Catálogo de publicaciones - revistas

<jats:title>ABSTRACT</jats:title><jats:p>Neutrophils are considered ‘first‐line defence’ cells as they can be rapidly recruited to the site of the immune response. As key components of non‐specific immune mechanisms, neutrophils use phagocytosis, degranulation, and formation of neutrophil extracellular traps (NETs) to fight pathogens. Recently, immunoregulatory abilities of neutrophils associated with the secretion of several mediators, including cytokines and extracellular vesicles (EVs) containing, among other components, microRNAs (miRNAs), have also been reported. EVs are small structures released by cells into the extracellular space and are present in all body fluids. Microvesicles show the composition and status of the releasing cell, its physiological state, and pathological changes. Currently, EVs have gained immense scientific interest as they act as transporters of epigenetic information in intercellular communication. This review summarises findings from recent scientific reports that have evaluated the utility of miRNA molecules as biomarkers for effective diagnostics or even as start‐points for new therapeutic strategies in neutrophil‐mediated immune reactions. In addition, this review describes the current state of knowledge on miRNA molecules, which are endogenous regulators of gene expression besides being involved in the regulation of the immune response.</jats:p>

<jats:title>ABSTRACT</jats:title><jats:p>Most tooth‐bearing non‐mammalian vertebrates have the capacity to replace their teeth throughout life. This capacity was lost in mammals, which replace their teeth only once at most. Not surprisingly, continuous tooth replacement has attracted much attention. Classical morphological studies (e.g. to analyse patterns of replacement) are now being complemented by molecular studies that investigate the expression of genes involved in tooth formation. This review focuses on ray‐finned fish (actinopterygians), which have teeth often distributed throughout the mouth and pharynx, and more specifically on teleost fish, the largest group of extant vertebrates. First we highlight the diversity in tooth distribution and in tooth replacement patterns. Replacement tooth formation can start from a distinct (usually discontinuous and transient) dental lamina, but also in the absence of a successional lamina, e.g. from the surface epithelium of the oropharynx or from the outer dental epithelium of a predecessor tooth. The relationship of a replacement tooth to its predecessor is closely related to whether replacement is the result of a prepattern or occurs on demand. As replacement teeth do not necessarily have the same molecular signature as first‐generation teeth, the question of the actual trigger for tooth replacement is discussed. Much emphasis has been laid in the past on the potential role of epithelial stem cells in initiating tooth replacement. The outcome of such studies has been equivocal, possibly related to the taxa investigated, and the permanent or transient nature of the dental lamina. Alternatively, replacement may result from local proliferation of undifferentiated progenitors, stimulated by hitherto unknown, perhaps mesenchymal, factors. So far, the role of the neurovascular link in continuous tooth replacement has been poorly investigated, despite the presence of a rich vascularisation surrounding actinopterygian (as well as chondrichthyan) teeth and despite a complete arrest of tooth replacement after nerve resection. Lastly, tooth replacement is possibly co‐opted as a process to expand the number of teeth in a dentition ontogenetically whilst conserving features of the primary dentition. That neither a dental lamina, nor stem cells appear to be required for tooth replacement places teleosts in an advantageous position as models for tooth regeneration in humans, where the dental lamina regresses and epithelial stem cells are considered lost.</jats:p>

<jats:title>ABSTRACT</jats:title><jats:p>Weed communities influence the dynamics of ecosystems, particularly in disturbed environments where anthropogenic activities often result in higher pollution. Understanding the dynamics existing between native weed communities and invasive species in disturbed environments is crucial for effective management and normal ecosystem functioning. Recognising the potential resistance of native weed communities to invasion in disturbed environments can help identify suitable native plants for restoration operations. This review aims to investigate the adaptations exhibited by native and non‐native weeds that may affect invasions within disturbed environments. Factors such as ecological characteristics, altered soil conditions, and adaptations of native weed communities that potentially confer a competitive advantage relative to non‐native or invasive weeds in disturbed environments are analysed. Moreover, the roles of biotic interactions such as competition, mutualistic relationships, and allelopathy in shaping the invasion resistance of native weed communities are described. Emphasis is given to the consideration of the resistance of native weeds as a key factor in invasion dynamics that provides insights for conservation and restoration efforts in disturbed environments. Additionally, this review underscores the need for further research to unravel the underlying mechanisms and to devise targeted management strategies. These strategies aim to promote the resistance of native weed communities and mitigate the negative effects of invasive weed species in disturbed environments. By delving deeper into these insights, we can gain an understanding of the ecological dynamics within disturbed ecosystems and develop valuable insights for the management of invasive species, and to restore long‐term ecosystem sustainability.</jats:p>

<jats:title>ABSTRACT</jats:title><jats:p>Motion is a crucial part of the natural world, yet our understanding of how animals avoid predation whilst moving remains rather limited. Although several theories have been proposed for how antipredator defence may be facilitated during motion, there is often a lack of supporting empirical evidence, or conflicting findings. Furthermore, many studies have shown that motion often ‘breaks’ camouflage, as sudden movement can be detected even before an individual is recognised. Whilst some static camouflage strategies may conceal moving animals to a certain extent, more emphasis should be given to other modes of camouflage and related defences in the context of motion (e.g. flicker fusion camouflage, active motion camouflage, motion dazzle, and protean motion). Furthermore, when motion is involved, defence strategies are not necessarily limited to concealment. An animal can also rely on motion to mislead predators with regards to its trajectory, location, size, colour pattern, or even identity. In this review, we discuss the various underlying antipredator strategies and the mechanisms through which they may be linked to motion, conceptualising existing empirical and theoretical studies from two perspectives – concealing and misleading effects. We also highlight gaps in our understanding of these antipredator strategies, and suggest possible methodologies for experimental designs/test subjects (i.e. prey and/or predators) and future research directions.</jats:p>

<jats:title>ABSTRACT</jats:title><jats:p>Metabolism includes anabolism and catabolism, which play an essential role in many biological processes. Chromatin modifications are post‐translational modifications of histones and nucleic acids that play important roles in regulating chromatin‐associated processes such as gene transcription. There is a tight connection between metabolism and chromatin modifications. Many metabolic enzymes and metabolites coordinate cellular activities with alterations in nutrient availability by regulating gene expression through epigenetic mechanisms such as DNA methylation and histone modifications. The dysregulation of gene expression by metabolism and epigenetic modifications may lead to diseases such as diabetes and cancer. Recent studies reveal that metabolic enzymes and metabolites specifically regulate chromatin modifications, including modification types, modification residues and chromatin regions. This specific regulation has been implicated in the development of human diseases, yet the underlying mechanisms are only beginning to be uncovered. In this review, we summarise recent studies of the molecular mechanisms underlying the metabolic regulation of histone and DNA modifications and discuss how they contribute to pathogenesis. We also describe recent developments in technologies used to address the key questions in this field. We hope this will inspire further in‐depth investigations of the specific regulatory mechanisms involved, and most importantly will shed lights on the development of more effective disease therapies.</jats:p>

<jats:title>ABSTRACT</jats:title><jats:p>In biogeography, vicariance and long‐distance dispersal are often characterised as competing scenarios. However, they are related concepts, both relying on collective geological, ecological, and phylogenetic evidence. This is illustrated by freshwater fishes, which may immigrate to islands either when freshwater connections are temporarily present and later severed (vicariance), or by unusual means when ocean gaps are crossed (long‐distance dispersal). Marine barriers have a strong filtering effect on freshwater fishes, limiting immigrants to those most capable of oceanic dispersal. The roles of vicariance and dispersal are debated for freshwater fishes of the Greater Antilles. We review three active hypotheses [Cretaceous vicariance, Greater Antilles–Aves Ridge (GAARlandia), long‐distance dispersal] and propose long‐distance dispersal to be an appropriate model due to limited support for freshwater fish use of landspans. Greater Antillean freshwater fishes have six potential source bioregions (defined from faunal similarity): Northern Gulf of México, Western Gulf of México, Maya Terrane, Chortís Block, Eastern Panamá, and Northern South America. Faunas of the Greater Antilles are composed of taxa immigrating from many of these bioregions, but there is strong compositional disharmony between island and mainland fish faunas (&gt;90% of Antillean species are cyprinodontiforms, compared to &lt;10% in Northern Gulf of México and Northern South America, and ≤50% elsewhere), consistent with a hypothesis of long‐distance dispersal. Ancestral‐area reconstruction analysis indicates there were 16 or 17 immigration events over the last 51 million years, 14 or 15 of these by cyprinodontiforms. Published divergence estimates and evidence available for each immigration event suggests they occurred at different times and by different pathways, possibly with rafts of vegetation discharged from rivers or washed to sea during storms. If so, ocean currents likely provide critical pathways for immigration when flowing from one landmass to another. On the other hand, currents create dispersal barriers when flowing perpendicularly between landmasses. In addition to high salinity tolerance, cyprinodontiforms collectively display a variety of adaptations that could enhance their ability to live with rafts (small body size, viviparity, low metabolism, amphibiousness, diapause, self‐fertilisation). These adaptations likely also helped immigrants establish island populations after arrival and to persist long term thereafter. Cichlids may have used a pseudo bridge (Nicaragua Rise) to reach the Greater Antilles. Gars (Lepisosteidae) may have crossed the Straits of Florida to Cuba, a relatively short crossing that is not a barrier to gene flow for several cyprinodontiform immigrants. Indeed, widespread distributions of Quaternary migrants (<jats:italic>Cyprinodon</jats:italic>, <jats:italic>Gambusia</jats:italic>, <jats:italic>Kryptolebias</jats:italic>), within the Greater Antilles and among neighbouring bioregions, imply that long‐distance dispersal is not necessarily inhibitory for well‐adapted species, even though it appears to be virtually impossible for all other freshwater fishes.</jats:p>

<jats:title>ABSTRACT</jats:title><jats:p>For centuries, Gram‐negative pathogens have infected the human population and been responsible for numerous diseases in animals and plants. Despite advancements in therapeutics, Gram‐negative pathogens continue to evolve, with some having developed multi‐drug resistant phenotypes. For the successful control of infections caused by these bacteria, we need to widen our understanding of the mechanisms of host–pathogen interactions. Gram‐negative pathogens utilise an array of effector proteins to hijack the host system to survive within the host environment. These proteins are secreted into the host system <jats:italic>via</jats:italic> various secretion systems, including the integral Type III secretion system (T3SS). The T3SS spans two bacterial membranes and one host membrane to deliver effector proteins (virulence factors) into the host cell. This multifaceted process has multiple layers of regulation and various checkpoints. In this review, we highlight the multiple strategies adopted by these pathogens to regulate or maintain virulence <jats:italic>via</jats:italic> the T3SS, encompassing the regulation of small molecules to sense and communicate with the host system, as well as master regulators, gatekeepers, chaperones, and other effectors that recognise successful host contact. Further, we discuss the regulatory links between the T3SS and other systems, like flagella and metabolic pathways including the tricarboxylic acid (TCA) cycle, anaerobic metabolism, and stringent cell response.</jats:p>

<jats:title>ABSTRACT</jats:title><jats:p>The intracellular coral–dinoflagellate symbiosis is the engine that underpins the success of coral reefs, one of the most diverse ecosystems on the planet. However, the breakdown of the symbiosis and the loss of the microalgal symbiont (i.e. coral bleaching) due to environmental changes are resulting in the rapid degradation of coral reefs globally. There is an urgent need to understand the cellular physiology of coral bleaching at the mechanistic level to help develop solutions to mitigate the coral reef crisis. Here, at an unprecedented scope, we present novel models that integrate putative mechanisms of coral bleaching within a common framework according to the triggers (initiators of bleaching, e.g. heat, cold, light stress, hypoxia, hyposalinity), cascades (cellular pathways, e.g. photoinhibition, unfolded protein response, nitric oxide), and endpoints (mechanisms of symbiont loss, e.g. apoptosis, necrosis, exocytosis/vomocytosis). The models are supported by direct evidence from cnidarian systems, and indirectly through comparative evolutionary analyses from non‐cnidarian systems. With this approach, new putative mechanisms have been established within and between cascades initiated by different bleaching triggers. In particular, the models provide new insights into the poorly understood connections between bleaching cascades and endpoints and highlight the role of a new mechanism of symbiont loss, i.e. ‘symbiolysosomal digestion’, which is different from symbiophagy. This review also increases the approachability of bleaching physiology for specialists and non‐specialists by mapping the vast landscape of bleaching mechanisms in an atlas of comprehensible and detailed mechanistic models. We then discuss major knowledge gaps and how future research may improve the understanding of the connections between the diverse cascade of cellular pathways and the mechanisms of symbiont loss (endpoints).</jats:p>

<jats:title>ABSTRACT</jats:title><jats:p>The core principle shared by most theories and models of succession is that, following a major disturbance, plant–environment feedback dynamics drive a directional change in the plant community. The most commonly studied feedback loops are those in which the regrowth of the plant community causes changes to the abiotic (e.g. soil nutrients) or biotic (e.g. dispersers) environment, which differentially affect species availability or performance. This, in turn, leads to shifts in the species composition of the plant community. However, there are many other PE feedback loops that potentially drive succession, each of which can be considered a model of succession.</jats:p><jats:p>While plant–environment feedback loops in principle generate predictable successional trajectories, succession is generally observed to be highly variable. Factors contributing to this variability are the stochastic processes involved in feedback dynamics, such as individual mortality and seed dispersal, and extrinsic causes of succession, which are not affected by changes in the plant community but do affect species performance or availability. Both can lead to variation in the identity of dominant species within communities. This, in turn, leads to further contingencies if these species differ in their effect on their environment (priority effects). Predictability and variability are thus intrinsically linked features of ecological succession.</jats:p><jats:p>We present a new conceptual framework of ecological succession that integrates the propositions discussed above. This framework defines seven general causes: landscape context, disturbance and land‐use, biotic factors, abiotic factors, species availability, species performance, and the plant community. When involved in a feedback loop, these general causes drive succession and when not, they are extrinsic causes that create variability in successional trajectories and dynamics. The proposed framework provides a guide for linking these general causes into causal pathways that represent specific models of succession.</jats:p><jats:p>Our framework represents a systematic approach to identifying the main feedback processes and causes of variation at different successional stages. It can be used for systematic comparisons among study sites and along environmental gradients, to conceptualise studies, and to guide the formulation of research questions and design of field studies. Mapping an extensive field study onto our conceptual framework revealed that the pathways representing the study's empirical outcomes and conceptual model had important differences, underlining the need to move beyond the conceptual models that currently dominate in specific fields and to find ways to examine the importance of and interactions among alternative causal pathways of succession. To further this aim, we argue for integrating long‐term studies across environmental and anthropogenic gradients, combined with controlled experiments and dynamic modelling.</jats:p>

<jats:title>ABSTRACT</jats:title><jats:p>Social norms – rules governing which behaviours are deemed appropriate or inappropriate within a given community – are typically taken to be uniquely human. Recently, this position has been challenged by a number of philosophers, cognitive scientists, and ethologists, who have suggested that social norms may also be found in certain non‐human animal communities. Such claims have elicited considerable scepticism from norm cognition researchers, who doubt that any non‐human animals possess the psychological capacities necessary for normative cognition. However, there is little agreement among these researchers about what these psychological prerequisites are. This makes empirical study of animal social norms difficult, since it is not clear what we are looking for and thus what should count as behavioural evidence for the presence (or absence) of social norms in animals. To break this impasse, we offer an approach that moves beyond contested psychological criteria for social norms. This approach is inspired by the animal culture research program, which has made a similar shift away from heavily psychological definitions of ‘culture’ to become organised around a cluster of more empirically tractable concepts of culture. Here, we propose an analogous set of constructs built around the core notion of a <jats:italic>normative regularity</jats:italic>, which we define as <jats:italic>a socially maintained pattern of behavioural conformity within a community</jats:italic>. We suggest methods for studying potential normative regularities in wild and captive primates. We also discuss the broader scientific and philosophical implications of this research program with respect to questions of human uniqueness, animal welfare and conservation.</jats:p>