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991.
Meimberg H Milan NF Karatassiou M Espeland EK McKay JK Rice KJ 《Molecular ecology》2010,19(23):5308-5319
Multiple introductions can play a prominent role in explaining the success of biological invasions. One often cited mechanism is that multiple introductions of invasive species prevent genetic bottlenecks by parallel introductions of several distinct genotypes that, in turn, provide heritable variation necessary for local adaptation. Here, we show that the invasion of Aegilops triuncialis into California, USA, involved multiple introductions that may have facilitated invasion into serpentine habitats. Using microsatellite markers, we compared the polymorphism and genetic structure of populations of Ae. triuncialis invading serpentine soils in California to that of accessions from its native range. In a glasshouse study, we also compared phenotypic variation in phenological and fitness traits between invasive and native populations grown on loam soil and under serpentine edaphic conditions. Molecular analysis of invasive populations revealed that Californian populations cluster into three independent introductions (i.e. invasive lineages). Our glasshouse common garden experiment found that all Californian populations exhibited higher fitness under serpentine conditions. However, the three invasive lineages appear to represent independent pathways of adaptation to serpentine soil. Our results suggest that the rapid invasion of serpentine habitats in California may have been facilitated by the existence of colonizing Eurasian genotypes pre‐adapted to serpentine soils. 相似文献
992.
993.
Kevin C Burns 《Plant signaling & behavior》2010,5(1):9-13
Color is a common feature of animal defense. Herbivorous insects are often colored in shades of green similar to their preferred food plants, making them difficult for predators to locate. Other insects advertise their presence with bright colors after they sequester enough toxins from their food plants to make them unpalatable. Some insects even switch between cryptic and aposomatic coloration during development.1 Although common in animals, quantitative evidence for color-based defense in plants is rare. After all, the primary function of plant leaves is to absorb light for photosynthesis, rather than reflect light in ways that alter their appearance to herbivores. However, recent research is beginning to challenge the notion that color-based defence is restricted to animals.Key words: aposomatic colouration, cryptic colouration, herbivory, moa, plant defenseTemperate deciduous forests provide what is arguably the most extraordinary display of color in nature. Prior to leaf-fall in autumn, the leaves of many deciduous tree species in Asia, Europe and North America turn red, leading to brilliantly colored landscapes. Once thought to be a by-product of chlorophyll re-absorption prior to leaf abscission, autumn flushes in red leaf colors are now known to result from the active synthesis of red-colored pigments.2,3 Although the exact reason for the production of red-colored pigments prior to leaf-fall is unknown, it has recently been hypothesized to be a form of defense.4 Aphids are common phloem-feeding herbivores in deciduous forests, which disperse from the forest floor into tree crowns in autumn, and the synthesis of red pigments could signal the timing of leaf fall and the reduction in the supply of photosynthate.5,6 Although there are also physiological explanations,7 red leaf colors could be a reliable signal of unpalatably to herbivores.8Lev-Yadun and Holopainen9 recently showed that there are fewer red-colored deciduous tree species in Europe than in North America, and they speculate that historical processes are the cause. During the advance and retreat of glaciers in the Pleistocene, the European Alps would have hindered the movement of plants and their herbivores in response to long-term climate change. Mountain ranges in North America run perpendicular to the equator, which would facilitate these migrations. Therefore, if red leaves are signals to herbivores, geographic differences in leaf pigmentation may be ‘anachronistic’.10 In other words, they may result from historical coevolutionary dynamics between plants and their herbivores, rather than present day selection pressures alone.Despite these important insights, our understanding of color-based defense in plants is in its infancy and progress hinges on quantitative tests in other parts of the globe. Previous work is also restricted largely to aposomatic, or warning colors.11 Given that cryptic coloration is widespread in animals, it might also be common in plants. Yet we are far from determining if this is true.Here, I discuss several New Zealand plant species that seem to be colored in ways that would make them difficult for herbivores to locate. I suggest that these plants are anachronisms; their unusual appearance is the result of selection from flightless browsing birds called moa, which went extinct following the arrival of humans in New Zealand 750 years ago. I also discuss the difficulties associated with testing for cypsis in plants and finish by outlining a methodological approach to test for color-based defense in plants when the putative herbivores are either unknown or extinct. 相似文献
994.
Kimberly Pelak Kevin V. Shianna Dongliang Ge Jessica M. Maia Mingfu Zhu Jason P. Smith Elizabeth T. Cirulli Jacques Fellay Samuel P. Dickson Curtis E. Gumbs Erin L. Heinzen Anna C. Need Elizabeth K. Ruzzo Abanish Singh C. Ryan Campbell Linda K. Hong Katharina A. Lornsen Alexander M. McKenzie Nara L. M. Sobreira Julie E. Hoover-Fong Joshua D. Milner Ruth Ottman Barton F. Haynes James J. Goedert David B. Goldstein 《PLoS genetics》2010,6(9)
We present the analysis of twenty human genomes to evaluate the prospects for identifying rare functional variants that contribute to a phenotype of interest. We sequenced at high coverage ten “case” genomes from individuals with severe hemophilia A and ten “control” genomes. We summarize the number of genetic variants emerging from a study of this magnitude, and provide a proof of concept for the identification of rare and highly-penetrant functional variants by confirming that the cause of hemophilia A is easily recognizable in this data set. We also show that the number of novel single nucleotide variants (SNVs) discovered per genome seems to stabilize at about 144,000 new variants per genome, after the first 15 individuals have been sequenced. Finally, we find that, on average, each genome carries 165 homozygous protein-truncating or stop loss variants in genes representing a diverse set of pathways. 相似文献
995.
Kevin M. Waters Daniel O. Stram Mohamed T. Hassanein Lo?c Le Marchand Lynne R. Wilkens Gertraud Maskarinec Kristine R. Monroe Laurence N. Kolonel David Altshuler Brian E. Henderson Christopher A. Haiman 《PLoS genetics》2010,6(8)
It has been recently hypothesized that many of the signals detected in genome-wide association studies (GWAS) to T2D and other diseases, despite being observed to common variants, might in fact result from causal mutations that are rare. One prediction of this hypothesis is that the allelic associations should be population-specific, as the causal mutations arose after the migrations that established different populations around the world. We selected 19 common variants found to be reproducibly associated to T2D risk in European populations and studied them in a large multiethnic case-control study (6,142 cases and 7,403 controls) among men and women from 5 racial/ethnic groups (European Americans, African Americans, Latinos, Japanese Americans, and Native Hawaiians). In analysis pooled across ethnic groups, the allelic associations were in the same direction as the original report for all 19 variants, and 14 of the 19 were significantly associated with risk. In summing the number of risk alleles for each individual, the per-allele associations were highly statistically significant (P<10−4) and similar in all populations (odds ratios 1.09–1.12) except in Japanese Americans the estimated effect per allele was larger than in the other populations (1.20; Phet = 3.8×10−4). We did not observe ethnic differences in the distribution of risk that would explain the increased prevalence of type 2 diabetes in these groups as compared to European Americans. The consistency of allelic associations in diverse racial/ethnic groups is not predicted under the hypothesis of Goldstein regarding “synthetic associations” of rare mutations in T2D. 相似文献
996.
The membrane origin of autophagosomes has long been a mystery and it may involve multiple sources. In this punctum, we discuss our recent finding that the plasma membrane contributes to the formation of pre-autophagic structures via clathrin-mediated endocytosis. Our study suggests that Atg16L1 interacts with clathrin heavy-chain/AP2 and is also localized on vesicles (positive for clathrin or cholera toxin B) close to the plasma membrane. Live-cell imaging studies revealed that the plasma membrane contributes to Atg16L1-positive structures and that this process and autophagosome formation are impaired by knockdowns of genes regulating clathrin-mediated endocytosis.Key words: autophagy, plasma membrane, endocytosis, phagophore, originWhere do autophagosomes get their membrane from? Although the field of autophagy has grown tremendously since its discovery a few decades ago, the origin(s) of the membranes that contribute to autophagosome biogenesis has been a mystery among autophagy researchers until recently. Mammalian autophagosomes are formed randomly throughout the cytoplasm via a process that involves elongation and fusion of phagophores to form double-membraned autophagosomes. This process involves two ubiquitin-like conjugation systems: conjugation of Atg12 to Atg5 that later forms a macromolecular complex with Atg16L1, and conjugation of phosphatidylethanolamine (PE) with Atg8/LC3-I. The Atg12-Atg5-Atg16L1 complex is targeted to the preautophagic structures, which then acquire Atg8. Atg12-Atg5-Atg16L1 dissociates from completed autophagosomes, while LC3-PE (LC3-II) is associated both with pre-autophagic structures and completed autophagosomes.Some recent studies have explored the contribution of membranes from different organelles supporting the general idea that autophagosomes derive membranes from pre-existing organelles. It is quite possible that there may be multiple membrane sources involved. A few groups have revisited the hypothesis that the endoplasmic reticulum (ER) may be one of the membrane donors. High-resolution 2D electron microscopy (EM) and 3D EM-tomography studies have revealed connections between the ER and the growing autophagosomes. Whether the ER contributes to general autophagy or a specific form of autophagy, reticulophagy, remains to be determined. In addition, it has not been shown if ER membrane is required for autophagosome formation. Recently another study has reported that autophagosomes receive lipids from the outer mitochondrial membrane, but only under starvation conditions, again fueling the multiple-membrane source hypothesis.We have now found evidence for plasma membrane contribution to pre-autophagic structures via endocytosis. Unlike the previous studies, which have focused on LC3- positive structures, we looked specifically at the Atg5-, Atg12- and Atg16-positive pre-autophagic structures, an idea that stemmed from our finding that clathrin heavy-chain immunoprecipitates with Atg16L1. We think that this interaction is partly mediated by the adaptor protein AP2, since knockdown of AP2 decreases the clathrin heavy-chain-Atg16L1 interaction. Immunogold EM also shows clathrin localization on Atg16L1-labeled vesicles close to the plasma membrane.These findings led us to test whether knockdown of proteins involved in clathrin-mediated endocytosis affected Atg16L1-positive pre-autophagic structures. Indeed, knockdown of key proteins in the clathrin-mediated endocytic pathway results in a decrease in the formation of Atg16L1-positive structures both under basal or autophagy-induced conditions (starvation or trehalose treatment). This correlates with a decrease in the number of LC3-labeled autophagosomes. When we directly analyzed vesicle fusion by livecell microscopy, we observed that vesicles endocytosed from the plasma membrane fuse to the Atg16L1-positive vesicles close to the plasma membrane. This was confirmed by immuno-EM when we found cholera toxin B-labeling (used to label plasma membrane that is subsequently internalized by endocytosis) on Atg16L1-vesicles. We noticed that overexpression of an Atg16L1 mutant that does not bind clathrin heavy-chain does not form Atg16L1-vesicular structures in the way we see with wild-type Atg16L1, suggesting that the binding of Atg16L1 to AP2/clathrin is required for the subsequent formation of the Atg16L1 vesicles.When we blocked endocytic vesicle scission (using both genetic and chemical inhibitors) we found that Atg16L1 strongly immunoprecipitates with clathrin-heavy chain probably due to the accumulation of clathrin-Atg16L1 structures at the plasma membrane that failed to pinch off. This was strongly supported by our fluorescence microscopy and immuno-EM studies that showed what we predicted—accumulation of Atg16L1 at the plasma membrane. This suggests that Atg16L1 in a complex with AP2/clathrin is targeted to the plasma membrane and subsequently internalized as Atg16L1-positive structures. Thus, our data strongly suggest that plasma membrane contributes to early autophagic precursors that subsequently mature to form phagophores (Fig. 1).Open in a separate windowFigure 1Plasma membrane contributes to the formation of early autophagic precursors. Previous studies show that delivery of fully formed autophagosomes to lysosomes requires fusion of such autophagosomes with early or late endosomes to form amphisomes, which are Atg16L1-negative, LC3-positive and are also positive for endosomal markers. We show that blocking clathrin-mediated endocytosis inhibits formation of Atg16L1-positive structures that mature to form phagophores and later autophagosomes. These Atg16L1-vesicles are positive for other early autophagosomal markers like Atg5 and Atg12, but are negative for early endosomal markers like EEA1, suggesting that they are high up in the autophagosome biogenesis cascade. Inhibition of dynamin with Dynsasore or the use of a dominant negative K44A mutant blocks scission and results in Atg16L1 accumulation on the plasma membrane, suggesting that endosomal scission is critical for this process.Although previous studies suggest that completely formed autophagosomes need to fuse with early or late endosomes in order for subsequent autophagosomelysosome fusion to occur, they did not look at the formation of pre-autophagic structures. Our study shows that active endocytosis is required both for the formation of autophagosomes, when very early endocytic intermediates immediately pinching off the plasma membrane (not early endosomes) fuse with Atg16L1-positive structures to form phagophores, and also for maturation of autophagosomes when early or late endosomes fuse with Atg16L1-negative but LC3-positive autophagosomes to form amphisomes. Since blocking clathrin-mediated endocytosis does not completely abrogate autophagosome formation, we believe that other endocytic pathways may have a similar role. Depending on the cell type or the physiological conditions, the contributions from the different endocytic pathways may vary accordingly. It will be interesting to know if the endocytic pathway continuously delivers membrane for early steps in autophagy as the preautophagic structures grow and mature to form autophagosomes, deriving membrane from other sources. 相似文献
997.
Kevin K. Schrader Anna Andolfi Charles L. Cantrell Alessio Cimmino Stephen O. Duke Weste Osbrink David E. Wedge Antonio Evidente 《化学与生物多样性》2010,7(9):2261-2280
Phytotoxic microbial metabolites produced by certain phytopathogenic fungi and bacteria, and a group of phytotoxic plant metabolites including Amaryllidacea alkaloids and some derivatives of these compounds were evaluated for algicide, bactericide, insecticide, fungicide, and herbicide activities in order to discover natural compounds for potential use in the management and control of several important agricultural and household structural pests. Among the various compounds evaluated: i) ophiobolin A was found to be the most promising for potential use as a selective algicide; ii) ungeremine was discovered to be bactericidal against certain species of fish pathogenic bacteria; iii) cycasin caused significant mortality in termites; iv) cavoxin, ophiobolin A, and sphaeropsidin A were most active towards species of plant pathogenic fungi; and v) lycorine and some of its analogues (1‐O‐acetyllycorine and lycorine chlorohydrate) were highly phytotoxic in the herbicide bioassay. Our results further demonstrated that plants and microbes can provide a diverse and natural source of compounds with potential use as pesticides. 相似文献
998.
Rogelio Zamilpa Elizabeth F. Lopez Ying Ann Chiao Qiuxia Dai Gladys P. Escobar Kevin Hakala Susan T. Weintraub Merry L. Lindsey 《Proteomics》2010,10(11):2214-2223
Matrix metalloproteinase‐9 (MMP‐9) deletion has been shown to improve remodeling of the left ventricle post‐myocardial infarction (MI), but the mechanisms to explain this improvement have not been fully elucidated. MMP‐9 has a broad range of in vitro substrates, but relevant in vivo substrates are incompletely defined. Accordingly, we evaluated the infarct regions of wild‐type (wt) and MMP‐9 null (null) mice using a proteomic strategy. Wt and null groups showed similar infarct sizes (48±3 in wt and 45±3% in null), indicating that both groups received an equal injury stimulus. Left ventricle infarct tissue was homogenized and analyzed by 2‐DE and MS. Of 31 spot intensity differences, the intensities of 9 spots were higher and 22 spots were lower in null mice compared to wt (all p<0.05). Several extracellular matrix proteins were identified in these spots by MS, including fibronectin, tenascin‐C, thrombospondin‐1, and laminin. Fibronectin was observed on the gels at a lower than expected molecular weight in the wt group, which suggested substrate cleavage, and the lower molecular weight spot was observed at lower intensity in the MMP‐9 null group, which suggested cleavage by MMP‐9. Immunoblotting confirmed the presence of fibronectin cleavage products in the wt samples and lower levels in the absence of MMP‐9. In conclusion, examining infarct tissue from wt and MMP‐9 null mice by proteomic analysis provides a powerful and unique method to identify in vivo candidate MMP substrates. 相似文献
999.
1000.
Mariannaea aquaticola sp. nov. is described, illustrated, and compared with closely related taxa. Phylogenetic analysis of rDNA ITS and 28S sequences
show that Mariannaea aquaticola has affinity with Nectriaceae, which is in agreement with other Mariannaea species. Other morphologically similar genera such as Verticillium and Clonostachys are shown to be phylogenetically distant to Mariannaea. The generic concept of Mariannaea is discussed, and the affinity to Nectriaceous teleomorphs is suggested as additional generic character. A key to Mariannaea species is provided. 相似文献