Search UNB Scholar
About UNB Scholar
UNB Scholar is an institutional repository initiative of UNB Libraries intended to collect, preserve, showcase, and promote the open access scholarly output of the UNB community. Use UNB Scholar to explore specific collections, or search all content in the repository. Material submitted to the repository will also be freely discoverable online through Google and other major search engines.
UNB Libraries welcomes submissions to UNB Scholar. Find out more about depositing your publications!
Communities in DSpace
Select a community to browse its collections.
Recent Submissions
Item type:Item, Symbiont Reintroduction Alters Tumor Progression and Life-History Traits in the Tumor-Bearing Freshwater Cnidarian Hydra oligactis(Wiley, 2026-04-13) Stepanskyy, Nikita; Meliani, Jordan; Tökölyi, Jácint; Nedelcu, Aurora M.; Ujvari, Beata; Thomas, Frédéric; Dujon, Antoine M.Environmental changes can disrupt long-standing host–symbiont associations and influence tumor dynamics; however, how these two aspects interact remains poorly understood, particularly when previously co-evolved symbionts are reintroduced into tumor-prone hosts. We experimentally reintroduced a native commensal ciliate symbiont (Kerona pediculus) into two long-term cultured symbiont-free lines of the freshwater cnidarian, Hydra oligactis, differing in tumor affliction: one harbors a transmissible tumor, and one has historically low spontaneous tumor incidence. Unexpectedly, spontaneous tumors emerged at high frequency in the latter, independently of ciliate acquisition, fundamentally reshaping the experimental framework and enabling comparisons of how symbiont reintroduction affects hosts with either transmissible or de novo tumors. While ciliate infection did not alter tumor incidence, it slightly accelerated tumor onset, increased the likelihood of supernumerary tentacle formation, and reduced asexual reproduction (particularly at high symbiont densities) across tumor contexts. Spontaneous tumors appeared later than transmissible tumors, were less often associated with supernumerary tentacles, and induced an earlier reproductive burst. Our findings show that symbiont reintroduction and tumor context shape tumor dynamics and life-history traits in tumor-bearing hosts, emphasizing the potential role of symbiotic history and tumor evolutionary context when assessing the outcomes of such pressures in vulnerable host populations.Item type:Item, Selection for Function in Early Life: Implications for Early-Onset Pathologies(Wiley, 2026-04-10) Asselin, Klara; Dujon, Antoine M.; Capp, Jean-Pascal; Lemaître, Jean-François; Pirard, Florence; Vaiman, Daniel; Ujvari, Beata; Pujol, Pascal; DeGregori, James; Nedelcu, Aurora M.; Thomas, FrédéricPersistent pathological structures, such as tumors, fibrotic nodules, granulomas, microbial biofilms, or protein aggregates, are traditionally viewed as age-related conditions that emerge after reproduction, when natural selection is less effective at eliminating traits expressed late in life. However, some pathologies with robust and organized architectures can arise surprisingly early, challenging this classical perspective. We recently proposed that intra-organismal selection for function, a selective process operating within organisms and acting on non-reproducing entities by favoring structural configurations that enhance stability, robustness, and novelty generation, may play a role in aging. Here, we suggest that this same process can also operate well before the so-called selection shadow (i.e., life stages where natural selection is too weak to purge deleterious mutations). We identify three non-mutually exclusive mechanisms that may promote this early-life action: (i) initial local adaptive benefits, such as improved tissue repair or containment of infection; (ii) limited or context-specific fitness costs, allowing structurally stable but abnormal configurations to persist undetected; and (iii) rapid environmental changes that reshape tissue-level selective landscapes, driven by pollutants, endocrine disruptors, or novel diets. Recognizing early-onset organized pathologies as by-products of eco-evolutionary tissue dynamics, rather than as mere developmental errors, reframes their biological significance and opens new therapeutic avenues. Instead of targeting cells exclusively, future strategies could focus on disrupting the functional architecture of pathological tissues and structures, offering novel means to prevent or control early-life diseases shaped by internal selection forces.Item type:Item, Selection for Function in Complex Distributed Pathological Systems(Wiley, 2026-02-02) Thomas, Frédéric; Dujon, Antoine M.; Vaiman, Daniel; Eberl, Gerard; Alix-Panabières, Catherine; Pujol, Pascal; Ujvari, Beata; Meliani, Jordan; Nedelcu, Aurora M.; Capp, Jean-PascalPathological processes are often conceptualized as localized phenomena anchored in a primary tumor, a focal lesion, or a single organ. However, growing evidence indicates that many diseases persist and progress as complex distributed systems, maintained by interactions among multiple sites. Building on the emerging framework of selection for function, which can be applied to understand the evolutionary persistence of both replicating and non-replicating entities, we propose that metastases, amyloidoses, fibroses, autoimmune syndromes, granulomatous diseases, and multifocal reproductive disorders can all be understood as complex evolving pathological systems within individuals. In these contexts, local units such as metastatic nodules, amyloid plaques, or fibrotic foci act as semi-autonomous entities, yet achieve collective persistence through systemic flows, feedback loops, and network-level interactions, where local structuration gives rise to systemic effects. At certain points, lesions that produce mediators can trigger systemic alterations that, in turn, favor the emergence and persistence of additional lesions. This creates a vicious cycle in which local and systemic dynamics reinforce one another, helping these specific pathological networks to overcome host defense mechanisms and persist (i.e., be ‘selected’ via differential persistence). This perspective unifies seemingly disparate conditions under the principle of system persistence, reframing pathology as an emergent organizational property of a pathological system rather than as isolated local breakdowns of organismal components. It also carries important implications for evolutionary medicine, suggesting a taxonomy of diseases that distinguishes localized from distributed functional pathologies. Clinically, it underscores the need to go beyond focal interventions, advocating instead for therapies that disrupt pathological connectivity, destabilize network coherence, and monitor systemic biomarkers of disease persistence. Recognizing the role of selection for function in the emergence and persistence of complex pathological systems opens new avenues for both theoretical integration and therapeutic innovation in evolutionary medicine.Item type:Item, Multicellular cooperation and the hallmarks of cancer: A new foundation(Oxford Academic, 2025-09-19) Maley, Carlo C.; Boddy, Amy M.; Nedelcu, Aurora M.; Aktipis, AthenaMulticellularity evolved independently several times across the tree of life. In all cases, these events were dependent on various types of cellular cooperation. We previously identified five universal foundations of cellular cooperation that are required in all complex multicellular lineages to allow the collection of cells to function and reproduce as a whole (i.e. a multicellular individual). These include: proliferation inhibition, controlled cell death, resource allocation, division of labor, and maintenance of the extracellular environment. We propose that there is a sixth universal foundation of multicellularity that breaks down in cancer: proximity maintenance. By staying in close proximity, cells can more easily provide benefits for one another, communicate, coordinate their behavior, and evolve increased size and complexity. Here, we revisit and further develop the five original foundations of multicellular cooperation in the context of the evolution of multicellularity from unicellular ancestors and their implications for cancer progression. In our previous work, we suggested that the breakdown of all these cooperative behaviors is reflected in the universal hallmarks of cancer. Similarly, the breakdown of proximity maintenance maps to another hallmark of cancer—activating invasion and metastasis.Item type:Item, The Role of Selection for Function in Aging and Chronic Diseases: A Novel Evolutionary Perspective(Wiley, 2025-09-05) Dujon, Antoine M.; Asselin, Klara; Lemaître, Jean François; Capp, Jean-Pascal; Pujol, Pascal; Ujvari, Beata; DeGregori, James; Nedelcu, Aurora M.; Thomas, FrédéricAging, and by extension age-related diseases, has traditionally been understood through classical evolutionary genetic models, such as the mutation accumulation and antagonistic pleiotropy theories. However, these frameworks primarily focus on the declining efficacy of organismal-level selection against mutations with deleterious effects in late life. Here, we propose a novel hypothesis: many chronic diseases associated with aging may emerge, at least in part, as a result of selection acting at lower organizational levels, including non-replicative biological entities, enabled by the relaxation of selective pressures that constrained within-organism evolutionary processes in early life. This hypothesis is built on the recently proposed concept of selection for function that extends the evolutionary process to non-replicative entities. While Darwinian selection acting at the organismal level strongly constrains within-organism evolution during an organism's reproductive lifespan, these constraints weaken with age. As a consequence, lower-level non-replicative entities, such as benign and malignant tumors, atherosclerotic plaques, and neurodegenerative aggregates, may experience a form of selection that favors those with increased stability, organization, and long-term persistence, sometimes at the cost to host fitness. These entities do not evolve via long-term differential reproduction, but rather certain configurations of their structure persist preferentially over others due to environmental constraints, microenvironmental selection, and internal stabilization mechanisms. Understanding aging through the lens of selection for function at the level of internal non-replicative entities provides new insights into the evolution of chronic diseases and opens novel therapeutic avenues aimed at disrupting internal functional organization, rather than merely targeting cellular proliferation/abnormalities or disease symptoms.
