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Developmental plasticity

About: Developmental plasticity is a research topic. Over the lifetime, 1721 publications have been published within this topic receiving 103438 citations.


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TL;DR: The phenotypic plasticity of a broad suite of morphological and life history traits is integrated and shared among species from three geographically independent lineages of mycalesine butterflies, despite considerable periods of independent evolution and exposure to disparate environments.
Abstract: Developmental plasticity is thought to have profound macro-evolutionary effects, for example, by increasing the probability of establishment in new environments and subsequent divergence into independently evolving lineages. In contrast to plasticity optimized for individual traits, phenotypic integration, which enables a concerted response of plastic traits to environmental variability, may affect the rate of local adaptation by constraining independent responses of traits to selection. Using a comparative framework, this study explores the evolution of reaction norms for a variety of life history and morphological traits across five related species of mycalesine butterflies from the Old World tropics. Our data indicate that an integrated response of a suite of key traits is shared amongst these species. Interestingly, the traits that make up the functional suite are all known to be regulated by ecdysteroid signalling in Bicyclus anynana, one of the species included in this study, suggesting the same underlying hormonal regulator may be conserved within this group of polyphenic butterflies. We also detect developmental thresholds for the expression of alternative morphs. The phenotypic plasticity of a broad suite of morphological and life history traits is integrated and shared among species from three geographically independent lineages of mycalesine butterflies, despite considerable periods of independent evolution and exposure to disparate environments. At the same time, we have detected examples of evolutionary change where independent traits show different patterns of reaction norms. We argue that the expression of more robust phenotypes may occur by shifting developmental thresholds beyond the boundaries of the typical environmental variation.

48 citations

Journal ArticleDOI
TL;DR: Early-life epigenotyping may find utility as a prognostic marker of metabolic dysfunction for identification and treatment of at-risk individuals and may have implications for the perpetuation of ill-health.
Abstract: The unrelenting rise in global rates of non-communicable disease has necessitated a thorough re-evaluation of the current use of adult- and lifestyle-based strategies to curb the growing epidemic. There is a rapidly emerging set of epidemiological, experimental and clinical data suggesting that developmental factors play a considerable role in determining individual disease risk later in life. This phenomenon is known as the Developmental Origins of Health and Disease (DOHaD). Developmental factors, such as maternal and paternal nutrition, gestational diabetes mellitus, and even the normative range of developmental experiences, may evoke the processes of developmental plasticity which enable an organism to change its developmental trajectory in response to environmental cues. However in the event of a mismatch between the early and mature environment, such anticipatory responses may become maladaptive and lead to elevated risk of disease. The evo-devo and eco-evo-devo framework for DOHaD has more recently been supported by mechanistic insights enabled by rapid advances in epigenetic research. Increasing evidence suggests that developmental plasticity may be effected by epigenetically mediated modulation of the expression of specific genes. These mechanisms include DNA methylation, histone modifications and noncoding RNA activity. A growing number of animal studies also point towards the transgenerational inheritance of epigenetic marks, which may have implications for the perpetuation of ill-health. However early-life epigenotyping may find utility as a prognostic marker of metabolic dysfunction for identification and treatment of at-risk individuals.

48 citations

Journal ArticleDOI
TL;DR: It is proposed that the pattern of feedforward inhibition is less dynamic than the patternof feedforward excitation at the site of plasticity, and initially in the adjustment process the preexisting pattern ofFeedforward GABAergic inhibition opposes changes in the auditory space map and tends to preserve the established response properties of the network.
Abstract: We studied the influence of GABA-mediated inhibition on adaptive adjustment of the owl's auditory space map during the initial phase of plasticity. Plasticity of the auditory space map was induced by subjecting owls to a chronic prismatic displacement of the visual field. In the initial stages of plasticity, inhibition suppressed responses to behaviorally appropriate, newly functional excitatory inputs. As a result, adaptive changes in excitatory input were only partially expressed as postsynaptic spike activity. This masking effect of inhibition on map plasticity did not depend on the activity of NMDA receptors at the synapses that supported the newly learned responses. On the basis of these results, we propose that the pattern of feedforward inhibition is less dynamic than the pattern of feedforward excitation at the site of plasticity. As a result, initially in the adjustment process the preexisting pattern of feedforward GABAergic inhibition opposes changes in the auditory space map and tends to preserve the established response properties of the network. The implications of this novel role of inhibition for the functional plasticity of the brain are discussed.

48 citations

Journal ArticleDOI
TL;DR: It is found that high-frequency bursts are necessary to trigger LTP and that this burst-dependent plasticity depends on presynaptic NMDA receptors and nitric oxide (NO) signaling and a mechanistic plasticity model based on NO and calcium signaling is developed.

48 citations

Journal ArticleDOI
TL;DR: This work discusses epigenetics as an adaptive mechanism of developmental plasticity and uses signaling theory to provide an evolutionary context for DOHaD phenomena within a generation and applies life‐course epidemiology conceptual models to inform study design and analytical strategies that are capable of parsing out the potential effects of process errors in the relationships among an organism's early environment, DNA methylation, and phenotype in a future environment.
Abstract: Developmental plasticity, a phenomenon of importance in both evolutionary biology and human studies of the developmental origins of health and disease (DOHaD), enables organisms to respond to their environment based on previous experience without changes to the underlying nucleotide sequence. Although such phenotypic responses should theoretically improve an organism's fitness and performance in its future environment, this is not always the case. Herein, we first discuss epigenetics as an adaptive mechanism of developmental plasticity and use signaling theory to provide an evolutionary context for DOHaD phenomena within a generation. Next, we utilize signalling theory to identify determinants of adaptive developmental plasticity, detect sources of random variability - also known as process errors that affect maintenance of an epigenetic signal (DNA methylation) over time, and discuss implications of these errors for an organism's health and fitness. Finally, we apply life-course epidemiology conceptual models to inform study design and analytical strategies that are capable of parsing out the potential effects of process errors in the relationships among an organism's early environment, DNA methylation, and phenotype in a future environment. Ultimately, we hope to foster cross-talk and interdisciplinary collaboration between evolutionary biology and DOHaD epidemiology, which have historically remained separate despite a shared interest in developmental plasticity.

48 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202316
202244
202172
202076
201953
201864