Models of Experimentally Derived Competitive Effects Predict Biogeographical Differences in the Abundance of Invasive and Native Plant Species

<div><p>Mono-dominance by invasive species provides opportunities to explore determinants of plant distributions and abundance; however, linking mechanistic results from small scale experiments to patterns in nature is difficult. We used experimentally derived competitive effects of an invader in North America, <i>Acroptilon repens</i>, on species with which it co-occurs in its native range of Uzbekistan and on species with which it occurs in its non-native ranges in North America, in individual-based models. We found that competitive effects yielded relative abundances of <i>Acroptilon</i> and other species in models that were qualitatively similar to those observed in the field in the two ranges. In its non-native range, <i>Acroptilon</i> can occur in nearly pure monocultures at local scales, whereas such nearly pure stands of <i>Acroptilon</i> appear to be much less common in its native range. Experimentally derived competitive effects of <i>Acroptilon</i> on other species predicted <i>Acroptilon</i> to be 4–9 times more proportionally abundant than natives in the North American models, but proportionally equal to or less than the abundance of natives in the Eurasian models. Our results suggest a novel way to integrate complex combinations of interactions simultaneously, and that biogeographical differences in the competitive effects of an invader correspond well with biogeographical differences in abundance and impact.</p></div

Mean extinction time for native species in different competitive scenarios.

<p>Mean extinction time for native species in different competitive scenarios (<i>RII_{N on}_A</i>  = 0.15 and 0.25) between <i>Acroptilon</i> and species native to North America and Europe. <i>Pseudoroegneria spicata</i> in North America and <i>Melilotus officinalis</i> were not included because they were never eliminated from the models.</p

A Novel and Practical Synthesis of Ramelteon

An efficient and practical process for the synthesis of ramelteon <b>1</b>, a sedative-hypnotic, is described. Highlights in this synthesis are the usage of acetonitrile as nucleophilic reagent to add to 4,5-dibromo-1,2,6,7-tetrahydro-8<i>H</i>-indeno­[5,4-<i>b</i>]­furan-8-one <b>2</b> and the subsequent hydrogenation which successfully implement four processes (debromination, dehydration, olefin reduction, and cyano reduction) into one step to produce the ethylamine compound <b>13</b> where dibenzoyl-l-tartaric acid is selected both as an acid to form the salt in the end of hydrogenation and as the resolution agent. Then, target compound <b>1</b> is easily obtained from <b>13</b> via propionylation. The overall yield in this novel and concise process is almost twice as much as those in the known routes, calculated on compound <b>2</b>

Induction of serum antibodies in response to infection of 1-day-old and 2-week-old chickens with parental and F protein cleavage site mutant APMV-4 viruses.

<p>Chickens were inoculated with each virus (256 HA units) by the intranasal route in the same experiment as <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0050598#pone-0050598-t002" target="_blank">Table 2</a>. Sera were collected at 14 dpi and evaluated for virus-specific antibodies by a hemagglutination inhibition assay using chicken erythrocytes.</p

Analysis of proteins present in virions of parental and F protein cleavage site mutant APMV-4 viruses, and cell-surface expression of the viral F protein.

<p>(A) Virus that was partially purified from infected chicken egg allantoic fluids by sucrose step gradients was separated by electrophoresis, and the gel was stained with Coomassie brilliant blue. Lanes: 1. Biologically-derived APMV-4, 2. rAPMV-4, 3. rAPMV-4/Fc type 3-Q, 4. rAPMV-4/Fc type 5-Q, 5. rAMPV-4/Fc BC, 6. rAMPV-4/Fc Las, 7. rAMPV-4/Fc SV, and 8. rAMPV-4/Fc PIV-1 (B) Incorporation of wild-type and mutated F proteins into the virions was further analyzed by Western blot. The separated proteins in the gel (8%) under reducing condition (in panel A) were transferred into a membrane, and the F protein was detected by using an antiserum raised against a synthetic peptide from the F protein of APMV-4. (C) Surface expression of the F protein on infected DF1 cells. DF1 cells were infected with each virus (MOI of 0.1) and, at 24 h post-infection, were stained with anti-peptide antiserum against the F protein followed by anti-Alexa Fluor 488 antibody, and were analyzed by flow cytometry.</p

Replication of parental and F protein cleavage site mutant APMV-4 viruses in 3-week-old ducks.

a<p>Groups of 3-week-old ducks were inoculated with each virus by the combined intranasal and intratracheal routes. Three birds from each group were sacrificed, and tissues samples (brain, trachea, lung, and spleen) were collected on 4 dpi and homogenized. To confirm the virus replication, aliquots (100 µl each) of the collected samples were inoculated into three eggs, and allantoic fluids were collected on 3 dpi. Virus replication was determined by hemagglutination assay.</p

Virus isolation from the indicated tissue harvested from mice 3 dpi with APMV serotypes 1 to 9^*.

*<p>Mice in groups of 3 were inoculated with 50 ìl of allantoic fluid containing 2⁷ HA units of each APMV serotype except serotype 5, which contained 3×10³ PFU/ml of cell culture harvested virus. The control group was inoculated with normal allantoic fluid. Tissues were harvested 3 dpi and homogenized, and clarified supernatant fluid was inoculated into 9-day-old embryonated eggs and tested for virus 4 days later by HA assay.</p><p>+  = each + indicates isolation of virus from one mice.</p><p>-  = no virus was isolated.</p><p>ND = not detected.</p

Serum antibody responses against APMV serotypes 1–9 in infected mice^a.

<p>All the values are averages from three independent experiments.</p>a<p>Mice in groups of 3 were inoculated as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016776#pone-0016776-t001" target="_blank">Table 1</a>. Serum samples were collected before inoculation and 14 dpi.</p>b<p>The hemagglutination inhibition (HI) titer is expressed as the reciprocal of the highest serum dilution causing complete inhibition of four HA units of NDV.</p><p>-  = not detected.</p

Growth kinetics of parental and F protein cleavage site mutant APMV-4 viruses in the brains of 1-day-old chicks.

<p>Ten 1-day-old SPF chicks were inoculated with the indicated parental or mutant viruses via the intracerebral route. Two birds in each group were sacrificed daily until 5 dpi. Brain tissue samples were harvested and virus titers were determined by limiting dilution in DF1 cells and immunostaining with antiserum against the N protein of APMV-4. Each bar represents mean and standard error of the mean of duplicate samples.</p

Replication of APMVs in 1-day- and 2-week-old chickens.

<p>Groups of (A) 1-day- or (B) 2-week-old chickens were inoculated with each virus (256 HA units) by the intranasal route. Three birds from each group were sacrificed on 3 dpi (1-day-old chicks) or 4 dpi (2-week-old chickens), and virus titers in the collected tissues samples (brain, trachea, lung, and spleen) were determined by limiting dilution in DF1 cells and immunostaining with polyclonal antibodies raised against the respective N protein.</p