HKT2;2/1, a K+-permeable transporter identified in a salt tolerant rice cultivar through surveys of natural genetic polymorphism

We have investigated OsHKT2;1 natural variation in a collection of 49 cultivars with different levels of salt tolerance and geographical origins. The effect of identified polymorphism on OsHKT2;1 activity was analysed through heterologous expression of variants in Xenopus oocytes. OsHKT2;1 appeared to be a highly conserved protein with only five possible amino acid substitutions that have no substantial effect on functional properties. Our study, however, also identified a new HKT isoform, No-OsHKT2;2/1 in Nona Bokra, a highly salt-tolerant cultivar. No-OsHKT2;2/1 probably originated from a deletion in chromosome 6, producing a chimeric gene. Its 5¢ region corresponds to that of OsHKT2;2, whose full-length sequence is not present in Nipponbare but has been identified in Pokkali, a salt-tolerant rice cultivar. Its 3¢ region corresponds to that of OsHKT2;1. No-OsHKT2;2/1 is essentially expressed in roots and displays a significant level of expression at high Na+ concentrations, in contrast to OsHKT2;1. Expressed in Xenopus oocytes or in Saccharomyces cerevisiae, No-OsHKT2;2/1 exhibited a strong permeability to Na+ and K+, even at high external Na+ concentrations, like OsHKT2;2, and in contrast to OsHKT2;1. Our results suggest that No-OsHKT2;2/1 can contribute to Nona Bokra salt tolerance by enabling root K+ uptake under saline conditions.

3.2 Lorenzo Greene, Lincoln University History Professor, 1933-72

In late August, Lloyd Gaines filled out an application after conferring with Dr. Lorenzo Greene and one of his civics instructors at Vashon High School, Zaid D. Lenoir.

2.1 Lloyd Gaines close up image

Charles Hamilton Houston and other NAACP attorneys assembled in early October 1939 to take depositions in preparation for the hearing scheduled a week later in Columbia to determine whether the university had complied with the Gaines decision. Attorneys took depositions from all of the instructors of the new LU law school as their preparation for the court proceedings wound down. The deposition of Lloyd Gaines was next. Attorneys planned to ask Gaines whether he considered Lincoln to be as good of a law school as Missouri and whether he planned to enroll. Called for questioning, Gaines did not respond. He could not be located anywhere. Lloyd’s mother, Callie Gaines, recalled that in January her son “left here to go to Kansas City to make a speech. That’s the last I saw of him.” While in Kansas City, Gaines spoke at the Centennial Methodist Church. He also looked for work, but not finding any caught a train for Chicago, telling people in Kansas City that he would stay a few days and return home.

UMA ÁNALISE EXEGÉTICA DA PORÇÃO DE MIQUEIAS 2,1-5: A SITUAÇÃO SOCIOECONÔMICA EM JUDÁ E SUAS IMPLICAÇÕES NA HERANÇA DOS CAMPONESES NA SEFELÁ JUDAÍTA NO SÉCULO VIII A.C.

Esta pesquisa procura examinar, à luz da metodologia exegética, a perícope de Miqueias 2,1-5, a fim de reconstruir o cenário no qual emergiu a dura crítica social do profeta. O texto apresenta, em sua análise literária, características de um dito profético coeso, em estilo poético. Sua estrutura encontra-se dividida em duas unidades (denúncia e castigo), sendo que cada uma das unidades possui outras duas subunidades (genérica e específica). O gênero literário harmoniza-se com um dito profético de julgamento geralmente conhecido como oráculo ai . A análise da dimensão histórica situa o acontecimento fundante em 701 a.C., na Sefelá judaíta. Numa análise investigativa do conteúdo da denúncia norteado pelo modelo teórico do modo de produção tributário, observa-se um conflito entre dois grupos. Nesse conflito, Miqueias faz uma acusação a um grupo de poder em Judá que planeja e executa ações criminosas contra a herança camponesa. O castigo descreve a conspiração e o plano divino contra esse grupo de poder. Javé havia planejado um mal idêntico ao que eles haviam cometido, desonra e privação de suas possessões. Os valores culturais de honra e vergonha subjazem a esse oráculo. Por descumprirem seus deveres junto a Javé e ao povo, os criminosos perderiam todos os seus direitos e, sobretudo, a honra perante a própria comunidade. Com base no modelo teórico do modo de produção tributário, constata-se que, na situação social em Judá no oitavo século, prevalecia um conflito entre campo e cidade. As comunidades aldeãs pagavam tributo à cidade em forma de produtos e serviços. A excessiva arrecadação de tributo e as falhas no sistema de ajuda mútua forçaram os indivíduos e famílias a contrair dívidas, a hipotecar suas terras herdadas dos pais e eventualmente perdê-las. O profeta Miqueias é o porta-voz do protesto da classe campesina que resolve reagir aos desmandos praticados pela elite citadina. Para ele, Javé escuta a queixa dos que estão sendo oprimidos e intervém na história tomando o partido do oprimido.(AU)

UMA ÁNALISE EXEGÉTICA DA PORÇÃO DE MIQUEIAS 2,1-5: A SITUAÇÃO SOCIOECONÔMICA EM JUDÁ E SUAS IMPLICAÇÕES NA HERANÇA DOS CAMPONESES NA SEFELÁ JUDAÍTA NO SÉCULO VIII A.C.

Esta pesquisa procura examinar, à luz da metodologia exegética, a perícope de Miqueias 2,1-5, a fim de reconstruir o cenário no qual emergiu a dura crítica social do profeta. O texto apresenta, em sua análise literária, características de um dito profético coeso, em estilo poético. Sua estrutura encontra-se dividida em duas unidades (denúncia e castigo), sendo que cada uma das unidades possui outras duas subunidades (genérica e específica). O gênero literário harmoniza-se com um dito profético de julgamento geralmente conhecido como oráculo ai . A análise da dimensão histórica situa o acontecimento fundante em 701 a.C., na Sefelá judaíta. Numa análise investigativa do conteúdo da denúncia norteado pelo modelo teórico do modo de produção tributário, observa-se um conflito entre dois grupos. Nesse conflito, Miqueias faz uma acusação a um grupo de poder em Judá que planeja e executa ações criminosas contra a herança camponesa. O castigo descreve a conspiração e o plano divino contra esse grupo de poder. Javé havia planejado um mal idêntico ao que eles haviam cometido, desonra e privação de suas possessões. Os valores culturais de honra e vergonha subjazem a esse oráculo. Por descumprirem seus deveres junto a Javé e ao povo, os criminosos perderiam todos os seus direitos e, sobretudo, a honra perante a própria comunidade. Com base no modelo teórico do modo de produção tributário, constata-se que, na situação social em Judá no oitavo século, prevalecia um conflito entre campo e cidade. As comunidades aldeãs pagavam tributo à cidade em forma de produtos e serviços. A excessiva arrecadação de tributo e as falhas no sistema de ajuda mútua forçaram os indivíduos e famílias a contrair dívidas, a hipotecar suas terras herdadas dos pais e eventualmente perdê-las. O profeta Miqueias é o porta-voz do protesto da classe campesina que resolve reagir aos desmandos praticados pela elite citadina. Para ele, Javé escuta a queixa dos que estão sendo oprimidos e intervém na história tomando o partido do oprimido.(AU)

The Thrombospondin Receptor CD47 (IAP) Modulates and Associates with α2β1 Integrin in Vascular Smooth Muscle Cells

The carboxyl-terminal domain of thrombospondin-1 enhances the migration and proliferation of smooth muscle cells. Integrin-associated protein (IAP or CD47) is a receptor for the thrombospondin-1 carboxyl-terminal cell-binding domain and binds the agonist peptide 4N1K (kRFYVVMWKk) from this domain. 4N1K peptide stimulates chemotaxis of both human and rat aortic smooth muscle cells on gelatin-coated filters. The migration on gelatin is specifically blocked by monoclonal antibodies against IAP and a β1 integrin, rather than αvβ3 as found previously for 4N1K-stimulated chemotaxis of endothelial cells on gelatin. Both human and rat smooth muscle cells displayed a weak migratory response to soluble type I collagen; however, the presence of 4N1K peptide or intact thrombospondin-1 provoked a synergistic chemotactic response that was partially blocked by antibodies to α2 and β1 integrin subunits and to IAP. A combination of antiα2 and IAP monoclonal antibodies completely blocked chemotaxis. RGD peptide and antiαvβ3 mAb were without effect. 4N1K and thrombospondin-1 did not augment the chemotactic response of smooth muscle cells to fibronectin, vitronectin, or collagenase-digested type I collagen. Complex formation between α2β1 and IAP was detected by the coimmunoprecipitation of both α2 and β1 integrin subunits with IAP. These data suggest that IAP can associate with α2β1 integrin and modulate its function.

Functional Hierarchy of Simultaneously Expressed Adhesion Receptors: Integrin α2β1 but Not CD44 Mediates MV3 Melanoma Cell Migration and Matrix Reorganization within Three-dimensional Hyaluronan-containing Collagen MatricesV⃞

Haptokinetic cell migration across surfaces is mediated by adhesion receptors including β1 integrins and CD44 providing adhesion to extracellular matrix (ECM) ligands such as collagen and hyaluronan (HA), respectively. Little is known, however, about how such different receptor systems synergize for cell migration through three-dimensionally (3-D) interconnected ECM ligands. In highly motile human MV3 melanoma cells, both β1 integrins and CD44 are abundantly expressed, support migration across collagen and HA, respectively, and are deposited upon migration, whereas only β1 integrins but not CD44 redistribute to focal adhesions. In 3-D collagen lattices in the presence or absence of HA and cross-linking chondroitin sulfate, MV3 cell migration and associated functions such as polarization and matrix reorganization were blocked by anti-β1 and anti-α2 integrin mAbs, whereas mAbs blocking CD44, α3, α5, α6, or αv integrins showed no effect. With use of highly sensitive time-lapse videomicroscopy and computer-assisted cell tracking techniques, promigratory functions of CD44 were excluded. 1) Addition of HA did not increase the migratory cell population or its migration velocity, 2) blocking of the HA-binding Hermes-1 epitope did not affect migration, and 3) impaired migration after blocking or activation of β1 integrins was not restored via CD44. Because α2β1-mediated migration was neither synergized nor replaced by CD44–HA interactions, we conclude that the biophysical properties of 3-D multicomponent ECM impose more restricted molecular functions of adhesion receptors, thereby differing from haptokinetic migration across surfaces.

Angiogenesis promoted by vascular endothelial growth factor: Regulation through α1β1 and α2β1 integrins

Vascular endothelial growth factor (VEGF), also known as vascular permeability factor, is a cytokine of central importance for the angiogenesis associated with cancers and other pathologies. Because angiogenesis often involves endothelial cell (EC) migration and proliferation within a collagen-rich extracellular matrix, we investigated the possibility that VEGF promotes neovascularization through regulation of collagen receptor expression. VEGF induced a 5- to 7-fold increase in dermal microvascular EC surface protein expression of two collagen receptors—the α1β1 and α2β1 integrins—through induction of mRNAs encoding the α1 and α2 subunits. In contrast, VEGF did not induce increased expression of the α3β1 integrin, which also has been implicated in collagen binding. Integrin α1-blocking and α2-blocking antibodies (Ab) each partially inhibited attachment of microvascular EC to collagen I, and α1-blocking Ab also inhibited attachment to collagen IV and laminin-1. Induction of α1β1 and α2β1 expression by VEGF promoted cell spreading on collagen I gels which was abolished by a combination of α1-blocking and α2-blocking Abs. In vivo, a combination of α1-blocking and α2-blocking Abs markedly inhibited VEGF-driven angiogenesis; average cross-sectional area of individual new blood vessels was reduced 90% and average total new vascular area was reduced 82% without detectable effects on the pre-existing vasculature. These data indicate that induction of α1β1 and α2β1 expression by EC is an important mechanism by which VEGF promotes angiogenesis and that α1β1 and α2β1 antagonists may prove effective in inhibiting VEGF-driven angiogenesis in cancers and other important pathologies.

Molecular cytogenetic delineation of a novel critical genomic region in chromosome bands 11q22.3-923.1 in lymphoproliferative disorders.

Aberrations of the long arm of chromosome 11 are among the most common chromosome abnormalities in lymphoproliferative disorders (LPD). Translocations involving BCL1 at 11q13 are strongly associated with mantle cell lymphoma. other nonrandom aberrations, especially deletions and, less frequently, translocations, involving bands 11q21-923 have been identified by chromosome banding analysis. To date, the critical genomic segment and candidate genes involved in these deletions have not been identified. In the present study, we have analyzed tumors from 43 patients with LPD (B-cell chronic lymphocytic leukemia, n = 40; mantle cell lymphoma, n = 3) showing aberrations of bands 11q21-923 by fluorescence in situ hybridization. As probes we used Alu-PCR products from 17 yeast artificial chromosome clones spanning chromosome bands 11q14.3-923.3, including a panel of yeast artificial chromosome clones recognizing a contiguous genomic DNA fragment of approximately 9-10 Mb in bands 11q22.3-923.3. In the 41 tumors exhibiting deletions, we identified a commonly deleted segment in band 11q22.3-923.1; this region is approximately 2-3 Mb in size and contains the genes coding for ATM (ataxia telangiectasia mutated), RDX (radixin), and FDX1 (ferredoxin 1). Furthermore, two translocation break-points were localized to a 1.8-Mb genomic fragment contained within the commonly deleted segment. Thus, we have identified a single critical region of 2-3 Mb in size in which 11q14-923 aberrations in LPD cluster. This provides the basis for the identification of the gene(s) at 11q22.3-923.1 that are involved in the pathogenesis of LPD.

Sistemas y Procesos en Publicidad y Relaciones Públicas. Tema 3, parte 1 (curso 2011-2012)

Resumen del Tema 3 (parte 1), para los grupos 1,2,3 y 4.

Modifications post-traductionnelles des canaux calciques cardiaques de type L : identification des résidus asparagine qui participent à la glycosylation de la sous-unité auxiliaire CaVα2δ1

Les canaux calciques de type L CaV1.2 sont principalement responsables de l’entrée des ions calcium pendant la phase plateau du potentiel d’action des cardiomyocytes ventriculaires. Cet influx calcique est requis pour initier la contraction du muscle cardiaque. Le canal CaV1.2 est un complexe oligomérique qui est composé de la sous-unité principale CaVα1 et des sous-unités auxiliaires CaVβ et CaVα2δ1. CaVβ joue un rôle déterminant dans l’adressage membranaire de la sous-unité CaVα1. CaVα2δ1 stabilise l’état ouvert du canal mais le mécanisme moléculaire responsable de cette modulation n’a pas été encore identifié. Nous avons récemment montré que cette modulation requiert une expression membranaire significative de CaVα2δ1 (Bourdin et al. 2015). CaVα2δ1 est une glycoprotéine qui possède 16 sites potentiels de glycosylation de type N. Nous avons donc évalué le rôle de la glycosylation de type-N dans l’adressage membranaire et la stabilité de CaVα2δ1. Nous avons d’abord confirmé que la protéine CaVα2δ1 recombinante, telle la protéine endogène, est significativement glycosylée puisque le traitement à la PNGase F se traduit par une diminution de 50 kDa de sa masse moléculaire, ce qui est compatible avec la présence de 16 sites Asn. Il s’est avéré par ailleurs que la mutation simultanée de 6/16 sites (6xNQ) est suffisante pour 1) réduire significativement la densité de surface de! CaVα2δ1 telle que mesurée par cytométrie en flux et par imagerie confocale 2) accélérer les cinétiques de dégradation telle qu’estimée après arrêt de la synthèse protéique et 3) diminuer la modulation fonctionnelle des courants générés par CaV1.2 telle qu’évaluée par la méthode du « patch-clamp ». Les effets les plus importants ont toutefois été obtenus avec les mutants N663Q, et les doubles mutants N348Q/N468Q, N348Q/N812Q, N468Q/N812Q. Ensemble, ces résultats montrent que Asn663 et à un moindre degré Asn348, Asn468 et Asn812 contribuent à la biogenèse et la stabilité de CaVα2δ1 et confirment que la glycosylation de type N de CaVα2δ1 est nécessaire à la fonction du canal calcique cardiaque de type L.