Relationship between phosphorus stoichiometric homeostasis and deepwater adaptability of submerged macrophytes in Erhai Lake, China: Insights from allometric plasticity.

The state transition theory suggests that the decline of submerged macrophytes in shallow lakes is closely associated with reduced stoichiometric homeostasis, particularly phosphorus homeostasis (HP). The degradation typically progresses from deeper to shallower regions, indicating a potential positive correlation between the deepwater adaptability (DA) and HP values of submerged macrophytes. Here, we investigated the distribution pattern of submerged macrophytes across different water depths of Erhai Lake to test this hypothesis. The results revealed a significant positive correlation between the DA and HP values of submerged macrophytes. Allometric analysis indicated that the morphological plasticity of submerged macrophytes was linked to their HP. Species with higher HP values, like Potamogeton maackianus, had robust plasticity strategies, particularly "real plasticity", that enabled them to cope with deeper water stress. In contrast, species with lower HP values (Ceratophyllum demersum and Hydrilla verticillata) experienced nutrient declines, which hindered their adaptation. Additionally, species with higher HP values exhibited closer connections within the plant traits-environment network, indicating that their morphological plasticity adjustments allow better adaptation to the environmental changes caused by increasing water depth. These results confirm the relationship between DA and HP in submerged macrophytes and explain the mechanisms underlying the correlation, thus expanding regime shift theory.

An appreciation of apex-to-base variation in xylem traits will lead to more precise understanding of xylem phenotypic plasticity.

Xylem air embolism is the primary cause of drought-related tree mortality. Phenotypic plasticity of xylem traits is key for species acclimation to environmental variability and evolution. It is widely believed that plants increase xylem embolism resistance in response to drought. However, I argue that this hypothesis, based on extensive literature, relies on sampling methods that overlook predictable anatomical patterns, potentially biasing our understanding of acclimation and adaptation strategies.

Nitrogen source and availability regulate plastic population dynamics in the marine diatom Thalassiosira weissflogii.

Variation in nitrogen (N) availability significantly influences population dynamics and the productivity of marine phytoplankton. As N availability in the ocean is conditioned by the N source, it is important to understand the capacity of phytoplankton organisms to adjust their physiology and dynamics under different N conditions. We investigated the growth dynamics of Thalassiosira weissflogii, a coastal diatom, in response to different N sources (Nitrate, NO3-; Ammonium, NH4+; urea, CH4N2O) and availabilities (45 and 5 µM). Our findings demonstrate that T. weissflogii can display plastic adjustments in population dynamics to different N sources. These responses evidenced a greater preference for NH4+ and urea than NO3-, particularly under high N availability. The relative growth rate (µ) is higher (1.18 ± 0.01) under NH4+-high treatment compared to NO3--high (1.01 ± 0.01). The carrying capacity (K) varied only among concentrations, indicating equal N utilization efficiency for biomass production. No effects of N source were detected under the low concentration, suggesting that the preference for NH4⁺ and urea was diminished by limited nitrogen supply due to potential interactions. These results provide valuable insights into the physiological flexibility of T. weissflogii to varying N conditions, shedding light on the ecological success and resilience of this species in highly variable coastal environments.

Latitudinal trends in an invasive plant: genetic differentiation, phenotypic plasticity, and the effects of heavy metals and herbivores on growth, defence, and reproductive characteristics.

BACKGROUND AND AIMS: Invasive species usually demonstrate remarkable adaptability across diverse environments, successfully inhabiting a wide variety of regions. This adaptability often links to genetic differentiation and phenotypic plasticity, leading to latitudinal trends in phenotypic traits. In this study, we collected seeds of invasive plant Phytolacca americana from different latitudes and planted them in homogeneous gardens to investigate the latitudinal variation of P. americana phenotypic traits and to evaluate the effects of herbivory and heavy metals on plant growth, defence, and reproductive characteristics. METHODS: P. americana seeds from different latitudes were planted in a homogeneous garden. For the experimental treatment, the seeds were divided into four groups: a heavy metal treatment group and its corresponding control group, and a cover treatment group with its corresponding control group. After the fruits matured, their growth, reproduction, and defence indicators were measured. KEY RESULTS: Significant latitudinal trends were observed in P. americana's growth and defence characteristics, including changes in branch number, underground biomass, total biomass, and leaf tannin content. Compared to previous field surveys on P. americana, our study found that the latitude trends in growth structure and defence traits were consistent. But the latitudinal trend of reproductive structure is different. Moreover, heavy metals and herbivory substantially influenced the plant's growth, reproduction, and defence mechanisms, further shaping its latitudinal patterns. CONCLUSIONS: The observed phenotypic variations in P. americana across latitudes can be largely attributed to the synergistic effects of phenotypic plasticity and genetic variation. At a broader geographical scale, adaptations to heavy metal stress and herbivory pressure among different P. americana populations involve distinct trade-offs related to growth, reproduction, and defence strategies.

Evolution of pH-sensitive transcription termination in Escherichia coli during adaptation to repeated long-term starvation.

Fluctuating environments that consist of regular cycles of co-occurring stress are a common challenge faced by cellular populations. For a population to thrive in constantly changing conditions, an ability to coordinate a rapid cellular response is essential. Here, we identify a mutation conferring an arginine-to-histidine (Arg to His) substitution in the transcription terminator Rho. The rho R109H mutation frequently arose in Escherichia coli populations experimentally evolved under repeated long-term starvation conditions, during which the accumulation of metabolic waste followed by transfer into fresh media results in drastic environmental pH fluctuations associated with feast and famine. Metagenomic sequencing revealed that populations containing the rho mutation also possess putative loss-of-function mutations in ydcI, which encodes a recently characterized transcription factor associated with pH homeostasis. Genetic reconstructions of these mutations show that the rho allele confers plasticity via an alkaline-induced reduction of Rho function that, when found in tandem with a ΔydcI allele, leads to intracellular alkalization and genetic assimilation of Rho mutant function. We further identify Arg to His substitutions at analogous sites in rho alleles from species that regularly experience neutral to alkaline pH fluctuations in their environments. Our results suggest that Arg to His substitutions in Rho may serve to rapidly coordinate complex physiological responses through pH sensing and shed light on how cellular populations use environmental cues to coordinate rapid responses to complex, fluctuating environments.

The 2024 roadmap for understanding marine species' resilience in a changing ocean.

Written to serve as a guideline for future research in this field, this roadmap provides some perspectives on the main developments and remaining challenges in the field of marine animal acclimatisation, adaptive potential and resilience to climate change. There has been extensive research conducted on the impact of climate change stress on marine animals, with studies recognising the potential for cross- and multi- generational impacts. Parents can potentially pass on resilience to offspring. The response of marine animals to climate change stressors is complex where utilising marginal and extreme systems as natural laboratories can help to address key research gaps and provide an understanding of the plastic and adaptive changes necessary for survival under stress.

Reprint: Acclimatization and Adaptive Capacity of Marine Species in a Changing Ocean.

To persist in an ocean changing in temperature, pH and other stressors related to climate change, many marine species will likely need to acclimatize or adapt to avoid extinction. If marine populations possess adequate genetic variation in tolerance to climate change stressors, species might be able to adapt to environmental change. Marine climate change research is moving away from single life stage studies where individuals are directly placed into projected scenarios ('future shock' approach), to focus on the adaptive potential of populations in an ocean that will gradually change over coming decades. This review summarizes studies that consider the adaptive potential of marine invertebrates to climate change stressors and the methods that have been applied to this research, including quantitative genetics, laboratory selection studies and trans- and multigenerational experiments. Phenotypic plasticity is likely to contribute to population persistence providing time for genetic adaptation to occur. Transgenerational and epigenetic effects indicate that the environmental and physiological history of the parents can affect offspring performance. There is a need for long-term, multigenerational experiments to determine the influence of phenotypic plasticity, genetic variation and transgenerational effects on species' capacity to persist in a changing ocean. However, multigenerational studies are only practicable for short generation species. Consideration of multiple morphological and physiological traits, including changes in molecular processes (eg, DNA methylation) and long-term studies that facilitate acclimatization will be essential in making informed predictions of how the seascape and marine communities will be altered by climate change.

Variable juvenile growth rates and offspring size: a response to anthropogenic shifts in prey size among populations.

Environmental variables, such as resource quality, shape growth in organisms, dictating body size, an important correlate of fitness. Variation in prey characteristics among populations is frequently associated with similar variation in predator body sizes. Anthropogenic alterations to prey landscapes impose novel ecological pressures on predators that may shift predator phenotypes. Research has focused on determining the adaptability of the phenotypic response by testing its genetic heritability. Here, we asked if anthropogenic shifts in prey size across the landscape correlate with juvenile growth rates among populations of watersnakes with divergent life-history phenotypes. We sought to determine if growth rate variation is the product of genetic adaptation or a non-heritable phenotypic response. Using a common-garden design, we measured growth of neonate snakes from fish farms varying in prey size. We found juvenile growth rates are faster for snakes with larger initial body sizes and from populations with larger average prey sizes. Our data suggest variability in juvenile grow rates within and among populations are not the product of genetic adaptation, but the indirect consequence of initial offspring size variation and prey consumption. We propose larger offspring sizes may favor increased juvenile growth rates, mediated through a larger morphological capacity to consume and process energy resources relative to smaller individuals. This experiment provides evidence supporting the growing body of literature that non-heritable responses may be significant drivers of rapid phenotypic divergence among populations across a landscape. This mechanism may explain the stability and colonization of populations in response to rapid, human-mediated, landscape changes.

Circadian disruption in cancer hallmarks: Novel insight into the molecular mechanisms of tumorigenesis and cancer treatment.

Circadian rhythms are 24-h rhythms governing temporal organization of behavior and physiology generated by molecular clocks composed of autoregulatory transcription-translation feedback loops (TTFLs). Disruption of circadian rhythms leads to a spectrum of pathologies, including cancer by triggering or being involved in different hallmarks. Clock control of phenotypic plasticity involved in tumorigenesis operates in aberrant dedifferentiating to progenitor-like cell states, generation of cancer stem cells (CSCs) and epithelial-to-mesenchymal transition (EMT) events. Circadian rhythms might act as candidates for regulatory mechanisms of cellular senescent and functional determinants of senescence-associated secretory phenotype (SASP). Reciprocal control between clock and epigenetics sheds light on post-transcriptional regulation of circadian rhythms and opens avenues for novel anti-cancer strategies. Additionally, disrupting circadian rhythms influences microbiota communities that could be associated with altered homeostasis contributing to cancer development. Herein, we summarize recent advances in support of the nexus between disruptions of circadian rhythms and cancer hallmarks of new dimensions, thus providing novel perspectives on potentially effective treatment approaches for cancer management.

Epigenetics Research in Evolutionary Biology: Perspectives on Timescales and Mechanisms.

Epigenetics research in evolutionary biology encompasses a variety of research areas, from regulation of gene expression to inheritance of environmentally mediated phenotypes. Such divergent research foci can occasionally render the umbrella term "epigenetics" ambiguous. Here I discuss several areas of contemporary epigenetics research in the context of evolutionary biology, aiming to provide balanced views across timescales and molecular mechanisms. The importance of epigenetics in development is now being assessed in many nonmodel species. These studies not only confirm the importance of epigenetic marks in developmental processes, but also highlight the significant diversity in epigenetic regulatory mechanisms across taxa. Further, these comparative epigenomic studies have begun to show promise toward enhancing our understanding of how regulatory programs evolve. A key property of epigenetic marks is that they can be inherited along mitotic cell lineages, and epigenetic differences that occur during early development can have lasting consequences on the organismal phenotypes. Thus, epigenetic marks may play roles in short-term (within an organism's lifetime or to the next generation) adaptation and phenotypic plasticity. However, the extent to which observed epigenetic variation occurs independently of genetic influences remains uncertain, due to the widespread impact of genetics on epigenetic variation and the limited availability of comprehensive (epi)genomic resources from most species. While epigenetic marks can be inherited independently of genetic sequences in some species, there is little evidence that such "transgenerational inheritance" is a general phenomenon. Rather, molecular mechanisms of epigenetic inheritance are highly variable between species.

No evidence for an up-regulation of female immune function in response to elevated risk of sexual conflict.

Sexual conflict is widespread among sexually reproducing organisms. Phenotypic plasticity in female resistance traits has the potential to moderate the harm imposed by males during mating, yet female plasticity has rarely been explored. In this experiment, we investigated whether female seed beetles invest more in immunocompetence, measured as phenoloxidase (PO) capacity, when exposed to cues signalling a greater risk of sexual conflict. Risk perception was manipulated by housing focal individuals alone or with a companion as developing larvae, followed by exposure to a mating-free male- or female-biased social environment when adults. We predicted that females exposed to cues of increased sexual conflict would have increased PO capacity. However, PO capacity did not differ between either larval or adult social treatments. Our results suggest that females may not perceive a risk to their fitness on the basis of increased male presence or are unable to adjust this aspect of their phenotype in response to that risk.

SOX10 mediates glioblastoma cell-state plasticity.

Phenotypic plasticity is a cause of glioblastoma therapy failure. We previously showed that suppressing the oligodendrocyte-lineage regulator SOX10 promotes glioblastoma progression. Here, we analyze SOX10-mediated phenotypic plasticity and exploit it for glioblastoma therapy design. We show that low SOX10 expression is linked to neural stem-cell (NSC)-like glioblastoma cell states and is a consequence of temozolomide treatment in animal and cell line models. Single-cell transcriptome profiling of Sox10-KD tumors indicates that Sox10 suppression is sufficient to induce tumor progression to an aggressive NSC/developmental-like phenotype, including a quiescent NSC-like cell population. The quiescent NSC state is induced by temozolomide and Sox10-KD and reduced by Notch pathway inhibition in cell line models. Combination treatment using Notch and HDAC/PI3K inhibitors extends the survival of mice carrying Sox10-KD tumors, validating our experimental therapy approach. In summary, SOX10 suppression mediates glioblastoma progression through NSC/developmental cell-state transition, including the induction of a targetable quiescent NSC state. This work provides a rationale for the design of tumor therapies based on single-cell phenotypic plasticity analysis.

Developmental programming of sarcoplasmic-reticulum function improves cardiac anoxia tolerance in turtles.

Oxygen deprivation during embryonic development can permanently remodel the vertebrate heart, often causing cardiovascular abnormalities in adulthood. While this phenomenon is mostly damaging, recent evidence suggests developmental hypoxia produces stress-tolerant phenotypes in some ectothermic vertebrates. Embryonic common snapping turtles (Chelydra serpentina) subjected to chronic hypoxia display improved cardiac anoxia tolerance after hatching, which is associated with altered Ca2+ homeostasis in heart cells (cardiomyocytes). Here we examined the possibility that changes in Ca2+ cycling, through the sarcoplasmic reticulum (SR), underlie the developmentally programmed cardiac phenotype of snapping turtles. We investigated this hypothesis by isolating cardiomyocytes from juvenile turtles that developed in either normoxia (21% O2; "N21") or chronic hypoxia (10% O2; "H10") and subjected the cells to anoxia/reoxygenation, either in the presence or absence of SR Ca2+-cycling inhibitors. We simultaneously measured cellular shortening, intracellular [Ca2+], and intracellular pH (pHi). Under normoxic conditions, N21 and H10 cardiomyocytes shortened equally, but H10 Ca2+ transients (Δ[Ca2+]i) were twofold smaller than N21 cells, and SR inhibition only decreased N21 shortening and Δ[Ca2+]i. Anoxia subsequently depressed shortening, Δ[Ca2+]i, and pHi in control N21 and H10 cardiomyocytes, yet H10 shortening and Δ[Ca2+]i recovered to pre-anoxic levels, partly due to enhanced myofilament Ca2+ sensitivity. SR blockade abolished the recovery of anoxic H10 cardiomyocytes and potentiated decreases in shortening, Δ[Ca2+]i, and pHi. Our novel results provide the first evidence of developmental programming of SR function and demonstrate that developmental hypoxia confers a long-lasting, superior anoxia-tolerant cardiac phenotype in snapping turtles, by enhancing myofilament Ca2+ sensitivity and modifying SR function.

Plasticity cannot fully compensate evolutionary differences in heat tolerance across fish species.

Understanding how evolution and phenotypic plasticity contribute to variation in heat tolerance is crucial to predict responses to warming. Here we analyze 272 thermal death time curves of 53 fish species acclimated to different temperatures and quantify their relative contributions. Analyses show that evolution and plasticity account, respectively, for 80.5 % and 12.4 % of the variation in elevation across curves, whereas their slope remained invariant. Evolutionary and plastic adaptive responses differ in magnitude, with heat tolerance increasing 0.54 ºC between species and 0.32 ºC within species for every 1 ºC increase in environmental temperatures. After successfully predicting critical temperatures under ramping conditions to validate these estimates, we show that fish populations can only partly ameliorate the impact of warming waters via thermal acclimation and this deficit in plasticity could increase as the warming accelerates.

Early-life variation in migration is subject to strong fluctuating survival selection in a partially migratory bird.

Population dynamic and eco-evolutionary responses to environmental variation and change fundamentally depend on combinations of within- and among-cohort variation in the phenotypic expression of key life-history traits, and on corresponding variation in selection on those traits. Specifically, in partially migratory populations, spatio-seasonal dynamics depend on the degree of adaptive phenotypic expression of seasonal migration versus residence, where more individuals migrate when selection favours migration. Opportunity for adaptive (or, conversely, maladaptive) expression could be particularly substantial in early life, through the initial development of migration versus residence. However, within- and among-cohort dynamics of early-life migration, and of associated survival selection, have not been quantified in any system, preventing any inference on adaptive early-life expression. Such analyses have been precluded because data on seasonal movements and survival of sufficient young individuals, across multiple cohorts, have not been collected. We undertook extensive year-round field resightings of 9359 colour-ringed juvenile European shags Gulosus aristotelis from 11 successive cohorts in a partially migratory population. We fitted Bayesian multi-state capture-mark-recapture models to quantify early-life variation in migration versus residence and associated survival across short temporal occasions through each cohort's first year from fledging, thereby quantifying the degree of adaptive phenotypic expression of migration within and across years. All cohorts were substantially partially migratory, but the degree and timing of migration varied considerably within and among cohorts. Episodes of strong survival selection on migration versus residence occurred both on short timeframes within years, and cumulatively across entire first years, generating instances of instantaneous and cumulative net selection that would be obscured at coarser temporal resolutions. Further, the magnitude and direction of selection varied among years, generating strong fluctuating survival selection on early-life migration across cohorts, as rarely evidenced in nature. Yet, the degree of migration did not strongly covary with the direction of selection, indicating limited early-life adaptive phenotypic expression. These results reveal how dynamic early-life expression of and selection on a key life-history trait, seasonal migration, can emerge across seasonal, annual, and multi-year timeframes, yet be substantially decoupled. This restricts the potential for adaptive phenotypic, microevolutionary, and population dynamic responses to changing seasonal environments.

Resource supply and intraspecific variation in inducible defense determine predator-prey interactions in an intraguild predation food web.

This study investigated the dynamics of reciprocal phenotypic plasticity entailing inducible defense and offense in freshwater ciliate communities in response to altered resource supply and the extent of intraspecific trait variation. Communities consisted of Euplotes octocarinatus (intraguild prey) capable of inducible defense to escape predation, Stylonychia mytilus (intraguild predator) capable of inducible offense to expand its prey spectrum, and Cryptomonas sp. (algal resource). The extent of inducible defense was tested in ten different Euplotes strains in response to freeze-killed Stylonychia concentrate, revealing significant differences in their width and length development. In a subsequent 30-day experiment, four strains were incubated in monoculture and mixture with Stylonychia under continuous and pulsed microalgae supply. The polyclonal Euplotes population outperformed the monoclonal populations, except one, which developed the most pronounced inducible defense and retained the highest biovolume. Stylonychia fluctuated in size, but dominated all communities irrespective of clonal composition. Pulsed resource supply promoted biovolume production of both species. However, periods of resource depletion resulted in more Stylonychia resting cysts, allowing Euplotes to resume growth. Our study provides new insights into interactions of induced defense and intraguild predation under variable environmental conditions, emphasizing the relevance of intraspecific trait variation for predator-prey interactions and community dynamics.

Trehalose mediates salinity-stress tolerance in natural populations of a freshwater crustacean.

Salinization poses an increasing problem worldwide, threatening freshwater organisms and raising questions about their ability to adapt. We explored the mechanisms enabling a planktonic crustacean to tolerate elevated salinity. By gradually raising water salinity in clonal cultures from 185 Daphnia magna populations, we showed that salt tolerance strongly correlates with native habitat salinity, indicating local adaptation. A genome-wide association study (GWAS) further revealed a major effect of the Alpha,alpha-trehalose-phosphate synthase (TPS) gene, suggesting that trehalose production facilitates salinity tolerance. Salinity-tolerant animals showed a positive correlation between water salinity and trehalose concentrations, while intolerant animals failed to produce trehalose. Animals with a non-functional TPS gene, generated through CRISPR-Cas9, supported the trehalose role in salinity stress. Our study highlights how a keystone freshwater animal adapts to salinity stress using an evolutionary mechanism known in bacteria, plants, and arthropods.

How does climate change impact social bees and bee sociality?

Climatic factors are known to shape the expression of social behaviours. Likewise, variation in social behaviour can dictate climate responses. Understanding interactions between climate and sociality is crucial for forecasting vulnerability and resilience to climate change across animal taxa. These interactions are particularly relevant for taxa like bees that exhibit a broad diversity of social states. An emerging body of literature aims to quantify bee responses to environmental change with respect to variation in key functional traits, including sociality. Additionally, decades of research on environmental drivers of social evolution may prove fruitful for predicting shifts in the costs and benefits of social strategies under climate change. In this review, we explore these findings to ask two interconnected questions: (a) how does sociality mediate vulnerability to climate change, and (b) how might climate change impact social organisation in bees? We highlight traits that intersect with bee sociality that may confer resilience to climate change (e.g. extended activity periods, diet breadth, behavioural thermoregulation) and we generate predictions about the impacts of climate change on the expression and distribution of social phenotypes in bees. The social evolutionary consequences of climate change will be complex and heterogeneous, depending on such factors as local climate and plasticity of social traits. Many contexts will see an increase in the frequency of eusocial nesting as warming temperatures accelerate development and expand the temporal window for rearing a worker brood. More broadly, climate-mediated shifts in the abiotic and biotic selective environments will alter the costs and benefits of social living in different contexts, with cascading impacts at the population, community and ecosystem levels.

The genetics of phenotypic plasticity. XVIII. Developmental limits restrict adaptive plasticity.

After environmental change, the trait evolution needed to rescue a population depends on the functional form of the plastic change (reaction norm) of that trait. Nearly all previous models of plasticity evolution for continuous traits have assumed that the functional form is linear, i.e., no limits on the range of plasticity. This paper examines the effect of developmental limits, modeled as a sigmoidal reaction norm, on evolutionary rescue after an abrupt environmental change and the subsequent evolution of plasticity, including genetic assimilation. We examined four different scenarios: (1) developmental limits only, (2) developmental limits plus a cost of plasticity, (3) developmental limits with developmental noise, and (4) developmental limits plus environmental variation. The probability of evolutionary rescue increased with an increase in phenotypic variation allowed by plastic development. With a smaller limit to the range of the plastic phenotype, the evolution of adaptive plasticity was limited, meaning the evolution of non-plastic genes was necessary. The addition of developmental constraints to the model did not speed up genetic assimilation, suggesting new theory is needed to understand empirical observations. The modeling framework presented here could be extended to different ecological and evolutionary conditions, alternative reaction norm shapes, the evolution of additional reaction norm parameters such as the range or the location of the inflection point on the environmental axis, or other function-valued traits.