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Niche construction through phenological plasticity: life history dynamics and ecological consequences.

The ability of an organism to alter the environment that it experiences has been termed 'niche construction'. Plants have several ways whereby they can determine the environment to which they are exposed at different life stages. This paper discusses three of these: plasticity in dispersal, flowering timing and germination timing. It reviews pathways through which niche construction alters evolutionary and ecological trajectories by altering the selective environment to which organisms are exposed, the phenotypic expression of plastic characters, and the expression of genetic variation. It provides examples whereby niche construction creates positive or negative feedbacks between phenotypes and environments, which in turn cause novel evolutionary constraints and novel life-history expression.

Biological Evolution↗

A direct experimental test of founder-flush effects on the evolutionary potential for assortative mating.

Founder-flush speciation models propose that population bottlenecks can enhance evolutionary potential for reproductive isolation. To test this prediction, we subjected bottlenecked (three-pair founder-flush) and nonbottlenecked populations of the housefly to 18 generations of selection for assortative mating. After the selection regime, we analysed videotaped courtship bouts in these lines to identify correlated responses to the selection protocol. The realized heritabilities for assortative mating for both the bottlenecked and nonbottlenecked treatments were very low, but still significant. The founder-flush populations had thus responded to selection as well as the nonbottlenecked populations, although not significantly greater (i.e. total increases in assortative mating were 9.6 and 8.6%, respectively). Multivariate analyses on the courtship repertoires found that, although both bottlenecked and nonbottlenecked treatments attained similar levels of assortative mating, the treatments exhibited different evolutionary solutions in their correlated responses. Specifically, the bottlenecked lines demonstrated a significantly more diverse set of evolutionary trajectories (i.e. significant shifts along the second principal component for courtship). This suggests that the bottlenecked lines had greater potential for the evolution of novel phenotypes as predicted by founder-induced speciation models. Our results, however, cannot distinguish whether the more variable evolutionary responses resulted from increased heritabilities in courtship components, reduced potential to follow the convergent evolutionary trajectories noted for the nonbottlenecked lines, or some combination of both general processes in determining the resultant multivariate phenotype.

Animals↗

Prenatal testosterone excess programs reproductive and metabolic dysfunction in the female.

Findings discussed in this review stress the importance of normal estrogen and androgen signaling at appropriate developmental time points in maintaining normal phenotypic expression, reproductive and metabolic function and document how inappropriate steroid signaling, at inopportune times can have undesirable outcomes. For example, inappropriate testosterone exposure during fetal life alters the developmental trajectory of the female culminating in a suite of disorders, which include intrauterine growth-retardation and postnatal catch up growth, phenotypic masculinization, reproductive neuroendocrine and ovarian disruptions leading to progressive loss of cyclicity and metabolic disruptions manifested as hyperinsulinemia.

Animals↗

Competitive regulation of plant allometry and a generalized model for the plant self-thinning process.

Taking into account the individual growth form (allometry) in a plant population and the effects of intraspecific competition on allometry under the population self-thinning condition, and adopting Ogawa's allometric equation 1/y = 1/axb + 1/c as the expression of complex allometry, the generalized model describing the change mode of r (the self-thinning exponential in the self-thinning equation, log M = K + log N, where M is mean plant mass, K is constant, and N is population density) was constructed. Meanwhile, with reference to the changing process of population density to survival curve type B, the exponential, r, was calculated using the software MATHEMATICA 4.0. The results of the numerical simulation show that (1) the value of the self-thinning exponential, r, is mainly determined by allometric parameters; it is most sensitive to change of b of the three allometric parameters, and a and c take second place; (2) the exponential, r, changes continuously from about -3 to the asymptote -1; the slope of -3/2 is a transient value in the population self-thinning process; (3) it is not a 'law' that the slope of the self-thinning trajectory equals or approaches -3/2, and the long-running dispute in ecological research over whether or not the exponential, r, equals -3/2 is meaningless. So future studies on the plant self-thinning process should focus on investigating how plant neighbor competition affects the phenotypic plasticity of plant individuals, what the relationship between the allometry mode and the self-thinning trajectory of plant population is and, in the light of evolution, how plants have adapted to competition pressure by plastic individual growth.

Mathematical Computing↗

Interaction between maternal effects and temperature affects diapause occurrence in the cricket Allonemobius socius.

The induction of diapause can be adaptive for egg survival during unfavorable conditions, while direct development can be advantageous under favorable conditions by allowing additional generations to exploit abundant resources. Therefore, the physiological capability of a female to respond to environmental cues indicative of habitat quality by producing eggs of the appropriate developmental phenotype should be under strong selection. Additionally, developing embryos may alter the developmental trajectory initiated by the female in response to changing environmental conditions. In this study, we used a cross-fostering approach to isolate the maternal effects of parental diapause history (not previously studied) and egg-laying temperature from the influence of the incubation environment experienced by the developing embryo on the proportion of diapause eggs produced by the striped ground cricket, Allonemobius socius. We found that an interaction between egg-incubation temperature and parental diapause history strongly affected the proportion of diapause eggs produced and the proportion of eggs that hatched within a 16-18 day incubation period, while egg-laying temperature and all other interactions did not. These novel results indicate that embryos can respond directly to the environmental conditions they experience during development, but that their ability to do so is influenced by maternal effects such as parental diapause history. The results of this study not only provide evidence, for the first time, of parental diapause history affecting diapause proportions, but also raise additional questions about the mechanism by which environmental information is transmitted from parent to offspring and how offspring are able to respond to conditions experienced during their own development.

Animals↗

Unraveling cellular dynamic changes in tumor evolution induced by long-term low dose-rate radiation.

BACKGROUND: In recent years, there has been a steady increase in professionals engaged in radioactive work. The biological impacts of long-term exposure to low dose-rate radiation remain elusive, as there is a dearth of systematic research in this field. METHODS: BEAS-2B cells were used to establish a cell model with continuous passaging after radiation exposure, which was subsequently subjected to in vivo tumorigenesis assays and in vitro malignant phenotype experiments. By scRNA-seq, we conducted copy number variation analysis, cell trajectory analysis, and cell communication analysis. Furthermore, we used FACS, molecular docking, multiplex immunohistochemistry, qRT-PCR, and co-immunoprecipitation to validate and further explore the molecular mechanisms driving tumor evolution. RESULTS: Long-term low dose-rate exposure is associated with a higher degree of malignancy, as evidenced by the induction of more CNV and EMT events, as well as the delayed activation of DNA repair pathways, which trigger increased genomic instability. The long-term low dose-rate specific ligand-receptor pair, ANGPTL4-SDC4, enhances cell malignancy by promoting angiogenesis in newly formed lung tumor cells. CONCLUSIONS: This study not only provides the first evidence and mechanistic explanation that long-term low dose-rate radiation leads to increased cellular malignancy but also offers valuable theoretical insights into the dynamic processes of early tumor evolution in lung cancer within the realm of tumor biology.

Humans↗

Reassessment of the environmental mechanisms controlling developmental polyphenism in spadefoot toad tadpoles.

Identifying the environmental mechanism(s) controlling developmental polyphenism is the first step in gaining a mechanistic and evolutionary understanding of the factors responsible for its expression and evolution. Tadpoles of the spadefoot toad Spea multiplicata can display either a "typical" omnivorous or a carnivorous phenotype. Exogenous thyroxine and feeding on conspecific tadpoles have been accepted as triggers for development of the carnivorous phenotype on the basis of a series of studies in the early 1990s. I repeated the thyroxine and conspecific-feeding assays and demonstrated that neither exogenous thyroxine nor feeding on conspecifics induces the carnivorous phenotype. Previous researchers used simple ratio statistics to argue that field-collected carnivores and thyroxine-treated tadpoles are similar, and my results supported these claims if I used the same simple ratio methodology. However, investigation of trait developmental trajectories and allometries for field-collected carnivores and thyroxine-treated and conspecific-fed tadpoles show that these phenotypes are profoundly different.

Adaptation, Physiological↗

Quasi-independence, homology and the unity of type: a topological theory of characters.

In this paper Lewontin's notion of "quasi-independence" of characters is formalized as the assumption that a region of the phenotype space can be represented by a product space of orthogonal factors. In this picture each character corresponds to a factor of a region of the phenotype space. We consider any region of the phenotype space that has a given factorization as a "type", i.e. as a set of phenotypes that share the same set of phenotypic characters. Using the notion of local factorizations we develop a theory of character identity based on the continuation of common factors among different regions of the phenotype space. We also consider the topological constraints on evolutionary transitions among regions with different regional factorizations, i.e. for the evolution of new types or body plans. It is shown that direct transition between different "types" is only possible if the transitional forms have all the characters that the ancestral and the derived types have and are thus compatible with the factorization of both types. Transitional forms thus have to go over a "complexity hump" where they have more quasi-independent characters than either the ancestral as well as the derived type. The only logical, but biologically unlikely, alternative is a "hopeful monster" that transforms in a single step from the ancestral type to the derived type. Topological considerations also suggest a new factor that may contribute to the evolutionary stability of "types". It is shown that if the type is decomposable into factors which are vertex irregular (i.e. have states that are more or less preferred in a random walk), the region of phenotypes representing the type contains islands of strongly preferred states. In other words types have a statistical tendency of retaining evolutionary trajectories within their interior and thus add to the evolutionary persistence of types.

Animals↗

Sperm mobility: phenotype in roosters (Gallus domesticus) determinedby concentration of motile sperm and straight line velocity.

Previous research demonstrated that sperm mobility, i.e., the net movement of a sperm population, is a quantitative trait of the domestic fowl. However, the cellular basis for this trait was unknown. In the present work, individual motile sperm were evaluated with a Hobson SpermTracker in order to identify one or more properties of motile sperm that could account for variation in sperm mobility observed among males. A method was validated for assessing sperm motion over an erythrocyte monolayer at body temperature. A small-scale experiment with roosters from the tails and center of a normal distribution of sperm mobility phenotypes (n = 33 roosters) demonstrated that straight line velocity (VSL) and motile concentration were critical to expression of phenotype. The importance of these variables was confirmed with a large-scale experiment using a representative subpopulation (n = 100 roosters). VSL of individual sperm at 41 degrees C ranged between 5 and 100 microm/sec. VSL averaged 32, 39, and 40 microm/sec for low, average, and high sperm mobility phenotypes. Sperm were diluted to 1.2 x 10(6)/ml for motion analysis. Mean motile concentrations were 0.52, 0.84, and 0.95 x 10(6)/ml for low, average, and high sperm mobility phenotypes. Motile concentration was correlated with sperm mobility (r = 0.71). VSL appeared to have an additive effect as it was correlated with straightness of sperm cell trajectory (r = 0.79).

Animals↗

The altered evolutionary trajectories of gene duplicates.

Gene duplication is widely regarded as the predominant mechanism by which genes with new functions and associated phenotypic novelties arise. However, the mutational events and population-genetic mechanisms that lead to the short-term preservation of duplicate genes are not necessarily the same as those exhibited by well-established paralogs en route to the origin of new beneficial features. Thus, although recent genome-wide analyses have revealed striking patterns of protein-sequence divergence among the members of surviving paralogous gene families, the mechanisms responsible for the historical development of these patterns remain unclear.

Animals↗

Ectopic expression of connectin reveals a repulsive function during growth cone guidance and synapse formation.

Connectin, a cell surface protein of the leucine-rich repeat family in Drosophila, is expressed on the surface of a subset of embryonic muscles (primarily lateral muscles), on the growth cones and axons of the motoneurons that innervate these muscles (primarily SNa motoneurons), and on several associated glial cells. When coupled with its ability to mediate homophilic cell adhesion, these results led to the suggestion that Connectin functions as an attractive signal for SNa pathfinding and targeting. In the present study, we ectopically expressed Connectin on ventral muscles normally innervated by SNb motoneurons. The SNb growth cones change both their morphology and their trajectory when they encounter ectopic Connectin-positive ventral muscles, displaying "bypass," "detour," and "stall" phenotypes. Moreover, SNb synapse formation is prevented by Connectin expression on ventral muscles. These results reveal a repulsive function for Connectin during motoneuron growth cone guidance and synapse formation.

Animals↗

Sex differences in psychopathy and antisocial personality disorder. A review and integration.

Although the correlates and causes of psychopathy and antisocial personality disorder (ASPD) have been the subject of extensive investigation, researchers in this area have until recently focused almost exclusively on males. As a consequence, relatively little is known about psychopathy and ASPD in females. In this paper, we review the empirical literature on sex differences in the base rates, mean symptom levels, correlates, and factor structure of psychopathy and ASPD. In addition, we discuss the potential sex-differentiated phenotypic expressions of psychopathy and ASPD (e.g., somatization disorder [SD]) as well as sex differences in the developmental trajectories of these conditions. There is suggestive evidence that these conditions may be differentially expressed across biological sex, although further investigation of this issue is warranted. We conclude with recommendations for future research in this area, including suggestions for embedding the study of sex differences in psychopathy and ASPD within a construct validational framework.

Antisocial Personality Disorder↗

Histochemical and immunohistochemical studies on the origin of the blue marlin heater cell phenotype.

The superior rectus muscle fibers of marlins, swordfish, sailfish and spearfish are modified for heat production at the expense of contractile ability. Although 'heater cells' are a muscle derivative (Block, 1986, 1991), the myoblast origin and developmental pathway of these thermogenic cells is unknown. To gain insight into heater cell origins, we characterized blue marlin superior rectus muscle and its heater tissue derivative with histochemical and immunological techniques. We specifically employed myosin ATPase and succinate dehydrogenase histochemical assays, and myosin heavy chain immunohistochemistry. Results revealed that marlin superior rectus muscles contain at least six distinct fiber types, and suggested the presence of both twitch and tonic fibers. Immunological results indicate that myosin is present within the thermogenic cells but not in myofibrillar lattices. The antibodies that recognized myosin in heater cells also labeled myosin in the twitch fibers of swimming muscle. In contrast, antibodies that labeled histologically defined tonic fibers did not label heater cells. These results suggest that heater cells and twitch fibers express the same myosin isoform, and establish a phenotypic connection between heater cells and twitch fibers. This conclusion is discussed in the context of the muscle-to-heater trajectory and the muscle fiber-type origin of heater cells.

Animals↗

Neurobehavioural disorders in the infant reeler mouse model: interaction of genetic vulnerability and consequences of maternal separation.

Studies on heterozygous (HZ) reeler mice suggest a relationship between reelin (a protein of extra cellular matrix) haploinsufficiency and the presence of altered neural networks and behaviour. Neonatal adverse and/or stimulating experiences might interfere with the emergence of this genetic-dependent phenotype. Repeated episodes of maternal separation early in ontogeny result in enduring neuroendocrine, neurochemical and behavioural alterations in the offspring. Therefore, in order to investigate whether developmental indexes of neurobehavioural disorders can be studied in the infant reeler mouse model, and whether ontogenetic adverse experiences may question or improve its suitability, homozygous reeler (RL), heterozygous (HZ) and wild-type (WT) mouse pups underwent maternal separation (SEP, 5h/day) or handling (H, 3min/day) on PND 2-6. As expected, a sex difference appeared, for measure of emotional and communicative behaviour in infant mice. On PND 7, compared to other genotypes, RL mouse pups from the H control group, showed reduced levels of ultrasound (USV) production and of locomotion. Surprisingly, this deficit in RL mice was fully reverted by maternal separation. Maternal separation per se reduced social motivation in the homing test at PND 9 in WT mice, with no effects on HZ and RL ones. Additionally, female pups emitted much lower levels of ultrasound production than males within the H control group. Such a baseline sex difference, however, disappeared in the SEP group. The present results provide evidence that unusual stress and related hormonal stimulation early in development may (i) independently shape individual phenotype and (ii) interact with a genetic make-up to substantially modify its "natural" developmental trajectories.

Animals↗

Proteins as Regulators of Metabolic Changes in Sepsis: Alterations in Body Fluids, Immune Cells, and Organs through the Eyes of Proteomics.

Sepsis is a life-threatening syndrome characterized by a dysregulated host response to infection and profound metabolic alterations that contribute to immune dysfunction and organ failure. This Review synthesizes proteomic evidence on sepsis-associated alterations in proteins involved in metabolic pathways across circulating biofluids, immune cells, and organs. Across plasma and urine, proteomic studies identify disturbances in lipoprotein-associated pathways, redox homeostasis, mitochondrial function, and substrate metabolism, indicating that protein signatures of metabolic dysregulation are systemic and detectable across biofluids. In immune cells, monocytes and neutrophils, proteomic analyses reveal a shift toward glycolysis with concurrent impairment of mitochondrial pathways alongside phenotype-dependent differences in lipid and redox-related programs. Organ-level studies further show that metabolic responses are heterogeneous, with distinct trajectories in the kidney, heart, liver, lung, skeletal muscle, and brain. These observations support the concept that sepsis involves compartment-specific remodeling of metabolism-associated protein networks rather than a single convergent metabolic state. Proteomics also highlights potential translational opportunities by identifying metabolism-associated proteins linked to disease severity, clinical phenotypes, and biologically distinct patient subgroups, although the current evidence remains largely exploratory and context-dependent. Overall, proteomics provides a complementary framework for understanding the molecular regulation of sepsis-associated metabolic dysfunction and may refine biological stratification and therapeutic targeting, particularly when integrated with longitudinal sampling and multiomic data.

Humans↗

Systolic and diastolic heart failure: different phenotypes of the same disease?

Traditional pathophysiological concepts of chronic heart failure have largely focused on the haemodynamic consequences of ventricular systolic dysfunction. How these concepts relate to the pathophysiology of diastolic heart failure, i.e., heart failure with a preserved ejection fraction is, however, unclear, causing uncertainty about pathophysiology, diagnosis and management. Recent measurements of regional myocardial systolic function in patients with diastolic heart failure indicate that systolic and diastolic heart failure may be more closely related than previously anticipated. Rather than being considered as separate diseases with a distinct pathophysiology, systolic and diastolic heart failure may be merely different clinical presentations within a phenotypic spectrum of one and the same disease. In this review, we will interpret these new insights in a broader conceptual context of chronic heart failure and design novel paradigms in which systolic and diastolic heart failure jointly progress in a pathophysiological time trajectory of only one disease.

Diastole↗

The emergence of a syndrome-specific personality profile in young children with Down syndrome.

For decades, researchers and practitioners have attempted to find evidence for a personality stereotype in individuals with Down syndrome that includes a pleasant, affectionate, and passive behaviour style. However, a more nuanced exploration of personality-motivation in Down syndrome reveals complexity beyond this pleasant stereotype, including reports of a less persistent motivational orientation and an over-reliance on social behaviours during cognitively-challenging tasks. It is hypothesised that the personality-motivation profile observed in individuals with Down syndrome emerges as a result of the cross-domain relations between more primary (cognitive, social-emotional) aspects of the Down syndrome behavioural phenotype. Young children with Down syndrome show a general profile of delays in the development of instrumental thinking coupled with emerging relative strengths in social-emotional functioning. If it is true that a less persistent motivational orientation emerges as a secondary phenotypic result of more primary strengths in social functioning and deficits in instrumental (means-end) thinking, it may be possible to alter the developmental trajectory of this personality-motivation profile with targeted and time-sensitive intervention. Implications for intervention planning are discussed.

Affect↗