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Invasive plants may promote predator-mediated feedback that inhibits further invasion.

ABSTRACT: Understanding the impacts of invasive species requires placing invasion within a full community context. Plant invaders are often considered in the context of herbivores that may drive invasion by avoiding invaders while consuming natives (enemy escape), or inhibit invasion by consuming invaders (biotic resistance). However, predators that attack those herbivores are rarely considered as major players in invasion. Invasive plants often promote predators, generally by providing improved habitat. Here, we show that predator-promoting invaders may initiate a negative feedback loop that inhibits invasion. By enabling top-down control of herbivores, predator-promoting invaders lose any advantage gained through enemy escape, indirectly favoring natives. In cases where palatable invaders encounter biotic resistance, predator promotion may allow an invader to persist, but not dominate. Overall, results indicate that placing invaders in a full community context may reveal reduced impacts of invaders compared to expectations based on simple plant-plant or plant-herbivore subsystems.

SUBMITTER: Smith LM

PROVIDER: S-EPMC4475373 | biostudies-literature | 2015 Jun

REPOSITORIES: biostudies-literature

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Invasive plants may promote predator-mediated feedback that inhibits further invasion.

Smith Lauren M LM Schmitz Oswald J OJ

Ecology and evolution 20150525 12

Understanding the impacts of invasive species requires placing invasion within a full community context. Plant invaders are often considered in the context of herbivores that may drive invasion by avoiding invaders while consuming natives (enemy escape), or inhibit invasion by consuming invaders (biotic resistance). However, predators that attack those herbivores are rarely considered as major players in invasion. Invasive plants often promote predators, generally by providing improved habitat. ...[more]

PMID: 26120430

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Project description:Rationale: Colitis-associated colorectal cancer (CAC) usually exhibits an accelerated disease progression, an increased resistance to therapeutic drugs and a higher mortality rate than sporadic colorectal cancer (CRC). PIAS3 is a member of the protein inhibitor of activated STAT (PIAS) family; however, little is known about the expression and biological functions of PIAS3 in CAC. The aim of our study was to investigate the biological mechanisms of PIAS3 in CAC. Methods: PIAS3 expression was examined in colon tissues of CAC/CRC patients and azoxymethane-dextran sulfate sodium (AOM-DSS)-induced mice. The role of PIAS3 was studied using a series of in vitro, in vivo and clinical approaches. Results: Downregulated PIAS3 expression, upregulated miR-18a expression and highly activated NF-κB and STAT3 were observed in colon tissues of CAC/CRC patients and AOM-DSS-induced mice. In vitro experiments revealed that PIAS3 significantly inhibited the activation of NF-κB and STAT3 and demonstrated that activated NF-κB and STAT3 transcriptionally regulated miR-18a level, and up-regulation of miR-18a expression led to defective PIAS3 expression. Moreover, PIAS3-mediated autoregulatory feedback loops (PIAS3/NF-κB/miR-18a and PIAS3/STAT3/miR-18a) were verified in vitro and were found to regulate cell proliferation. Additionally, modulation of the feedback loops via overexpression of PIAS3 or knockdown of miR-18a significantly inhibited cell proliferation in a mouse CRC xenograft model. Furthermore, upregulation of PIAS3 by intracolonic administration of PIAS3 lentivirus or anti-miR-18a lentivirus in AOM-DSS-induced mice led to dramatically reduced tumor sizes/numbers, whereas knockdown of PIAS3 in CAC mice significantly promoted tumor growth. Conclusion: Our data clearly show that PIAS3-mediated feedback loops control cell proliferation and function as robust driving forces for CAC progression. Targeting these highly activated feedback loops might offer promising therapeutic strategies for CAC.

Project description:Specialist predators with oscillating dynamics are often strongly affected by the population dynamics of their prey, yet they are not always the cause of prey cycling. Only those that exert strong (delayed) regulation of their prey can be. Inferring predator-prey coupling from time series therefore requires contrasting models with top-down versus bottom-up predator-prey dynamics. We study here the joint dynamics of population densities of the Icelandic gyrfalcon Falco rusticolus, and its prey, the rock ptarmigan Lagopus muta. The dynamics of both species are likely not only linked to each other but also to stochastic weather variables acting as confounding factors. We infer the degree of coupling between populations, as well as forcing by abiotic variables, using multivariate autoregressive models MAR(p), with p = 1 and 2 time lags. MAR(2) models, allowing for species to cycle independently from each other, further suggest alternative scenarios where a cyclic prey influences its predator but not the other way around (i.e., bottom-up scenarios). The classical MAR(1) model predicts that the time series exhibit predator-prey feedback (i.e., reciprocal dynamic influence between prey and predator), and that weather effects are weak and only affecting the gyrfalcon population. Bottom-up MAR(2) models produced a better fit but less realistic cross-correlation patterns. Simulations of MAR(1) and MAR(2) models further demonstrate that the top-down MAR(1) models are more likely to be misidentified as bottom-up dynamics than vice versa. We therefore conclude that predator-prey feedback in the gyrfalcon-ptarmigan system is likely the main cause of observed oscillations, though bottom-up dynamics cannot yet be excluded with certainty. Overall, we showed how to make more out of ecological time series by using simulations to gauge the quality of model identification, and paved the way for more mechanistic modeling of this system by narrowing the set of important biotic and abiotic drivers.

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Invasive plants may promote predator-mediated feedback that inhibits further invasion.

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Invasive plants may promote predator-mediated feedback that inhibits further invasion.

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