Biological Reviews最新文献

Historically, a vertebrate-centric paradigm has framed our interpretation of molluscan endocrinology, with considerable research focusing on vertebrate-type steroid hormones (e.g. oestrogens, testosterone). However, contradictory evidence on the occurrence of vertebrate-type steroid hormones in molluscan tissues, and a lack of the specific steroidogenesis enzymes involved in producing these steroids has fuelled an ongoing debate about the ability of molluscs to biosynthesise vertebrate-type steroids de novo. Consequently, the exploration of other hormonal pathways that may exist in the phylum remains a significant knowledge gap. This study systematically identified, combined and evaluated evidence from 147 eligible studies (published between 2012 and 2021) on the occurrence of hormones, hormone receptors and hormone-metabolising enzymes in Mollusca according to the 2015 PRISMA-P systematic review guidelines and the 2020 COSTER guidelines. The data collected are holistically summarised and visualised in a fully searchable, interactive and openly accessible online database using Tableau Public 2023.1 software. A critical appraisal assessment (Risk-of-Bias tool) accompanied by tailor-made guidelines as well as a narrative synthesis using comparative endocrinology is presented. Strikingly, 95% of studies measuring hormones in molluscs did not investigate the hormones' ability to bind to their respective receptors. Moreover, many studies either used methods now considered unreliable (e.g. lack specificity) to identify relevant biomolecules (i.e. hormones, receptors, enzymes) or did not employ robust internal validation steps, with 83% of all studies not independently repeating their experiments. This highlights an urgent need for greater experimental rigour in the field. Most studies were also found to be heavily skewed towards vertebrate-type sex steroidogenesis, with 66% measuring 17β-oestradiol in mollusc tissues, despite unconvincing evidence that molluscs can biosynthesise vertebrate-type steroids. By contrast, the retinoic acid signalling pathway, known to be more evolutionarily conserved (and a target of environmental pollution), has received far less attention. However, a limited number of studies are now looking beyond vertebrate-type sex steroids, notably those looking at thyroid hormones, phytosterols (plant sterols) and ecdysteroids (insect steroids) in molluscs. These studies should act as a catalyst to spark interest in further exploration of understudied or unexplored hormonal pathways in Mollusca to elucidate fully the endocrinology of this important phylum.

Three categories of explanations exist for why we age: mechanistic theories, which omit reference to evolutionary forces; weakening force of selection theories, which posit that barriers exist that prevent evolutionary forces from optimising fitness in ageing; and optimisation theories, which posit that evolutionary forces actually select for ageing under the constraints that exist due to limited energy and other resources. We now have a broad data set of observed features of ageing against which these categories of theories can be tested, including results of interventions like caloric restriction, features of long-lived organisms, the existence of mortality rate plateaus, longevity of eusocial insect queens, and the malleability of lifespan. Optimisation theories are the only ones that fit all the observed data. Moreover, this category of theory makes a very ordinary claim, consistent with significant other data: evolution by natural selection is operating in ageing. It is actually quite extraordinary, either implicitly or explicitly, to claim that natural selection fails to operate, as the other categories of theories do. A key prediction of optimisation theories that differs from other theories is that mutations that extend lifespan should generally reduce fitness under natural conditions. Contrary to some suggestions in the literature, to date the available evidence supports this prediction. Optimisation theories have several implications, including that lifespan should be relatively easy to manipulate by tapping into existing biological mechanisms, and that the geroscience hypothesis, which states that intervention on the rate of ageing should also modulate the incidence of age-related diseases, is likely to be correct.

The biological effects of weak magnetic fields have long been a subject of scientific inquiry, with increasing evidence supporting their influence on biochemical, physiological, and behavioural processes. This review describes three primary mechanisms of magnetoreception that have been identified in migrating animals: use of magnetite in sensitive cells, sensitive electroreceptors, and spin dynamics in cryptochrome radical pairs. It also critically examines the potential of the radical-pair mechanism to serve as a universal explanation for the diverse non-sensory biological effects of weak magnetic fields, including extremely low-frequency magnetic fields, static magnetic fields, and hypomagnetic conditions. Understanding how weak magnetic fields influence radical-pair processes could revolutionize our approach to bioelectromagnetic interactions and provide new avenues for development of medical and technological applications. Future research should focus on direct real-time monitoring of radical-pair-mediated biochemical reactions, evaluating the interplay between magnetic fields, light exposure, and temperature, and refining theoretical models to bridge the gap between quantum-scale interactions and macroscopic biological effects. Addressing these questions will be essential in determining whether the radical-pair mechanism can serve as a unifying principle in magnetobiology.

Glycolysis is a fundamental metabolic pathway central to the bioenergetics and physiology of virtually all living organisms. In this comprehensive review, we explore the intricate biochemical principles and evolutionary origins of glycolytic pathways, from the classical Embden-Meyerhof-Parnas (EMP) pathway in humans to various prokaryotic and alternative glycolytic routes. By examining glycolysis across the tree of life, we explore its presence and adaptation in prokaryotes, archaea, bacteria, animals and plants, and the extension of glycolysis into sulfosugar metabolism. Further, we discuss the role of unwanted side reactions, thermodynamic principles, and metabolic control principles that underpin glycolysis and the broader metabolic network, and summarise advanced methods for quantifying glycolytic activity, including new analytical methods, alongside kinetic, constraint-based, and machine-learning based modelling. With a focus on the Pasteur, Crabtree, and Warburg effects, this review further discusses the roles of glycolysis in health and disease, highlighting its impact on global metabolic operations, inborn errors, and various pathologies as well as its role in biotechnology and metabolic engineering.

We examine two standard phylogenetic-biogeographic patterns and how these are interpreted by current ancestral-area algorithms. In the first pattern, a basal, paraphyletic grade is restricted to one part of its clade's overall range. In the second pattern, the clades of a group overlap in one central area but are allopatric elsewhere, resulting in a 'star pattern'. Ancestral-area algorithms will calculate a localised centre of origin for both patterns in the area of overlap. Yet both patterns can also be derived by vicariance (causing the allopatry) and subsequent range expansion by normal dispersal (causing the overlap). In this model, ancestors of allopatric clades were already widespread and polymorphic before the modern clades began to diverge. The overlap region is not a centre of origin, it is a region of secondary range expansion. There is no reason to assume that basal grades occupy ancestral areas or habitats. There is also no need to use a priori areas in biogeographic analysis. Instead, the distributional relationships among the clade localities can be examined directly. Distribution has emerged as a critical factor in molecular systematics, as many clades are defined more easily by their geographic distribution than by traditional morphological characters. Thus, it makes sense to review the precise geometry of the distributions in a study group, including details of allopatry, disjunction, overlap and others. A distinction is drawn here between secondary clade overlap that has developed following the origin of the clades, and primary clade overlap (true sympatry) that developed with the origin of the clades. In current practice, distribution maps have been replaced in biogeographic analysis by outputs from ancestral-area analyses. But if the main clades recovered in a study are mapped, simple, distinctive features, such as allopatry, marginal overlap and disjunction often become evident, and we encourage authors to map their clades. The patterns discussed here, for example, the star pattern centred on New Zealand, are repeated in unrelated groups. Thus, the regions interpreted in ancestral-area analysis as centres of origin can be re-interpreted as phylogenetic-biogeographic breaks (nodes) in widespread ancestors. The method proposed here - 'allopatry indicates vicariance; overlap indicates dispersal' - is simpler to apply than the current algorithms, and the results are much simpler, with a single cause explaining many distribution patterns, rather than each component clade of a biogeographic pattern having a separate history.

Social inequality among individuals is a common cause of conflict in the animal kingdom. In eusocial insects, such as ants, bees, wasps, and termites, for example, the large differences in reproductive potential between castes result in conflicts over caste fate during development. Here, we present the first comprehensive review on caste fate conflict, drawing on data from diverse taxa and recent theoretical advances. In many eusocial species, caste fate is determined by differential feeding, which results in caste fate being socially controlled, thereby aligning larval development with the collective needs of the colony. However, in some taxa, mechanisms of individual self-determination disrupt this balance, leading to overproduction of reproductive individuals at the expense of workers, with significant costs to colony fitness. Such conflicts are particularly pronounced in some stingless bees and lower termites, where larvae can bypass social control to determine their own caste fate. Indications of caste conflict can also be found in other groups, such as in some parasitic ants and in ant hybrid zones. Overall, the observed dynamics illustrate how conflicts in biological systems can be resolved in favour of either individual or collective interests, and how this affects the functioning of higher levels of organisation.

Ants and phloem-feeding hemipterans have established one of the most widespread and best-known mutualisms on Earth. In this mutualism, known as trophobiosis, ants feed on honeydew excreted by phloem-feeding hemipterans and, in exchange, protect hemipterans from their antagonists. Parasitoid wasps are among the main groups of antagonists of phloem-feeding hemipterans. Like trophobiosis, the interaction between trophobiotic ants and parasitoids of phloem-feeding hemipterans has evolved over millions of years and is widely distributed both geographically and phylogenetically. Ants protect phloem-feeding hemipterans from their parasitoids in many different ways, with outcomes for parasitoids that vary from altered reproduction or development to death. Consequently, parasitoids have evolved a series of behavioural, chemical, and morphological adaptations that reduce or limit the impact of trophobiotic ants. Our review shows that research on these interactions is asymmetric and strongly biased towards certain taxa and ecosystems, mostly aphids that feed on temperate crops. It will be necessary to broaden the range of taxa and ecosystems studied to evaluate how these interactions have shaped the evolution of phloem-feeding hemipterans, their parasitoids, and trophobiotic ants. While, in general, the presence of trophobiotic ants reduces the top-down regulation of phloem-feeding hemipterans by parasitoids, recent findings suggest that the mechanisms that explain this reduction are more complex than expected. By reviewing these interactions, the limitations of past research, and the advantages of current techniques, we provide perspectives to understand: (i) the mechanisms that ants use to protect hemipterans from parasitoids; (ii) the strategies evolved by parasitoids to counteract these ants; and (iii) the multiple factors that modulate the effects of trophobiotic ants on parasitoids of hemipterans. We suggest that a better understanding of these interactions will improve the management of phloem-feeding hemipterans, which constitute one of the most damaging groups of pests to global agriculture.

Epigenetics refers to heritable changes in genome function that occur without direct alterations to the DNA sequence. A multitude of environmental contaminants can influence the epigenetic marks of a genome. Changes of epigenetic marks including DNA methylation, histone modifications, and non-coding RNAs can induce alterations at the gene transcription level, potentially leading to physiological long-term changes that can be inherited transgenerationally. (Eco)Toxicoepigenetics is thus an emerging field of research focusing on linking environmental exposure with epigenome alterations, with a high postulated relevance for improved ecological risk assessment at the regulatory level. Despite its huge potential, fundamental knowledge is scarce and scattered concerning epigenetic regulation in relevant ecotoxicological model species and mechanisms of interaction between environmental contaminants and the epigenome. This is a paramount challenge for the efficient implementation of (eco)toxicoepigenetics that is not often recognised in the literature. Herein, we provide updated knowledge regarding the main epigenetic modifications that occur on ecotoxicologically relevant models and summarize the differences in epigenetic patterns between vertebrate and invertebrate species that are routinely used as test organisms in ecotoxicology. We also systematically revise what is known on the mechanisms through which environmental contaminants can modulate the epigenome, using three legacy contaminants of the aquatic compartment for which appreciable information exists concerning ecotoxicologically relevant species. Future directions for (eco)toxicoepigenetics research are discussed in the context of the existing knowledge, with particular emphasis on the much-needed characterization of the epigenomes of ecotoxicological models and the need to understand better the mechanisms underlying the modulation of epigenetic marks and related machinery by environmental contaminants. This review will hopefully stimulate future research contributing to the continuous incorporation of epigenetic studies in ecotoxicology and the development and implementation of effective epigenetic-based ecotoxicological biomarkers for environmental stress assessment.

Traits that affect organismal fitness are often highly genetically variable. This genetic variation is vital for populations to adapt to their environments, but it is also surprising given that nature - after all - 'selects' the best genotypes at the expense of those that fall short. Explaining the extensive genetic variation of fitness-related traits is thus a longstanding puzzle in evolutionary biology, with cascading implications for ecology, conservation, and human health. Balancing selection - an umbrella term for scenarios in which natural selection maintains genetic variation - is a century-old explanation to resolve this puzzle that has gained recent momentum from genome-scale methods for detecting it. Yet evaluating whether balancing selection can, in fact, resolve the puzzle is challenging, given the logistical constraints of distinguishing balancing selection from alternative hypotheses and the daunting collection of theoretical models that formally underpin this debate. Here, we track the development of balancing selection theory over the last century and provide an accessible review of this rich collection of models. We first outline the range of biological scenarios that can generate balancing selection. We then examine how fundamental features of genetic systems - non-random mating between individuals, ploidy levels, genetic drift, linkage, and genetic architectures of traits - have been progressively incorporated into the theory. We end by linking these theoretical predictions to ongoing empirical efforts to understand the evolutionary processes that explain genetic variation.