Mineral nutrient supply, cell wall adjustment and the control of leaf growth

The possibility that changes in the plasticity of expanding cell walls are involved in regulating early leaf growth responses to nutrient deficiencies in monocot plants was investigated. Intact maize seedlings (Zea mays L.) which were hydroponically grown with their roots in low-nutrient solution (1 mol m^?3 CaCl₂) showed early inhibition of first-leaf growth, as compared with seedlings on complete nutrient solution. This early inhibition of leaf growth was not associated with reduced cell production. However, segmental elongation along the cell expansion zone at the base of the leaf and the lengths of mature epidermal cells were reduced by the low-nutrient treatment. Solute (osmotic) potentials in the expanding leaf tissues were unchanged. In contrast, low-nutrient treatments significantly altered leaf plasticity, i.e. the irreversible extension caused by applying a small force in the direction of leaf growth. For example, in vivo plasticity decreased, along with leaf growth, after transfer of seedlings from complete nutrient solution to low-nutrient solution for 15 h. Conversely, in vivo plasticity increased, along with leaf growth, after transfer of plants previously grown on low-nutrient solution to complete nutrient solution for 15 h. The nutrient treatments also induced similar changes in the in vitro plasticity of the expanding leaf cell walls. There were no consistent changes in elasticity. Thus, reductions in the plasticity of expanding leaf cell walls appear to be involved in controlling the early inhibition of maize leaf growth by root imposition of nutrient stress.     

Maternal dopamine exposure provides offspring starvation resistance in Daphnia

The neurotransmitter dopamine has been shown to play an important role in modulating behavioral, morphological, and life history responses to food abundance. However, costs of expressing high dopamine levels remain poorly studied and are essential for understanding the evolution of the dopamine system. Negative maternal effects on offspring size from enhanced maternal dopamine levels have previously been documented in Daphnia. Here, we tested whether this translates into fitness costs in terms of lower starvation resistance in offspring. We exposed Daphnia magna mothers to aqueous dopamine (2.3 or 0 mg/L for the control) at two food levels (ad libitum vs. 30% ad libitum) and recorded a range of maternal life history traits. The longevity of their offspring was then quantified in the absence of food. In both control and dopamine treatments, mothers that experienced restricted food ration had lower somatic growth rates and higher age at maturation. Maternal food restriction also resulted in production of larger offspring that had a superior starvation resistance compared to ad libitum groups. However, although dopamine exposed mothers produced smaller offspring than controls at restricted food ration, these smaller offspring survived longer under starvation. Hence, maternal dopamine exposure provided an improved offspring starvation resistance. We discuss the relative importance of proximate and ultimate causes for why D. magna may not evolve toward higher endogenous dopamine levels despite the fitness benefits this appears to have.     

A data-driven framework to model the organism–environment system

Organisms modify their development and function in response to the environment. At the same time, the environment is modified by the activities of the organism. Despite the ubiquity of such dynamical interactions in nature, it remains challenging to develop models that accurately represent them, and that can be fitted using data. These features are desirable when modeling phenomena such as phenotypic plasticity, to generate quantitative predictions of how the system will respond to environmental signals of different magnitude or at different times, for example, during ontogeny. Here, we explain a modeling framework that represents the organism and environment as a single coupled dynamical system in terms of inputs and outputs. Inputs are external signals, and outputs are measurements of the system in time. The framework uses time-series data of inputs and outputs to fit a nonlinear black-box model that allows to predict how the system will respond to novel input signals. The framework has three key properties: it captures the dynamical nature of the organism–environment system, it can be fitted with data, and it can be applied without detailed knowledge of the system. We study phenotypic plasticity using in silico experiments and demonstrate that the framework predicts the response to novel environmental signals. The framework allows us to model plasticity as a dynamical property that changes in time during ontogeny, reflecting the well-known fact that organisms are more or less plastic at different developmental stages.     

Neurotrophins,but not depolarization,regulate substance P expression in the developing optic tectum

Neurotransmitter expression can be regulated by both activity and neurotrophins in a number of in vitro systems. We examined whether either of these factors was likely to play a role in the in vivo optic nerve‐dependent regulation of a substance P‐like immunoreactive (SP‐ir) population of cells in the developing optic tectum of the frog. In contrast to our previous results with the adult system, blocking tectal cell responses to glutamate release by retinal ganglion cells with 6‐cyano‐7‐nitroquinoxaline‐2,3 dione (CNQX) did not affect the percent of SP‐ir cells in the developing tectum. Treatment with d‐(‐)‐2‐amino‐5‐phosphonovaleric acid (d‐AP‐5) was also ineffective in this regard, although both it and CNQX treatment disrupted visual map topography. Chronic treatment with brain‐derived neurotrophic factor (BDNF) and neurotrophin‐4/5 (NT‐4/5) produced increases in SP‐ir cells in the treated lobes of normal animals, which were significant in the case of NT‐4/5. Both substances also prevented the decrease of SP cells that would otherwise occur in the deafferented lobe of unilaterally optic nerve‐transected tadpoles. These changes in the percent of SP‐ir cells occurred without any detectable changes in the overall number of tectal cells. NGF had no effect on SP expression. Nor did it affect topographic map formation, which was disrupted by treatment with either BDNF or NT‐4/5. Our results demonstrate that different mechanisms regulate SP expression in the developing and adult tectum. They indicate that neurotrophin levels in the developing optic tectum may selectively regulate a specific neuropeptide‐expressing population of cells. © 2001 John Wiley & Sons, Inc. J Neurobiol 48: 131–149, 2001     

INCREASED RESIDUAL VARIANCE AT DEVELOPMENTAL SWITCH POINTS: STATISTICAL ARTIFACT OR INDICATOR OF EXPOSED GENOTYPIC INFLUENCE?

Discussing the organization of developmental switches, West-Eberhard (2003) proposed the use of regression residual plots to locate the neutral point of the switch, which is characterized by maximum genotypic influence on the resulting phenotype. However, statistical artifacts due to measurement error in nonlinear models might account for a substantial proportion of the increase of residuals variance at the switch point. Simulations based on field data show that increases in residual variance occur as artifacts when normal amounts of measurement error are present, even in absence of any genotypic variance. The results suggest that interpretation of nonlinear variation in thresold traits is problematic and requires considering this statistical effect. A method to estimate the weight of genotypic contribution to residual variance is proposed, and its assumptions and limitations are discussed.     

Intrinsic and environmental response pathways that regulate root system architecture

Root system development is an important agronomic trait. The right architecture in a given environment allows plants to survive periods of water of nutrient deficit, and compete effectively for resources. Root systems also provide an optimal system for studying developmental plasticity, a characteristic feature of plant growth. This review proposes a framework for describing the pathways regulating the development of complex structures such as root systems: intrinsic pathways determine the characteristic architecture of the root system in a given plant species, and define the limits for plasticity in that species. Response pathways co-ordinate environmental cues with development by modulating intrinsic pathways. The current literature describing the regulation of root system development is summarized here within this framework. Regulatory pathways are also organized based on their specific developmental effect in the root system. All the pathways affect lateral root formation, but some specifically target initiation of the lateral root, while others target the development and activation of the lateral root primordium, or the elongation of the lateral root. Finally, we discuss emerging approaches for understanding the regulation of root system architecture.     

Carry‐over Effects of Size at Metamorphosis in Red‐eyed Treefrogs: Higher Survival but Slower Growth of Larger Metamorphs

Most animals have complex life histories, composed of a series of ecologically distinct stages, and the transitions between stages are often plastic. Anurans are models for research on complex life cycles. Many species exhibit plastic timing of and size at metamorphosis, due to both environmental constraints on larval growth and development and adaptive plastic responses to environmental variation. Models predicting optimal timing of metamorphosis balance cost/benefit ratios across stages, assuming that size affects growth and mortality rates in each stage. Much research has documented such effects in the larval period, but we lack an equal understanding of juvenile growth and mortality. Here, we examine how variation in size at metamorphosis in the Neotropical red‐eyed treefrog, Agalychnis callidryas, affects post‐metamorphic growth, foraging, and behavior in the lab as well as growth and survival in the field. Surprisingly, many individuals lost mass for weeks after metamorphosis. In the lab, larger metamorphs lost more mass following metamorphosis, ate similar amounts, had lower food conversion efficiencies, and grew more slowly after mass loss ceased than did smaller ones. In field cages larger metamorphs were more likely to survive than smaller ones; just one froglet died in the lab. Our data suggest that size‐specific differences in physiology and behavior influence these trends. Comparing across species and studies, large size at metamorphosis generally confers higher survival; size effects on growth rates vary substantially among species, in both magnitude and direction, but may be stronger in the tropics.     

Trade-offs limiting the evolution of coloniality: ecological displacement rates used to measure small costs

Multicellular organisms that benefit from division of labour are presumably descended from colonial species that initially derived benefits from larger colony size, before the evolution of specialization. Life in a colony can have costs as well as benefits, but these can be hard to measure. We measured physiological costs to life in a colony using a novel method based on population dynamics, comparing growth rates of unicells and kairomone-induced colonies of a green alga Desmodesmus subspicatus against a reference co-occurring species. Coloniality negatively affected growth during the initial log growth phase, while no adverse effect was detected under nutrient-limited competitive conditions. The results point to costs associated with traits involved in rapid growth rather than those associated with efficient growth under resource scarcity. Some benefits of coloniality (e.g. defence from herbivory) may be different from when this trait evolved, but our approach shows how costs would have depended on conditions.     

Nicotine induces dendritic spine remodeling in cultured hippocampal neurons

Cholinergic neurons in the CNS are involved in synaptic plasticity and cognition. Both muscarinic and nicotinic acetylcholine receptors (nAChRs) influence plasticity and cognitive function. The mechanism underlying nAChR‐induced plasticity, however, has remained elusive. Here, we demonstrate morphological changes in dendritic spines following activation of α4β2* nAChRs, which are expressed on glutamatergic pre‐synaptic termini of cultured hippocampal neurons. Exposure of the neurons to nicotine resulted in a lateral enlargement of spine heads. This was abolished by dihydro‐β‐erythroidine, an antagonist of α4β2* nAChRs, but not by α‐bungarotoxin, an antagonist of α7 nAChRs. Tetanus toxin or a mixture of 2‐amino‐5‐phosphonovaleric acid and 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione, antagonists of NMDA‐ and AMPA‐type glutamate receptors, blocked the nicotine‐induced spine remodeling. In addition, nicotine exerted full spine‐enlarging response in the post‐synaptic neuron whose β2 nAChR expression was knocked down. Finally, pre‐treatment with nicotine enhanced the Ca²⁺‐response of the neurons to glutamate. These data suggest that nicotine influences the activity of glutamatergic neurotransmission through the activation of pre‐synaptic α4β2 nAChRs, resulting in the modulation of spinal architecture and responsiveness. The present findings may represent one of the cellular mechanisms underlying cholinergic tuning of brain function.