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排序方式: 共有813条查询结果,搜索用时 343 毫秒
91.
Ann F. Budd Flavia L. D. Nunes Ernesto Weil John M. Pandolfi 《Evolutionary ecology》2012,26(2):265-290
Recent advances in morphometrics and genetics have led to the discovery of numerous cryptic species in coral reef ecosystems.
A prime example is the Montastraea annularis scleractinian coral species complex, in which morphological, genetic, and reproductive data concur on species boundaries,
allowing evaluation of long-term patterns of speciation and evolutionary innovation. Here we test for cryptic species in the
Atlantic species, Montastraea cavernosa, long recognized as polymorphic. Our modern samples consist of 94 colonies collected at four locations (Belize, Panamá, Puerto
Rico in the Caribbean; S?o Tomé in the Eastern Atlantic). Our fossil samples consist of 78 colonies from the Plio-Pleistocene
of Costa Rica and Panamá. Landmark morphometric data were collected on thin sections of 46 modern and 78 fossil colonies.
Mahalanobis distances between colonies were calculated using Bookstein coordinates, revealing two modern and four fossil morphotypes.
The remaining 48 of the 94 modern colonies were assigned to morphotype using discriminant analysis of calical measurements.
Cross-tabulation and multiple comparisons tests show no significant morphological differences among geographic locations or
water depths. Patterns of variation within and among fossil morphotypes are similar to modern morphotypes. DNA sequence data
were collected for two polymorphic nuclear loci (β-tub1 and β-tub2) on all 94 modern colonies. Haplotype networks show that both genes consist of two clades, but morphotypes are not associated
with genetic clades. Genotype frequencies and two-locus genotype assignments indicate genetic exchange across clades, and
ϕst values show no genetic differentiation between morphotypes at different locations. Taken together, our morphological and
genetic results do not provide evidence for cryptic species in M. cavernosa, but indicate instead that this species has an unusually high degree of polymorphism over a wide geographic area and persisting
for >25 million years (myr). 相似文献
92.
H Inuzuka D Gao LW Finley W Yang L Wan H Fukushima YR Chin B Zhai S Shaik AW Lau Z Wang SP Gygi K Nakayama J Teruya-Feldstein A Toker MC Haigis PP Pandolfi W Wei 《Cell》2012,150(1):179-193
Aberrant Skp2 signaling has been implicated as a driving event in tumorigenesis. Although the underlying molecular mechanisms remain elusive, cytoplasmic Skp2 correlates with more aggressive forms of breast and prostate cancers. Here, we report that Skp2 is acetylated by p300 at K68 and K71, which is a process that can be antagonized by the SIRT3 deacetylase. Inactivation of SIRT3 leads to elevated Skp2 acetylation, which leads to increased Skp2 stability through impairment of the Cdh1-mediated proteolysis pathway. As a result, Skp2 oncogenic function is increased, whereby cells expressing an acetylation-mimetic mutant display enhanced cellular proliferation and tumorigenesis in vivo. Moreover, acetylation of Skp2 in the nuclear localization signal (NLS) promotes its cytoplasmic retention, and cytoplasmic Skp2 enhances cellular migration through ubiquitination and destruction of E-cadherin. Thus, our study identifies an acetylation-dependent regulatory mechanism governing Skp2 oncogenic function and provides insight into how cytoplasmic Skp2 controls cellular migration. 相似文献
93.
Manion M Rodriguez B Medvik K Hardy G Harding CV Schooley RT Pollard R Asmuth D Murphy R Barker E Brady KE Landay A Funderburg N Sieg SF Lederman MM 《PloS one》2012,7(1):e30306
Background
Type I interferons play important roles in innate immune defense. In HIV infection, type I interferons may delay disease progression by inhibiting viral replication while at the same time accelerating disease progression by contributing to chronic immune activation.Methods
To investigate the effects of type I interferons in HIV-infection, we obtained cryopreserved peripheral blood mononuclear cell samples from 10 subjects who participated in AIDS Clinical Trials Group Study 5192, a trial investigating the activity of systemic administration of IFNα for twelve weeks to patients with untreated HIV infection. Using flow cytometry, we examined changes in cell cycle status and expression of activation antigens by circulating T cells and their maturation subsets before, during and after IFNα treatment.Results
The proportion of CD38+HLA-DR+CD8+ T cells increased from a mean of 11.7% at baseline to 24.1% after twelve weeks of interferon treatment (p = 0.006). These frequencies dropped to an average of 20.1% six weeks after the end of treatment. In contrast to CD8+ T cells, the frequencies of activated CD4+ T cells did not change with administration of type I interferon (mean percentage of CD38+DR+ cells = 2.62% at baseline and 2.17% after 12 weeks of interferon therapy). As plasma HIV levels fell with interferon therapy, this was correlated with a “paradoxical” increase in CD8+ T cell activation (p<0.001).Conclusion
Administration of type I interferon increased expression of the activation markers CD38 and HLA DR on CD8+ T cells but not on CD4+ T cells of HIV+ persons. These observations suggest that type I interferons may contribute to the high levels of CD8+ T cell activation that occur during HIV infection. 相似文献94.
Hobbs RM Fagoonee S Papa A Webster K Altruda F Nishinakamura R Chai L Pandolfi PP 《Cell Stem Cell》2012,10(3):284-298
95.
The growth rate hypothesis (GRH) links growth rates with organism elemental stoichiometry. Support for the GRH was found for many animal species, but less so for plants. This is the first study to test the GRH in macroalgae. Tropical coral reef macroalgae from three lineages, Caulerpa serrulata (Chlorophyta), Laurencia intricata (Rhodophyta), and Sargassum polyphyllum (Phaeophyceae) were grown enriched with nitrogen or phosphorous and under control conditions at Heron Island on the Great Barrier Reef, Australia. Growth rate, photosynthesis, nucleic acid composition, and elemental stoichiometry were measured. Nutrient enrichment had positive effects on photosynthetic rates and on investment in RNA. However, growth rate was not correlated with either photosynthetic rates or RNA content; thus, we did not find support for the GRH in tropical macroalgae. Macroalgae, especially L. intricata, accumulated P to very high levels (>0.6% of dry weight). The growth rate response to tissue P concentrations was unimodal. Above 0.21%, P accumulation had negative effects on growth. Nitrogen was not stored, but evidence of futile cycling was observed. The capacity to store large amounts of P is probably an adaptation to the low and patchy nutrient environment of the tropical oceans. 相似文献
96.
M Pedrazzi M Averna B Sparatore M Patrone F Salamino M Marcoli G Maura C Cervetto D Frattaroli S Pontremoli E Melloni 《PloS one》2012,7(8):e44518
Background
Extracellular high mobility group box 1 (HMGB1) protein can operate in a synergistic fashion with different signal molecules promoting an increase of cell Ca2+ influx. However, the mechanisms responsible for this effect of HMGB1 are still unknown.Principal Findings
Here we demonstrate that, at concentrations of agonist per se ineffective, HMGB1 potentiates the activation of the ionotropic glutamate N-methyl-D-aspartate receptor (NMDAR) in isolated hippocampal nerve terminals and in a neuroblastoma cell line. This effect was abolished by the NMDA channel blocker MK-801. The HMGB1-facilitated NMDAR opening was followed by activation of the Ca2+-dependent enzymes calpain and nitric oxide synthase in neuroblastoma cells, resulting in an increased production of NO, a consequent enhanced cell motility, and onset of morphological differentiation. We have also identified NMDAR as the mediator of HMGB1-stimulated murine erythroleukemia cell differentiation, induced by hexamethylenebisacetamide. The potentiation of NMDAR activation involved a peptide of HMGB1 located in the B box at the amino acids 130–139. This HMGB1 fragment did not overlap with binding sites for other cell surface receptors of HMGB1, such as the advanced glycation end products or the Toll-like receptor 4. Moreover, in a competition assay, the HMGB1(130–139) peptide displaced the NMDAR/HMGB1 interaction, suggesting that it comprised the molecular and functional site of HMGB1 regulating the NMDA receptor complex.Conclusion
We propose that the multifunctional cytokine-like molecule HMGB1 released by activated, stressed, and damaged or necrotic cells can facilitate NMDAR-mediated cell responses, both in the central nervous system and in peripheral tissues, independently of other known cell surface receptors for HMGB1. 相似文献97.
Maura D Morello E du Merle L Bomme P Le Bouguénec C Debarbieux L 《Environmental microbiology》2012,14(8):1844-1854
Bacteriophages have been known to be present in the gut for many years, but studies of relationships between these viruses and their hosts in the intestine are still in their infancy. We isolated three bacteriophages specific for an enteroaggregative O104:H4 Escherichia coli (EAEC) strain responsible for diarrhoeal diseases in humans. We studied the replication of these bacteriophages in vitro and in vivo in a mouse model of gut colonization. Each bacteriophage was able to replicate in vitro in both aerobic and anaerobic conditions. Each bacteriophage individually reduced biofilms formed on plastic pegs and a cocktail of the three bacteriophages was found to be more efficient. The cocktail was also able to infect bacterial aggregates formed on the surface of epithelial cells. In the mouse intestine, bacteriophages replicated for at least 3 weeks, provided the host was present, with no change in host levels in the faeces. This model of stable and continuous viral replication provides opportunities for studying the long-term coevolution of virulent bacteriophages with their hosts within a mammalian polymicrobial ecosystem. 相似文献
98.
99.
Marcoli M Cervetto C Paluzzi P Guarnieri S Alloisio S Thellung S Nobile M Maura G 《Journal of neurochemistry》2008,105(6):2330-2342
Although growing evidence suggests that extracellular ATP might play roles in the control of astrocyte/neuron crosstalk in the CNS by acting on P2X7 receptors, it is still unclear whether neuronal functions can be attributed to P2X7 receptors. In the present paper, we investigate the location, pharmacological profile, and function of P2X7 receptors on cerebrocortical nerve terminals freshly prepared from adult rats, by measuring glutamate release and calcium accumulation. The preparation chosen (purified synaptosomes) ensures negligible contamination of non-neuronal cells and allows exposure of 'nude' release-regulating pre-synaptic receptors. To confirm the results obtained, we also carried out specific experiments on human embryonic kidney 293 cells which had been stably transfected with rat P2X7 receptors. Together, our findings suggest that (i) P2X7 receptors are present in a subpopulation of adult rat cerebrocortical nerve terminals; (ii) P2X7 receptors are localized on glutamatergic nerve terminals; (iii) P2X7 receptors play a significant role in ATP-evoked glutamate efflux, which involves Ca2+ -dependent vesicular release; and (iv) the P2X7 receptor itself constitutes a significant Ca2+ -independent mode of exit for glutamate. 相似文献
100.
The effect of deleting p110delta on the phenotype and function of PTEN-deficient B cells 总被引:3,自引:0,他引:3
Janas ML Hodson D Stamataki Z Hill S Welch K Gambardella L Trotman LC Pandolfi PP Vigorito E Turner M 《Journal of immunology (Baltimore, Md. : 1950)》2008,180(2):739-746
Control of the intracellular levels of phosphatidylinositol-(3, 4, 5)-trisphosphate by PI3K and phosphatase and tensin homolog (PTEN) is essential for B cell development and differentiation. Deletion of the PI3K catalytic subunit p110delta leads to a severe reduction in B1 and marginal zone (MZ) B cells, whereas deletion of PTEN results in their expansion. We have examined the relationship between these two molecules by generating mice with a B cell-specific deletion of PTEN (PTENB) and a concurrent germline deletion of p110delta. The expanded B1 cell population of PTENB mice was reduced to normal levels in PTENB/p110delta mutant mice, indicating a critical role for the p110delta isoform in the expansion of B1 cells. However, numbers of MZ B cells in the PTENB/p110delta mutants was intermediate between wild-type and PTENB-deficient mice, suggesting an additional role for other PI3K catalytic isoforms in MZ differentiation. Furthermore, the defective class switch recombination in PTENB B cells was only partially reversed in PTENB/p110delta double mutant B cells. These results demonstrate an epistatic relationship between p110delta and PTEN. In addition, they also suggest that additional PI3K catalytic subunits contribute to B cell development and function. 相似文献