912 resultados para ”we” identity
Resumo:
Pedro Giménez' is a white criolla variety cropped in Argentina, mainly in Mendoza and San Juan, being the most planted white variety destined for wine making in the country. Its origin remains unknown, as well as its relationship with Spanish variety 'Pedro Ximénez', mostly grown in Jerez, Spain. Previous works have probed that most of Criollas varieties existing in America at the moment, are the offspring of 'Muscat of Alexandria' x 'Criolla Chica'. The aim of the present work was to compare 'Pedro Giménez' with the Spanish variety 'Pedro Ximénez', and to establish its degree of relatedness to 'Muscat of Alexandria' and 'Criolla Chica'. Therefore we used a set of 18 nuclear SSR loci and 3 chloroplast SSR loci. 'Pedro Giménez' shared only 38% of the alleles under analysis with 'Pedro Ximénez', indicating that they are indeed two different varieties. In all 18 polymorphic nuclear SSR loci 'Pedro Giménez' shared 50% of its alleles with 'Muscat of Alexandria', while the other 50% of the alleles present in 'Pedro Giménez' were also present in 'Criolla Chica'. This data, along with those from the chloroplast SSR analysis, strongly suggest that 'Pedro Giménez' is the progeny of 'Muscat of Alexandria' x 'Criolla Chica', being the latest one the most likely female progenitor.
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Avian ecosystem services such as the suppression of pests are considered being of high ecological and economic importance in a range of ecosystems, especially in tropical agroforestry. But how bird predation success is related to the diversity and composition of the bird community, as well as local and landscape factors, is poorly understood. The author quantified arthropod predation in relation to the identity and diversity of insectivorous birds, using experimental exposure of artificial, caterpillar-like prey on smallholder cacao agroforestry systems, differing in local shade management and distance to primary forest. The bird community was assessed using both mist netting (targeting on active understory insectivores) and point count (higher completeness of species inventories) sampling. The study was conducted in a land use dominated area in Central Sulawesi, Indonesia, adjacent to the Lore Lindu National Park. We selected 15 smallholder cacao plantations as sites for bird and bat exclosure experiments in March 2010. Until July 2011, we recorded several data in this study area, including the bird community data, cacao tree data and bird predation experiments that are presented here. We found that avian predation success can be driven by single and abundant insectivorous species, rather than by overall bird species richness. Forest proximity was important for enhancing the density of this key species, but did also promote bird species richness. The availability of local shade trees had no effects on the local bird community or avian predation success. Our findings are both of economical as well as ecological interest because the conservation of nearby forest remnants will likely benefit human needs and biodiversity conservation alike.
Resumo:
Developmental commitment involves activation of lineage-specific genes, stabilization of a lineage-specific gene expression program, and permanent inhibition of inappropriate characteristics. To determine how these processes are coordinated in early T cell development, the expression of T and B lineage-specific genes was assessed in staged subsets of immature thymocytes. T lineage characteristics are acquired sequentially, with germ-line T cell antigen receptor-β transcripts detected very early, followed by CD3ɛ and terminal deoxynucleotidyl transferase, then pTα, and finally RAG1. Only RAG1 expression coincides with commitment. Thus, much T lineage gene expression precedes commitment and does not depend on it. Early in the course of commitment to the T lineage, thymocytes lose the ability to develop into B cells. To understand how this occurs, we also examined expression of well defined B lineage-specific genes. Although λ5 and Ig-α are not expressed, the μ0 and Iμ transcripts from the unrearranged IgH locus are expressed early, in distinct patterns, then repressed just before RAG1 expression. By contrast, RNA encoding the B cell receptor component Ig-β was found to be transcribed in all immature thymocyte subpopulations and throughout most thymocyte differentiation. Ig-β expression is down-regulated only during positive selection of CD4+CD8– cells. Thus several key participants in the B cell developmental program are expressed in non-B lineage-committed cells, and one is maintained even through commitment to an alternative lineage, and repressed only after extensive T lineage differentiation. The results show that transcriptional activation of “lymphocyte-specific” genes can occur in uncommitted precursors, and that T lineage commitment is a composite of distinct positive and negative regulatory events.
Resumo:
Sequence divergence acts as a potent barrier to homologous recombination; much of this barrier derives from an antirecombination activity exerted by mismatch repair proteins. An inverted repeat assay system with recombination substrates ranging in identity from 74% to 100% has been used to define the relationship between sequence divergence and the rate of mitotic crossing-over in yeast. To elucidate the role of the mismatch repair machinery in regulating recombination between mismatched substrates, we performed experiments in both wild-type and mismatch repair defective strains. We find that a single mismatch is sufficient to inhibit recombination between otherwise identical sequences, and that this inhibition is dependent on the mismatch repair system. Additional mismatches have a cumulative negative effect on the recombination rate. With sequence divergence of up to approximately 10%, the inhibitory effect of mismatches results mainly from antirecombination activity of the mismatch repair system. With greater levels of divergence, recombination is inefficient even in the absence of mismatch repair activity. In both wild-type and mismatch repair defective strains, an approximate log-linear relationship is observed between the recombination rate and the level of sequence divergence.
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A method for cell–cell and cell–liposome fusion at the single-cell level is described. Individual cells or liposomes were first selected and manipulated either by optical trapping or by adhesion to a micromanipulator-controlled ultramicroelectrode. Spatially selective fusion of the cell–cell or cell–liposome pair was achieved by the application of a highly focused electric field through a pair of 5-μm o.d. carbon-fiber ultramicroelectrodes. The ability to fuse together single cells opens new possibilities in the manipulation of the genetic and cellular makeup of individual cells in a controlled manner. In the study of cellular networks, for example, the alteration of the biochemical identity of a selected cell can have a profound effect on the behavior of the entire network. Fusion of a single liposome with a target cell allows the introduction of the liposomal content into the cell interior as well as the addition of lipids and membrane proteins onto the cell surface. This cell–liposome fusion represents an approach to the manipulation of the cytoplasmic contents and surface properties of single cells. As an example, we have introduced a membrane protein (γ-glutamyltransferase) reconstituted in liposomes into the cell plasma membrane.
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The several linked polymorphic genes of the MHC, which has been proposed as a prime determinant of sensed genetic individuality within species, is known to operate in mice by olfactory recognition in aspects of reproductive behavior that concern mate selection, thereby favoring outbreeding and heterozygosity, and also concern the maintenance of pregnancy. A single base-change can alter an individual MHC odortype, and the potential range of combinatorial MHC-determined odortypes is clearly vast. Following our findings that newborn mice already express their MHC odortype (which is detectable at 9 days of gestational age), we sought to determine whether MHC is involved in behavioral aspects of early development, such as rearing. In the studies presented herein, we report the ability and proclivity of mothers to recognize and preferentially retrieve syngeneic (genetically identical) pups from other pups differing only for MHC. Reciprocally, we report the ability of pups to recognize their familial environment, regardless of whether they had been nursed by their biological mothers or by foster mothers. Early learning experiences of the MHC environment are apparently a key element in survival, assuring maternal protection and promoting outbreeding.
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The vegetative development of the maize shoot can be divided into juvenile and adult phases based on the types of leaves produced at different times in shoot development. Models for the regulation of phase change make explicit predictions about when the identity of these types of leaves is determined. To test these models, we examined the timing of leaf type determination in maize. Clones induced in transition leaf primordia demonstrated that the juvenile and adult regions of these leaves do not become clonally distinct until after the primordium is 700 μm in length, implying that these cell fates were undetermined at this stage of leaf development. Adult shoot apices were cultured in vitro to induce rejuvenation. We found that leaf primordia as large as 3 mm in length can be at least partially rejuvenated by this treatment, and the location of rejuvenated tissue is correlated with the maturation pattern of the leaf. The amount and distribution of juvenile tissue in rejuvenated leaves suggests that rejuvenation occurs nearly simultaneously in all leaf primordia. In vitro culture rejuvenated existing leaf primordia and the P0 primordium, but did not change the identity of subsequent primordia or the total number of leaves produced by the shoot. This result suggests that leaf identity can be regulated independently of the identity of the shoot apical meristem, and it implies that vegetative phase change is not initiated by a change in the identity of the shoot apical meristem.
Resumo:
Advanced glycation endproducts (AGEs) are derivatives of nonenzymatic reactions between sugars and protein or lipids, and together with AGE-specific receptors are involved in numerous pathogenic processes associated with aging and hyperglycemia. Two of the known AGE-binding proteins isolated from rat liver membranes, p60 and p90, have been partially sequenced. We now report that the N-terminal sequence of p60 exhibits 95% identity to OST-48, a 48-kDa member of the oligosaccharyltransferase complex found in microsomal membranes, while sequence analysis of p90 revealed 73% and 85% identity to the N-terminal and internal sequences, respectively, of human 80K-H, a 80- to 87-kDa protein substrate for protein kinase C. AGE-ligand and Western analyses of purified oligosaccharyltransferase complex, enriched rough endoplasmic reticulum, smooth endoplasmic reticulum, and plasma membranes from rat liver or RAW 264.7 macrophages yielded a single protein of approximately 50 kDa recognized by both anti-p60 and anti-OST-48 antibodies, and also exhibited AGE-specific binding. Immunoprecipitated OST-48 from rat rough endoplasmic reticulum fractions exhibited both AGE binding and immunoreactivity to an anti-p60 antibody. Immune IgG raised to recombinant OST-48 and 80K-H inhibited binding of AGE-bovine serum albumin to cell membranes in a dose-dependent manner. Immunostaining and flow cytometry demonstrated the surface expression of OST-48 and 80K-H on numerous cell types and tissues, including mononuclear, endothelial, renal, and brain neuronal and glial cells. We conclude that the AGE receptor components p60 and p90 are identical to OST-48, and 80K-H, respectively, and that they together contribute to the processing of AGEs from extra- and intracellular compartments and in the cellular responses associated with these pathogenic substances.
Resumo:
High molecular weight kininogen (HK) and factor XII are known to bind to human umbilical vein endothelial cells (HUVEC) in a zinc-dependent and saturable manner indicating that HUVEC express specific binding site(s) for those proteins. However, identification and immunochemical characterization of the putative receptor site(s) has not been previously accomplished. In this report, we have identified a cell surface glycoprotein that is a likely candidate for the HK binding site on HUVECs. When solubilized HUVEC membranes were subjected to an HK-affinity column in the presence or absence of 50 microM ZnCl2 and the bound membrane proteins eluted, a single major protein peak was obtained only in the presence of zinc. SDS/PAGE analysis and silver staining of the protein peak revealed this protein to be 33 kDa and partial sequence analysis matched the NH2 terminus of gC1q-R, a membrane glycoprotein that binds to the globular "heads" of C1q. Two other minor proteins of approximately 70 kDa and 45 kDa were also obtained. Upon analysis by Western blotting, the 33-kDa band was found to react with several monoclonal antibodies (mAbs) recognizing different epitopes on gC1q-R. Ligand and dot blot analyses revealed zinc-dependent binding of biotinylated HK as well as biotinylated factor XII to the isolated 33-kDa HUVEC molecule as well as recombinant gC1q-R. In addition, binding of 125I-HK to HUVEC cells was inhibited by selected monoclonal anti-gC1q-R antibodies. C1q, however, did not inhibit 125I-HK binding to HUVEC nor did those monoclonals known to inhibit C1q binding to gC1q-R. Taken together, the data suggest that HK (and factor XII) bind to HUVECs via a 33-kDa cell surface glycoprotein that appears to be identical to gC1q-R but interact with a site on gC1q-R distinct from that which binds C1q.
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Sequence-specific interactions between aminoacyl-tRNA synthetases and their cognate tRNAs both ensure accurate RNA recognition and prevent the binding of noncognate substrates. Here we show for Escherichia coli glutaminyl-tRNA synthetase (GlnRS; EC 6.1.1.18) that the accuracy of tRNA recognition also determines the efficiency of cognate amino acid recognition. Steady-state kinetics revealed that interactions between tRNA identity nucleotides and their recognition sites in the enzyme modulate the amino acid affinity of GlnRS. Perturbation of any of the protein-RNA interactions through mutation of either component led to considerable changes in glutamine affinity with the most marked effects seen at the discriminator base, the 10:25 base pair, and the anticodon. Reexamination of the identity set of tRNA(Gln) in the light of these results indicates that its constituents can be differentiated based upon biochemical function and their contribution to the apparent Gibbs' free energy of tRNA binding. Interactions with the acceptor stem act as strong determinants of tRNA specificity, with the discriminator base positioning the 3' end. The 10:25 base pair and U35 are apparently the major binding sites to GlnRS, with G36 contributing both to binding and recognition. Furthermore, we show that E. coli tryptophanyl-tRNA synthetase also displays tRNA-dependent changes in tryptophan affinity when charging a noncognate tRNA. The ability of tRNA to optimize amino acid recognition reveals a novel mechanism for maintaining translational fidelity and also provides a strong basis for the coevolution of tRNAs and their cognate synthetases.
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The Arabidopsis MADS domain proteins AP1, AP3, PI, and AG specify floral organ identity. All of these proteins contain a MADS domain required for DNA binding and dimerization; a region termed L (linker between MADS domain and K domain), which plays an important role in dimerization specificity; the K domain, named for its similarity to the coiled-coil domain of keratin; and a C-terminal region of unknown function. To determine which regions of these proteins are responsible for their abilities to specify different organs, we have made a number of chimeric MADS box genes. The in vivo function of these chimeric genes was investigated by ectopic expression in transgenic Arabidopsis plants. The four proteins fall into two classes on the basis of regions responsible for their functional specificities. The L region and K domain define the functional specificities of AP3 and PI, while the MADS domain and L region define the functional specificities of AP1 and AG.
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In my previous article Racial Capitalism, I examined the ways in which white individuals and predominantly white institutions derive value from non-white racial identity. This process flows from our intense social and legal preoccupation with diversity. And it results in the commodification of non-white racial identity, with negative implications for both individuals and society. This Article picks up where Racial Capitalism left off in three ways. As a foundation, it first expands the concept of racial capitalism to identity categories more generally, explaining that individual in-group members and predominantly in-group institutions — usually individuals or institutions that are white, male, straight, wealthy, and so on — can and do derive value from out-group identities. Second, the Article turns from the overarching system of identity capitalism to the myriad ways that individual out-group members actively participate in that system. In particular, I examine how out-group members leverage their out-group status to derive social and economic value for themselves. I call such out-group participants identity entrepreneurs. Identity entrepreneurship is neither inherently good nor inherently bad. Rather, it is a complicated phenomenon with both positive and negative consequences. Finally, the Article considers the appropriate response to identity entrepreneurship. We should design laws and policies to maximize both individual agency and access to information for out-group members. Such reforms would protect individual choice while making clear the consequences of identity entrepreneurship both for individual identity entrepreneurs and for the out-group as a whole. A range of legal doctrines interact with and influence identity entrepreneurship, including employment discrimination under Title VII, rights of privacy and publicity, and intellectual property. Modifying these doctrines to take account of identity entrepreneurship will further progress toward an egalitarian society in which in-group and out-group identities are valued equally.
Proximodistal identity during vertebrate limb regeneration is regulated by Meis homeodomain proteins
Resumo:
The mechanisms by which cells obtain instructions to precisely re-create the missing parts of an organ remain an unresolved question in regenerative biology. Urodele limb regeneration is a powerful model in which to study these mechanisms. Following limb amputation, blastema cells interpret the proximal-most positional identity in the stump to reproduce missing parts faithfully. Classical experiments showed the ability of retinoic acid (RA) to proximalize blastema positional values. Meis homeobox genes are involved in RA-dependent specification of proximal cell identity during limb development. To understand the molecular basis for specifying proximal positional identities during regeneration, we isolated the axolotl Meis homeobox family. Axolotl Meis genes are RA-regulated during both regeneration and embryonic limb development. During limb regeneration, Meis overexpression relocates distal blastema cells to more proximal locations, whereas Meis knockdown inhibits RA proximalization of limb blastemas. Meis genes are thus crucial targets of RA proximalizing activity on blastema cells.
Resumo:
Recent research indicates that social identity theory offers an important lens to improve our understanding of founders as enterprising individuals, the venture creation process, and its outcomes. Yet, further advances are hindered by the lack of a valid scale that could be used to measure founders' social identities - a problem that is particularly severe because social identity is a multidimensional construct that needs to be assessed properly so that organizational phenomena can be understood. Drawing on social identity theory and the systematic classification of founders' social identities (Darwinians, Communitarians, Missionaries) provided in Fauchart and Gruber (2011), this study develops and empirically validates a 12-item scale that allows scholars to capture the multidimensional nature of social identities of entrepreneurs. Our validation tests are unusually comprehensive and solid, as we not only validate the developed scale in the Alpine region (where it was originally conceived), but also in 12 additional countries and the Anglo-American region. Scholars can use the scale to identify founders' social identities and to relate these identities to micro-level processes and outcomes in new firm creation. Scholars may also link founders' social identities to other levels of analysis such as industries (e.g., industry evolution) or whole economies (e.g., economic growth).
Resumo:
Social identity theory offers an important lens to improve understanding of founders as enterprising individuals, the venture creation process, and its outcomes. Yet, further advances are hindered by the lack of valid scales to measure founders’ social identities. Drawing on social identity theory and a systematic classification of founders’ social identities (Darwinians, Communitarians, and Missionaries), we develop and test a corresponding 15-item scale in the Alpine region and validate it in 13 additional countries and regions. The scale allows identifying founders’ social identities and relating them to processes and outcomes in entrepreneurship. The scale is available online in 15 languages.