The K+/H+ antiporter LeNHX2 increases salt tolerance by improving K+ homeostasis in transgenic tomato

The endosomal LeNHX2 ion transporter exchanges H⁺ with K⁺ and, to lesser extent, Na⁺. Here, we investigated the response to NaCl supply and K⁺ deprivation in transgenic tomato (Solanum lycopersicum L.) overexpressing LeNHX2 and show that transformed tomato plants grew better in saline conditions than untransformed controls, whereas in the absence of K⁺ the opposite was found. Analysis of mineral composition showed a higher K⁺ content in roots, shoots and xylem sap of transgenic plants and no differences in Na⁺ content between transgenic and untransformed plants grown either in the presence or the absence of 120 mm NaCl. Transgenic plants showed higher Na⁺/H⁺ and, above all, K⁺/H⁺ transport activity in root intracellular membrane vesicles. Under K⁺ limiting conditions, transgenic plants enhanced root expression of the high‐affinity K⁺ uptake system HAK5 compared to untransformed controls. Furthermore, tomato overexpressing LeNHX2 showed twofold higher K⁺ depletion rates and half cytosolic K⁺ activity than untransformed controls. Under NaCl stress, transgenic plants showed higher uptake velocity for K⁺ and lower cytosolic K⁺ activity than untransformed plants. These results indicate the fundamental role of K⁺ homeostasis in the better performance of LeNHX2 overexpressing tomato under NaCl stress.     

Mutants impaired in vacuolar metal mobilization identify chloroplasts as a target for cadmium hypersensitivity in Arabidopsis thaliana

Cadmium (Cd) is highly toxic to plants causing growth reduction and chlorosis. It binds thiols and competes with essential transition metals. It affects major biochemical processes such as photosynthesis and the redox balance, but the connection between cadmium effects at the biochemical level and its deleterious effect on growth has seldom been established. In this study, two Cd hypersensitive mutants, cad1‐3 impaired in phytochelatin synthase (PCS1), and nramp3nramp4 impaired in release of vacuolar metal stores, have been compared. The analysis combines genetics with measurements of photosynthetic and antioxidant functions. Loss of AtNRAMP3 and AtNRAMP4 function or of PCS1 function leads to comparable Cd sensitivity. Root Cd hypersensitivities conferred by cad1‐3 and nramp3nramp4 are cumulative. The two mutants contrast in their tolerance to oxidative stress. In nramp3nramp4, the photosynthetic apparatus is severely affected by Cd, whereas it is much less affected in cad1‐3. In agreement with chloroplast being a prime target for Cd toxicity in nramp3nramp4, the Cd hypersensitivity of this mutant is alleviated in the dark. The Cd hypersensitivity of nramp3nramp4 mutant highlights the critical role of vacuolar metal stores to supply essential metals to plastids and maintain photosynthetic function under Cd and oxidative stresses.     

P2Y2 receptor promotes intestinal microtubule stabilization and mucosal re‐epithelization in experimental colitis

P2Y₂ receptor expression is increased in intestinal epithelial cells (IECs) during inflammatory bowel diseases (IBDs). In this context, P2Y₂ stimulates PGE₂ release by IECs, suggesting a role in wound healing. For this study, we have used the non‐cancerous IEC‐6 cell line. IEC‐6 cell migration was determined using Boyden chambers and the single‐edged razor blade model of wounding. The receptor was activated using ATP, UTP, or 2‐thioUTP. Pharmacological inhibitors, a blocking peptide, a neutralizing antibody and interfering RNAs were used to characterize the signaling events. Focal adhesions and microtubule (MT) dynamics were determined by immunofluorescence using anti‐vinculin and anti‐acetylated‐α‐tubulin antibodies, respectively. In vivo, the dextran sodium sulfate mouse model of colitis was used to characterize the effects of P2Y₂ agonist 2‐thioUTP on remission. We showed that P2Y₂ increased cell migration and wound closure by recruiting Go protein with the cooperation of integrin α_v. Following P2Y₂ activation, we demonstrated that GSK3β activity was inhibited in response to Akt activation. This leads to MT stabilization and increased number of focal adhesions. In vivo, P2Y₂ activation stimulates remission, as illustrated by a reduction in the disease activity index values and histological scores as compared to control mice. These findings highlight a novel function for this receptor in IECs. They also illustrate that P2Y receptors could be targeted for the development of innovative therapies for the treatment of IBDs. J. Cell. Physiol. 228: 99–109, 2013. © 2012 Wiley Periodicals, Inc.     

Glucose transporter 2 expression is down regulated following P2X7 activation in enterocytes

With the diabetes epidemic affecting the world population, there is an increasing demand for means to regulate glycemia. Dietary glucose is first absorbed by the intestine before entering the blood stream. Thus, the regulation of glucose absorption by intestinal epithelial cells (IECs) could represent a way to regulate glycemia. Among the molecules involved in glycemia homeostasis, extracellular ATP, a paracrine signaling molecule, was reported to induce insulin secretion from pancreatic β cells by activating P2Y and P2X receptors. In rat's jejunum, P2X7 expression was previously immunolocalized to the apex of villi, where it has been suspected to play a role in apoptosis. However, using an antibody recognizing the receptor extracellular domain and thus most of the P2X7 isoforms, we showed that expression of this receptor is apparent in the top two‐thirds of villi. These data suggest a different role for this receptor in IECs. Using the non‐cancerous IEC‐6 cells and differentiated Caco‐2 cells, glucose transport was reduced by more than 30% following P2X7 stimulation. This effect on glucose transport was not due to P2X7‐induced cell apoptosis, but rather was the consequence of glucose transporter 2 (Glut2)'s internalization. The signaling pathway leading to P2X7‐dependent Glut2 internalization involved the calcium‐independent activation of phospholipase Cγ1 (PLCγ1), PKCδ, and PKD1. Although the complete mechanism regulating Glut2 internalization following P2X7 activation is not fully understood, modulation of P2X7 receptor activation could represent an interesting approach to regulate intestinal glucose absorption. J. Cell. Physiol. 228: 120–129, 2013. © 2012 Wiley Periodicals, Inc.     

The study of habitat use by censuses and molecular methods in birds: the case of two sympatric pigeons

Capsule Faecal DNA gives accurate results of habitat use.     

REACTION OF FIN WHALES BALAENOPTERA PHYSALUS TO AN EARTHQUAKE

ABSTRACT

Whales living within seismically active regions are subject to intense disturbances from strong sounds produced by earthquakes that can kill or injure individuals. Nishimura & Clark (1993) relate the possible effects of underwater earthquake noise levels in marine mammals, adducing that T-phase source signal level (10- to 30- Hz range) can exceed 200 dB re: 1 μPa at 1 m, for a magnitude 4–5 earthquake, sounds audible to fin whales which produce low frequency sounds of 16–20/25–44 Hz over 0.5–1s, typically of 183 dB re: 1 μPa at 1 m. Here we present the response of a fin whale to a 5.5 Richter scale earthquake that took place on 22 February 2005, in the Gulf of California. The whale covered 13 km in 26 min (mean speed = 30.2 km/h). We deduce that the sound heard by this whale might have triggered the costly energy expenditure of high speed swimming as a seismic-escape response. These observations support the hypothesis of Richardson et al. (1995) that cetaceans may flee from loud sounds before they are injured, when exposed to noise in excess of 140 dB re: 1 μPa 1 m.     

Diabetic liver injury from streptozotocin is regulated through the caspase-8 homolog cFLIP involving activation of JNK2 and intrahepatic immunocompetent cells

The endemic occurrence of obesity and the associated risk factors that constitute the metabolic syndrome have been predicted to lead to a dramatic increase in chronic liver disease. Non-alcoholic steatohepatitis (NASH) has become the most frequent liver disease in countries with a high prevalence of obesity. In addition, hepatic steatosis and insulin resistance have been implicated in disease progression of other liver diseases, including chronic viral hepatitis and hepatocellular carcinoma. The molecular mechanisms underlying the link between insulin signaling and hepatocellular injury are only partly understood. We have explored the role of the antiapoptotic caspase-8 homolog cellular FLICE-inhibitory protein (cFLIP) on liver cell survival in a diabetic model with hypoinsulinemic diabetes in order to delineate the role of insulin signaling on hepatocellular survival. cFLIP regulates cellular injury from apoptosis signaling pathways, and loss of cFLIP was previously shown to promote injury from activated TNF and CD95/Apo-1 receptors. In mice lacking cFLIP in hepatocytes (flip^−/−), loss of insulin following streptozotocin treatment resulted in caspase- and c-Jun N-terminal kinase (JNK)-dependent liver injury after 21 days. Substitution of insulin, inhibition of JNK using the SP600125 compound in vivo or genetic deletion of the mitogen-activated protein kinase (MAPK)9 (JNK2) in all tissues abolished the injurious effect. Strikingly, the difference in injury between wild-type and cFLIP-deficient mice occurred only in vivo and was accompanied by liver-infiltrating inflammatory cells with a trend toward increased amounts of NK1.1-positive cells and secretion of proinflammatory cytokines. Transfer of bone marrow from rag-1-deficient mice that are depleted from B and T lymphocytes prevented liver injury in flip^−/− mice. These findings support a direct role of insulin on cellular survival by alternating the activation of injurious MAPK, caspases and the recruitment of inflammatory cells to the liver. Thus, increasing resistance to insulin signaling pathways in hepatocytes appears to be an important factor in the initiation and progression of chronic liver disease.     

Vriesea friburgensis: A natural trap or a nurse plant in coastal sand dunes?

Positive interactions between plants play a fundamental role in environments with extreme conditions, such as coastal sand dunes, where the establishment of many species is limited by high temperature, and low availability of water and nutrients in the soil. The ability to store water and enrich the soil with nutrients characterizes bromeliads as potential nurse plants for other species. This study aimed to analyze the potential of the bromeliad Vriesea friburgensis to act as a nurse plant, and to compare this interaction in coastal dunes in herbaceous versus scrub vegetation. The study was performed on Santa Catarina Island in Brazil. Juveniles of other species associated with V. friburgensis were collected within and under bromeliad tanks and on adjacent plots beside each bromeliad. The abundance, species richness and height of juveniles were recorded. We found that abundance and richness of Vf‐associated juveniles were lower than those Vf‐not associated, in herbaceous vegetation (negative interaction). However, the height of some shrubs species, like Eupatorium casarettoi and Tibouchina urvilleana, was greater when Vf‐associated (positive interaction). In scrub vegetation, the abundance and richness of juveniles were not significantly affected by V. friburgensis presence (neutral interaction). However, the height of some shrubs and trees species, like Clusia criuva, Eugenia catharinae, Myrsine parvifolia and Ocotea pulchella, was greater when Vf‐associated. Species composition associated with V. friburgensis differed from the assemblage in adjacent plots, indicating that some species interact more with nurse plants, whereas others fail to develop when associated with this bromeliad; the difference between groups in species composition was less evident in scrub vegetation areas. Clusia criuva was considered an indicator species for Vf‐associated juveniles in both vegetation types. Despite the fact that these tank bromeliads do not function as nurse plants for some species, there are others that seem to be favoured by this interaction.