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121.
1.?A major goal in community ecology is to identify mechanisms that govern the assembly and maintenance of ecological communities. Current models of metacommunity dynamics differ chiefly in the relative emphasis placed on dispersal limitation and niche differentiation as causal mechanisms structuring ecological communities. Herein we investigate the relative roles of these two mechanisms in structuring primate communities in Africa, South America, Madagascar and Borneo. 2.?We hypothesized that if dispersal limitation is important in structuring communities, then community similarity should depend on geographical proximity even after controlling for ecological similarity. Conversely, if communities are assembled primarily through niche processes, then community similarity should be determined by ecological similarity regardless of geographical proximity. 3.?We performed Mantel and partial Mantel tests to investigate correlations among primate community similarity, ecological distance and geographical distance. Results showed significant and strongly negative relationships between diurnal primate community similarity and both ecological similarity and geographical distance in Madagascar, but significant and stronger negative relationships between community similarity and geographical distance in African, South American and Bornean metacommunities. 4.?We conclude that dispersal limitation is an important determinant of primate community structure and may play a stronger role in shaping the structure of some terrestrial vertebrate communities than niche differentiation. These patterns are consistent with neutral theory. We recommend tests of functional equivalence to determine the extent to which neutral theory may explain primate community composition.  相似文献   
122.
Hepatic δ-aminolevulinic acid synthetase was induced in rats injected with allylisopropylacetamide. The induction process was studied in relation to experimental perturbation of cytochrome P-450 in the liver. Animals were treated with either administered endotoxin or exogenous heme, both of which accelerate degradation of cytochrome P-450 heme. These manipulations were effective in blocking induction of δ-aminolevulinic acid synthetase, and the effect of each compound was proportional to its ability to stimulate degradation of cytochrome P-450 heme. The findings suggest that the heme moiety of cytochrome P-450 dissociates reversibly from its apoprotein and, prior to its degradation, mixes with endogenously synthesized heme to form a pool that regulates δ-aminolevulinic acid synthetase activity. A similar or identical heme fraction appears to mediate stimulation of heme oxygenase, which suggests that the regulation of δ-aminolevulinic acid synthetase and of heme oxygenase in the liver are closely interrelated.  相似文献   
123.
A series of ligands with varying heterocyclic cores and substituents that display a range of selectivity’s (up to >100x) for ER-β over ER- are reported.  相似文献   
124.
125.
The O-antigen (rfb) operon and related genes of MA6, an O rough:H7 Shiga-toxigenic Escherichia coli strain, were examined to determine the cause of the lack of O157 expression. A 1,310-bp insertion, homologous to IS629, was observed within its gne gene. trans complementation with a functional gne gene from O157:H7 restored O157 antigen expression in MA6.Shiga-toxigenic Escherichia coli (STEC) serotype O157:H7 carries O157 and H7 antigens, so these traits are extensively used in identification (1). Strain MA6, isolated from beef in Malaysia (8), carries the O157:H7 virulence factor genes, including the Shiga toxin 2 gene (stx2), the γ intimin allele (γ-eae), the enterohemolysin gene (ehxA), and the +93 uidA single nucleotide polymorphism (SNP) found only in O157:H7 strains (1). Multilocus sequence typing also showed MA6 to have the most common sequence type (ST-66) for O157:H7 strains. However, and in spite the fact that MA6 had per gene sequences essential for O157 antigen synthesis (2), no O157 antigen is expressed (O rough), and therefore, it is undetectable with serological assays used in O157:H7 analysis.The biosynthesis and assembly of E. coli O antigen are highly complex (9). The rfb operon (12 genes) (16), along with 3 ancillary genes outside of the rfb, is required for the biosynthesis of the 4 sugar nucleotide precursors and the assembly of the O unit (11). This is then linked to the core antigen, comprising an inner and an outer component, which require 3 other operons for biosynthesis and assembly (9). As defects in any of these genes could produce the O-null phenotype (13), we systematically examined these genes (Table (Table1)1) to elucidate the cause of the absence of O157 expression in MA6.

TABLE 1.

rfb operon genes, ancillary genes, and waa cluster genes examined in this study
CategoryGeneral functionaGene(s)
O-antigen (rfb) operonNucleotide sugar transferwbdN, wbdO, wbdP, wbdQ, wbdR
O-unit processingwzy, wzx
Nucleotide sugar synthesisper, gmd, fcl, manC, manB
waa core gene clustersStructure modificationwaaQ, waaP, waaY
Nucleotide sugar transferrfaG, rfaC
LPS core biosynthesis enzymewaaI, waaJ, waaD, waaL
Ancillary genesNucleotide sugar synthesismanA
O-unit processingwecA
Nucleotide sugar synthesisgne
Open in a separate windowaLPS, lipopolysaccharide.PCR and sequencing primers for the individual genes were designed from sequences for the O157:H7 strain EDL933 (GenBank accession no. AE005174). The 50-μl PCR mix contained 5 U of HotStar Taq (Qiagen, Valencia, CA), 1× polymerase buffer, 2.5 to 3.5 mM MgCl2, 400 μM each dNTP, 300 nM of each primer, and ∼100 ng of template DNA from either MA6 or the EDL931 reference strain. The “touchdown” PCR (10) consisted of 95°C for 15 min and 10 cycles of 95°C for 30 s, 69 to 60°C (−1°C/cycle) for 20 s, and 72°C for 1.5 min, followed by 35 cycles of 95°C for 30 s, 60°C for 20 s, and 72°C for 1.5 min, with a single step of 72°C for 1 min for final extension. Products were examined on a 1% agarose gel in Tris-borate-EDTA (TBE) buffer. Comparison of amplicons from respective genes from MA6 and EDL931 showed that no gross differences in size were observed for any of the rfb or related genes, suggesting the absence of major insertions or deletions. Consistently, contigs assembled from the MA6 amplicon were identical in sequence to those of EDL933 in GenBank, indicating the absence of base mutations in either the promoter or any of the open reading frames (ORF). One exception was the gne gene, encoding UDP-acetylgalactosamine (GalNAc)-4-epimerase, which is essential for the synthesis of one of the oligosaccharide subunits in the O antigen (14). When PCR primers that bound upstream of the putative promoter and downstream of the gne gene were used, an expected ∼1,400-bp product was obtained from EDL931 (Fig. (Fig.1,1, lane 3), but the MA6 amplicon was ∼2,700 bp (Fig. (Fig.1,1, lane 4). PCR of other O157:H7 strains all yielded the ∼1,400-bp product, while MA6 consistently produced the larger amplicon. Comparison of sequences to that of EDL933 showed the presence of a 1,310-bp insertion within the MA6 gne ORF at +385 that shared 96% homology to the insertion sequence 629 (IS629) (accession no. X51586) element. Furthermore, the deduced protein sequences for the putative orfA and orfB genes on the insert were 100% and 99% identical to those of the IS629 transposase in O157:H7 strains Sakai (accession no. NC_002695), and EDL933 and EC4115 (accession no. NC_011353), respectively.Open in a separate windowFIG. 1.Agarose gel electrophoresis of gne amplicons derived from EDL931 (O157:H7) and MA6. Lanes: 1, exACTGene (1 kb) plus molecular size ladder (Fisher BioReagents, Pittsburgh, PA); 2, negative control (reaction mix without DNA template); 3, EDL931; 4, MA6.To determine whether gne::IS629 (accession no. GU183138) caused the absence of O157 expression in MA6, the wild-type EDL931 gne ORF was amplified using primers that added BamHI and SacI restriction sites at the 5′ and 3′ termini, respectively. The purified amplicon was digested accordingly, ligated into pTrc99A vector (Stratagene, La Jolla, CA), and electroporated into E. coli DH5α (10). Transformants were selected on LB plates with 100 μg/ml ampicillin (Amp). Colonies that were Amp resistant (Ampr) were PCR amplified with vector-specific primers, and those carrying the insert were sequenced to confirm the presence of the wild-type gne insert in the construct (pGNE). For trans-complementation studies, pGNE was electroporated into MA6. Ampr transformants were PCR amplified with vector-specific primers as well as primers that annealed to sequences outside the gne gene and also not present on the vector, to confirm that they carried both pGNE and the gne::IS629 locus. Serological testing with the RIM O157:H7 latex kit (Remel, Lenexa, KS) confirmed that the Ampr MA6 transformants expressed O157 antigen.These results confirmed that gne::IS629 caused the O rough phenotype of MA6. Originally isolated from Shigella sonnei (7), IS629 has since been found, often in multiple copies, to cause gene disruptions in other enteric bacteria (6). fliC::IS629 caused nonmotility of an E. coli O111 strain (17), and wbaM::IS629 resulted in an O rough Shigella boydii strain (15). The IS629 recognition site remains unknown (5), so it is uncertain that there is an IS629 hot spot within the O157:H7 gne ORF. Other bacteria, like O157:H7, also have the gne gene positioned upstream of the rfb operon (12), but no gne::IS629 rough strains of these have been reported. This suggests that the IS629 insertion site within the gne of MA6 may have occurred as a result of a random mutation and that MA6 appears to be the only naturally occurring O rough O157:H7 strain that resulted from the gne::IS629 insertion.The O antigen is not required for growth but does confer protection (9), so the loss of the O antigen has been reported to make pathogens serum sensitive or less virulent (4). If that is so, we would expect MA6 to be less pathogenic than O157:H7; consistent with that speculation, MA6 has not been implicated in illness. Even so, while no O rough O157:H7 strains have caused disease, other O rough STEC strains have caused illnesses (3); hence, the virulence potential of MA6 remains undetermined.In conclusion, the absence of O157 antigen expression by MA6 is caused by gne::IS629. Occurrence of O rough:H7 strains like MA6 in food or clinical samples is of concern, as they are undetectable by the serological assays used to identify O157:H7. However, the IS629 insertion site within the O157:H7 gne ORF appears to have been due to a random mutational event, and therefore, MA6-like O rough mutants of O157:H7 are thus far uncommon.  相似文献   
126.
Laminins (comprised of alpha, beta, and gamma chains) are heterotrimeric glycoproteins integral to all basement membranes. The function of the laminin alpha5 chain in the developing intestine was defined by analysing laminin alpha5(-/-) mutants and by grafting experiments. We show that laminin alpha5 plays a major role in smooth muscle organisation and differentiation, as excessive folding of intestinal loops and delay in the expression of specific markers are observed in laminin alpha5(-/-) mice. In the subepithelial basement membrane, loss of alpha5 expression was paralleled by ectopic or accelerated deposition of laminin alpha2 and alpha4 chains; this may explain why no obvious defects were observed in the villous form and enterocytic differentiation. This compensation process is attributable to mesenchyme-derived molecules as assessed by chick/mouse alpha5(-/-) grafted associations. Lack of the laminin alpha5 chain was accompanied by a decrease in epithelial alpha3beta1 integrin receptor expression adjacent to the epithelial basement membrane and of Lutheran blood group glycoprotein in the smooth muscle cells, indicating that these receptors are likely mediating interactions with laminin alpha5-containing molecules. Taken together, the data indicate that the laminin alpha5 chain is essential for normal development of the intestinal smooth muscle and point to possible mesenchyme-derived compensation to promote normal intestinal morphogenesis when laminin alpha5 is absent.  相似文献   
127.
Almost all real-life decisions entail attribute conflict; every serious choice alternative is better than its competitors on some attribute dimensions but worse on others. In pre-decisional “coherence shifting,” the decision maker gradually softens that conflict psychologically to the point where one alternative is seen as dominant over its competitors, or nearly so. Specifically, weaknesses of the eventually chosen alternative come to be perceived as less severe and less important while its strengths seem more desirable and significant. The research described here demonstrates that difficult multiattribute decision problems are aversive and that pre-decisional coherence shifting aids individuals in regulating that emotional discomfort. Across three studies, attribute conflict was confirmed to be aversive (Study 1), and skin conductance responses and ratings of decision difficulty both decreased in participants who coherence shifted (Study 2). Coherence shifting was also diminished among decision makers who were depleted of regulatory resources, known to be required for common emotion regulation mechanisms. Further, coherence shifting was shown to be relatively common among people who reported strong suppression tendencies in everyday emotion regulation (Study 3). Overall, the data suggest that, at least in part, coherence shifting serves as a tool that helps decision makers manage the pre-decisional discomfort generated by attribute conflict. Theoretical and practical implications are discussed.  相似文献   
128.
The Tertiary relic genus Catalpa, containing 11 Old and New World species, has multiple nectaries in the junctions of the major veins on the lower leaf surfaces. The generalized structure of the nectaries consists of a single, basal cell, and a single row of vertically oriented secretory cells. The nectaries are small, and contain no vascular tissue. Glandular and nonglandular trichomes are also present on the leaves. The glandular trichomes are structurally very similar to the nectaries, and probably are their precursors. Development of multiple nectaries in the lower leaf surface vein axils is considered to be an advanced strategy for attracting beneficial insects to control or minimize the effects of herbivorous insects. Chinese and American species of Catalpa are closely related, and have greater numbers of nectaries in more locations on the lower leaf surface than west Indian species. Herbivory pressures in the West Indies are postulated to be lower than on the continents, i.e. Asia and North America.  相似文献   
129.
Ppz Ser/Thr protein phosphatases (PPases) are found only in fungi and have been proposed as potential antifungal targets. In Saccharomyces cerevisiae Ppz1 (ScPpz1) is involved in regulation of monovalent cation homeostasis. ScPpz1 is inhibited by two regulatory proteins, Hal3 and Vhs3, which have moonlighting properties, contributing to the formation of an unusual heterotrimeric PPC decarboxylase (PPCDC) complex crucial for CoA biosynthesis. Here we report the functional characterization of CnPpz1 (CNAG_03673) and two possible Hal3‐like proteins, CnHal3a (CNAG_00909) and CnHal3b (CNAG_07348) from the pathogenic fungus Cryptococcus neoformans. Deletion of CnPpz1 or CnHal3b led to phenotypes unrelated to those observed in the equivalent S. cerevisiae mutants, and the CnHal3b‐deficient strain was less virulent. CnPpz1 is a functional PPase and partially replaced endogenous ScPpz1. Both CnHal3a and CnHal3b interact with ScPpz1 and CnPpz1 in vitro but do not inhibit their phosphatase activity. Consistently, when expressed in S. cerevisiae, they poorly reproduced the Ppz1‐regulatory properties of ScHal3. In contrast, both proteins were functional monogenic PPCDCs. The CnHal3b isoform was crystallized and, for the first time, the 3D‐structure of a fungal PPCDC elucidated. Therefore, our work provides the foundations for understanding the regulation and functional role of the Ppz1‐Hal3 system in this important pathogenic fungus.  相似文献   
130.
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