences were obtained from 18 species for three loci and analysed using maximum parsimony, maximum likelihood and Bayesian inferences. Divergence dates were estimated for the internal transcribed spacer (ITS)‐based phylogeny using a relaxed molecular clock. Reconstruction of the ancestral geographical range was conducted using the Bayesian 50% majority rule consensus tree under a parsimony method. Results The backbone phylogenetic tree was fully supported, with Nephroma plumbeum as sister to all other species. Four strongly supported clades were detected: the Nephroma helveticum, the N. bellum, the N. laevigatum and the N. parile clades. The latter two share a common ancestor and each includes a widespread Holarctic species (N. laevigatum and N. parile, respectively) and all species endemic to Macaronesia. The data suggest a neo‐endemic origin of Macaronesian taxa, a recent range expansion from Macaronesia of both widespread species, a range expansion limited to the Mediteranean Basin and south‐western Europe for another taxon, and a long dispersal event that resulted in a speciation event in the western parts of North America. Main conclusions The Macaronesian endemic species belong to two sister clades and originated from a most recent common ancestor (MRCA) shared with one widely distributed taxon, either N. parile or N. laevigatum. Estimates of the mean divergence dates suggest that the endemics originated in the archipelagos after the rise of the volcanic islands, along with the ancestor to the now widespread species, which probably expanded their range beyond Macaronesia via long‐distance dispersal. This study provides the first phylogenetic evidence of Macaronesian neo‐endemism in lichenized fungi and provides support for the hypothesis that oceanic islands may serve as a source for the colonization of continents. However, further data are needed to properly assess the alternative hypothesis, namely colonization from western North America.     

Off‐host aggregation in the non‐fed,female brown dog tick,Rhipicephalus sanguineus (Latreille), is induced by tick excreta and enhanced by low relative humidity

We report that Rhipicephalus sanguineus (Ixodida: Ixodidae) faeces and its main component, guanine, act as assembly pheromones in short‐range Petri plate bioassays. Arrestment activity in response to guanine was lower than that in response to natural excreta, indicating the presence of other active ingredients in natural excreta. The selective removal of appendages was used to establish the important roles played by the palps and the front pair of legs in the detection of the pheromone. Reaction to chemically pure guanine at varying concentrations occurred without a dose response; thus only the presence of guanine, not a critical amount, is required to induce assembly. Higher speed and intensity of clustering occurred at 33% relative humidity (RH). We conclude that female adults of R. sanguineus are more prone to assemble under dry conditions that match the arid microhabitats preferred by this species and that this tendency allows this tick to reside in human dwellings and dog kennels that maintain standards of comfort at 30–50% RH. Cleaning or removing tick excreta‐covered surfaces on which ticks aggregate from within and around human dwellings may prove useful as a means of interfering with the establishment of off‐host clusters of R. sanguineus.     

Life‐history constraints in grassland plant species: a growth‐defence trade‐off is the norm

Plant growth can be limited by resource acquisition and defence against consumers, leading to contrasting trade‐off possibilities. The competition‐defence hypothesis posits a trade‐off between competitive ability and defence against enemies (e.g. herbivores and pathogens). The growth‐defence hypothesis suggests that strong competitors for nutrients are also defended against enemies, at a cost to growth rate. We tested these hypotheses using observations of 706 plant populations of over 500 species before and following identical fertilisation and fencing treatments at 39 grassland sites worldwide. Strong positive covariance in species responses to both treatments provided support for a growth‐defence trade‐off: populations that increased with the removal of nutrient limitation (poor competitors) also increased following removal of consumers. This result held globally across 4 years within plant life‐history groups and within the majority of individual sites. Thus, a growth‐defence trade‐off appears to be the norm, and mechanisms maintaining grassland biodiversity may operate within this constraint.     

Porcine growth hormone gene expression from viral promoters in transgenic swine

Abstract

The production of porcine growth hormone (pGH) from novel expression vectors containing the promoter/enhancer elements of the Moloney murine leukemia virus (MLV) LTR or the human cytomegalovirus (CMV) immediate early gene was examined in transgenic swine. Both fusion genes resulted in elevated levels of serum pGH, elevation of insulin‐like growth factor 1 (IGF‐1), and a pronounced decrease in carcass fat deposition. The two viral promoter/enhancer elements were constitutively active in the transgenic swine throughout the life of the animals. In individual swine, the CMV‐pGH transgene was expressed predominantly in the pancreas while the MLV‐pGH transgene was expressed in a wide variety of tissues. These swine were infertile, had insulin resistance, and demonstrated an accelerated form of osteochondritis dissicans. Our results show that excess pGH produces a phenotype identical to that seen in swine expressing heterologous growth hormones, and provides a baseline for assessing the overall efficiency of producing transgenic swine. Furthermore, our data suggests that unregulated pGH production, even at 15 times normal levels and independent of the tissue source, has adverse effects that outweigh the desired reduction in carcass fat deposition in transgenic swine.     

Surface Chirality of Gly‐Pro Dipeptide Adsorbed on a Cu(110) Surface

The adsorption of chiral Gly‐Pro dipeptide on Cu(110) has been characterized by combining in situ polarization modulation infrared reflection absorption spectroscopy (PM‐RAIRS) and X‐ray photoelectron spectroscopy (XPS). The chemical state of the dipeptide, and its anchoring points and adsorption geometry, were determined at various coverage values. Gly‐Pro molecules are present on Cu(110) in their anionic form (NH₂/COO⁻) and adsorb under a 3‐point binding via both oxygen atoms of the carboxylate group and via the nitrogen atom of the amine group. Low‐energy electron diffraction (LEED) and scanning tunneling microscopy (STM) have shown the presence of an extended 2D chiral array, sustained via intermolecular H‐bonds interactions. Furthermore, due to the particular shape of the molecule, only one homochiral domain is formed, creating thus a truly chiral surface. Chirality 27:411–416, 2015. © 2015 Wiley Periodicals, Inc.     

NEMO specifically recognizes K63‐linked poly‐ubiquitin chains through a new bipartite ubiquitin‐binding domain

An important property of NEMO, the core element of the IKK complex involved in NF‐κB activation, resides in its ability to specifically recognize poly‐ubiquitin chains. A small domain called NOA/UBAN has been suggested to be responsible for this property. We recently demonstrated that the C‐terminal Zinc Finger (ZF) of NEMO is also able to bind ubiquitin. We show here by ZF swapping and mutagenesis that this represents its only function. While neither NOA nor ZF shows any preference for K63‐linked chains, we demonstrate that together they form a bipartite high‐affinity K63‐specific ubiquitin‐binding domain. A similar domain can be found in two other proteins, Optineurin and ABIN2, and can be freely exchanged with that of NEMO without interfering with its activity. This suggests that the main function of the C‐terminal half of NEMO is to specifically bind K63‐linked poly‐ubiquitin chains. We also demonstrate that the recently described binding of NEMO to linear poly‐ubiquitin chains is dependent on the NOA alone and does not require the presence of the ZF.     

Hyperosmolarity enhanced susceptibility to renal tubular fibrosis by modulating catabolism of type I transforming growth factor‐β receptors

Hyperosmolarity plays an essential role in the pathogenesis of diabetic tubular fibrosis. However, the mechanism of the involvement of hyperosmolarity remains unclear. In this study, mannitol was used to evaluate the effects of hyperosmolarity on a renal distal tubule cell line (MDCK). We investigated transforming growth factor‐β receptors and their downstream fibrogenic signal proteins. We show that hyperosmolarity significantly enhances the susceptibility to exogenous transforming growth factor (TGF)‐β1, as mannitol (27.5 mM) significantly enhanced the TGF‐β1‐induced increase in fibronectin levels compared with control experiments (5.5 mM). Specifically, hyperosmolarity induced tyrosine phosphorylation on TGF‐β RII at 336 residues in a time (0–24 h) and dose (5.5–38.5 mM) dependent manner. In addition, hyperosmolarity increased the level of TGF‐β RI in a dose‐ and time‐course dependent manner. These observations may be closely related to decreased catabolism of TGF‐β RI. Hyperosmolarity significantly downregulated the expression of an inhibitory Smad (Smad7), decreased the level of Smurf 1, and reduced ubiquitination of TGF‐β RI. In addition, through the use of cycloheximide and the proteasome inhibitor MG132, we showed that hyperosmolarity significantly increased the half‐life and inhibited the protein level of TGF‐β RI by polyubiquitination and proteasomal degradation. Taken together, our data suggest that hyperosmolarity enhances cellular susceptibility to renal tubular fibrosis by activating the Smad7 pathway and increasing the stability of type I TGF‐β receptors by retarding proteasomal degradation of TGF‐β RI. This study clarifies the mechanism underlying hyperosmotic‐induced renal fibrosis in renal distal tubule cells. J. Cell. Biochem. 109: 663–671, 2010. © 2010 Wiley‐Liss, Inc.