Invasive species are organisms whose introduction and spread in exotic ranges result in a multitude of ecological impacts. Understanding the factors that constrain the exotic distributions of invasive species is of considerable interest. Biotic associations formed with taxa in the invaded community may be particularly important in shaping invader distributions. These associations emerge from interactions between the traits of the invasive species and some subset of the traits present in the invaded community. Focusing on how organism traits influence the outcomes of biotic interactions may inform predictions of invader distributions. This kind of trait-based approach may be most easily applied to systems where invaders specialize on particular hosts because such associations imply a close correspondence between the traits of the invader and hosts. This dissertation focuses on the South American cactus moth (Cactoblastis cactorum, Lepidoptera: Pyralidae), an invasive consumer in North America whose larvae infest prickly-pear cacti (Opuntia spp.). Chapter One is a brief introduction providing background and context to the presented research. In Chapter Two, I quantify Opuntia morphological and tissue macronutrient traits hypothesized to correlate with patterns of C. cactorum host use. Tissue macronutrient traits appear important in predicting C. cactorum infestation whereas a model containing Opuntia morphological traits had poor predictive ability. Chapter Three describes a method that uses host Opuntia identity and availability to estimate habitat suitability in order to predict the North American distribution of C. cactorum. I then simulate C. cactorum dispersal relative to scenarios of habitat suitability and Opuntia availability. Chapter Four alters the model in Chapter Three so that habitat suitability for C. cactorum is determined by the availability of trait-based groupings of Opuntia hosts. I then simulate C. cactorum dispersal via a different method from that described in Chapter Three. In Chapters Three and Four, I evaluate the degree of similarity among model predictions and the relative contribution of modeling constraints in generating variation in this similarity. Chapters Three and Four predictions were most affected by estimates of abiotic suitability and dispersal constraints, respectively. Chapter Five is a short summary of my results and a discussion of their more general applicability.

No description available.

Invasive species have become an increasing threat to many habitats worldwide. This research addressed the questions of whether several invasive woody plants can germinate, survive and grow in light levels typical of an undisturbed forest understory, and also whether alteration of the nitrogen cycle by one invader is likely to increase the rate of invasion by others.

The social, economic, and ecological costs of plant invasions are vast, through their ability to alter ecosystem structure and function. Invasive annual grasses are a nuisance in the American Southwest through promotion of the grass-fire cycle. Annual grasses such as Bromus rubens, Bromus tectorum, Schismus barbatus, and Schismus arabicus have invaded the Mojave Desert and increased fire occurrence, thus it is important to identify and characterize the areas where persistent invasion has occurred and subsequently fire risk is increased by understanding the distribution of these invasive grasses. Previous plot and landscape-scale research has revealed anthropogenic and biophysical correlates with the establishment and dominance of invasive annual grasses in the Mojave Desert. However, these previous studies have been limited in spatial and temporal scales. Here we use a remote sensing framework to map persistent and productive populations of invasive annual grass, called hot spots, in the entire Mojave Desert ecoregion over 12 years, identify important variables for predicting hot spot distribution, and identify the most invaded subregions. Hot spots were identified in over 5% of the Mojave Desert, and invasive grasses were detected in over 90% of the desert at least once. Our results indicate that soil texture, aspect, winter precipitation, and elevation are the most important predictive variables of invasive grass hot spots, while anthropogenic variables were the least useful. The most invaded subregions of the Mojave Desert were western Mojave basins, eastern Mojave mountain woodland and shrubland, western Mojave low ranges and arid footslopes, eastern Mojave basins, and eastern Mojave low ranges and footslopes.

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.

Yes / This data article is related to the research article entitled Proteomics of Tissue Factor silencing in cardiomyocytic cells reveals a new role for this coagulation factor in splicing machinery control by Lento et al [1]. Tissue Factor (TF) is the key player in the coagulation cascade, but it has additional functions ranging from angiogenesis, tumor invasion and, in the heart, the maintenance of the integrity of cardiac cells. This article reports the nano-LC-MSE analysis of the cardiomyocytic HL-1 cell line proteome and describes the results obtained from a Gene Ontology analysis of those proteins affected by TF-gene silencing.

No description available.

no / Burkholderia cepacia is known to invade and survive within respiratory epithelial cells. Previous studies have employed transformed cell lines and it is not known whether the bacterium is capable of manifesting the same phenomena in primary cell culture. Two strains of B. cepacia of environmental (NCTC 10661) and clinical origin (C1359) were examined for their ability to invade and survive (over a 24 h period) within type II pneumocytes in primary culture using a gentamicin¿ceftazidime antibiotic protection assay. Both strains of B. cepacia were capable of invasion of type II pneumocytes in primary culture. Strain C1359 was capable of multiplying intracellularly as indicated by a seven-fold increase in the numbers of bacteria from 4¿24 h, whereas strain 10661, although unable to replicate intracellularly, was found to survive in the pneumocytes for at least 24 h. Future studies on the invasiveness of B. cepacia can employ A549 cells as a valid surrogate for primary cell culture assays which are time-consuming, labour-intensive and expensive to perform.

La sénescence et l’apoptose sont deux mécanismes oncosupresseurs induits dans les lésions pré-malignes et capables de s’opposer à la prolifération cellulaire incontrôlée induite par l’activation d’oncogènes mitogéniques. Leur inhibition est nécessaire à la conversion d’une lésion bénigne en tumeur maligne. Nous avons démontré que les gènes embryonnaires TWIST1, TWIST2 et SNAI3 sont fréquemment réactivés dans les cancers humains. De par leur capacité à inactiver fonctionnellement la protéine oncosuppressive p53, ces facteurs embryonnaires permettent d’inhiber la sénescence et l’apoptose induites en réponse à l’activation d’oncoprotéines mitogéniques, de transformer in vitro des fibroblastes primaires murins et de leur accorder un pouvoir tumorigène. Dans les cellules épithéliales, cet échappement aux mécanismes de sauvegarde est associé à une transition épithélio-mésenchymateuse (EMT) et à l’acquisition conséquente de capacités de migration, d’invasion et d’auto-renouvellement. Ces résultats nous ont donc permis de mettre en exergue un lien étroit entre l’inhibition des systèmes de sauvegarde cellulaire et l’EMT et de proposer que la réactivation des gènes embryonnaires tels TWIST ou SNAI3 soit suffisante pour promouvoir la conversion maligne et la dissémination précoce des cellules cancéreuses / Senescence and apoptosis, the two main oncosuppressive mechanisms activated in premalignant tumors, restrict cell proliferation in response to mitogenic oncogene activation. Their inhibition is required for malignant conversion of benign lesions. We demonstrated that TWIST1, TWIST2 and SNAI3 embryonic genes are frequently reactivativated in human cancers. By functionally inactivating the p53 oncosuppressive protein, these embryonic factors override oncogene-induced senescence and apoptosis and cooperate in vitro with mitogenic oncoproteins in murine primary fibroblast transformation, providing cells with tumorigenic potential. In epithelial cells, failsafe program escape is associated with an epithelialmesenchymal transition (EMT), and the consequent acquisition of motility, invasive properties and selfrenewal capabilities. These data highlight an intimate crosstalk between failsafe program escape and EMT and suggest that reactivation of embryonic genes such as TWIST or SNAI3 is sufficient to promote both malignant conversion and early cancer cell dissemination

Les glioblastomes (GBMs) sont les tumeurs cérébrales primaires les plus courantes chez l’adulte avec un pronostic fatal dans les douze mois suivant le diagnostic. De nouvelles avancées dans la connaissance de la pathologie moléculaire des GBMs et de leurs régulateurs clés sont indispensables à l’émergence de nouvelles pistes thérapeutiques. Inositol Requiring Enzyme 1 α (IRE1α) est une protéine résidente du réticulum endoplasmique (RE) agissant en tant que détecteur proximal de l’Unfolded Protein Response (UPR) en conditions physiologiques ou pathologiques. IRE1α est une enzyme bivalente possédant une activité Ser/Thr kinase et endoribonucléasique (RNase). Récemment, des mutations ponctuelles dans le gène ERN1/IRE1α ont été détectées dans les cancers chez l’homme, (en particulier dans les GBMs), et IRE1α a été proposé comme un régulateur majeur de la progression tumorale parmi les protéines kinases. Dans ce travail, nous avons montré que le blocage des deux activités Set/thr kinase et RNase dans les cellules U87-MG réprime fortement l’angiogenèse tumorale, la perfusion des vaisseaux et l’expression de facteurs pro-angiogéniques dans des modèles tumoraux de xénogreffes. Ce changement phénotypique est accompagné d’une réponse dite« d’échappement » des cellules tumorales. Celles-ci envahissent le tissu cérébral sain par migration de long des vaisseaux (mécanismes appelé co-option vasculaire). De plus, ce phénotype a été montré comme étant fonctionnellement associé au processus de transition mésenchymateuse. Par mutagenèse dirigée, nous avons montré qu’IRE1α module les processus d’angiogenèse et d’invasion par ces deux domaines catalytiques : l’activité Ser/Thr kinase d’IRE1α est essentielle pour l’angiogenèse alors que le domaine RNase d’IRE1α contrôle le phénotype invasif et co-opté. IRE1α est ainsi identifié comme un régulateur clé de la croissance du glioblastome, agissant au carrefour de signalisations majeures dans le contrôle de l’adaptation de la cellule tumorale à son micro-environnement. / Glioblastomas (GBMs) are the most common primary brain tumors in humans and remain essentially incurable. New advances in the knowledge of GBM molecular pathology and their key regulators are crucial to identify new putative ways for GBM therapy. Inositol Requiring Enzyme 1 α (IRE1α) is a transmembrane Endoplasmic Reticulum (ER)-resident protein acting as proximal sensor of the Unfolded Protein Response (UPR) in both physiological and pathological situations. IRE1α is a bivalent enzyme, displaying Ser/Thr kinase and endoribonuclease (RNase) activities in its cytosolic side. Recently, single mutations in IRE1α gene were detected in human cancers, including GBM, and IRE1α was proposed as a major contributor to tumor progression among protein kinases. In this work, we have shown that blockade of both IRE1α Ser/Thr kinase and RNase activities in U87-MG cells highly repressed tumor angiogenesis, blood perfusion and the expression of pro-angiogenic factors in human xenograft tumor models. This phenotypic change is adversely associated to the so-called "evasive response" of tumors cells. The cells began to migrate along pre-existing brain capillaries and invade healthy tissue (a process named blood vessel co-option). Moreover, this phenotype was shown to be functionally linked to the mesenchymal differentiation process. By using site-directed mutagenesis, we demonstrated that IRE1α protein modulates both angiogenesis and invasive processes through its two catalytic domains: IRE1α Ser/Thr kinase domain was essential for IRE1-mediated angiogenesis, whereas IRE1's RNase domain drove the invasive, co-opted phenotype. IRE1α is therefore identified as a key regulator of glioma progression, acting at the crossroads of major signaling networks in the control of tumor cell adaptation to its microenvironment.