Many species of insects display dispersing and nondispersing morphs. Among these, aphids are one of the best examples of taxa that have evolved specialized morphs for dispersal versus reproduction. The dispersing morphs typically possess a full set of wings as well as a sensory and reproductive physiology that is adapted to flight and reproducing in a new location. In contrast, the nondispersing morphs are wingless and show adaptations to maximize fecundity. In this review, we provide an overview of the major features of the aphid wing dimorphism. We first provide a description of the dimorphism and an overview of its phylogenetic distribution. We then review what is known about the mechanisms underlying the dimorphism and end by discussing its evolutionary aspects.

We have developed miniature telemetry systems that capture neural, EMG, and acceleration signals from a freely moving insect or other small animal and transmit the data wirelessly to a remote digital receiver. The systems are based on custom low-power integrated circuits (ICs) that amplify, filter, and digitize four biopotential signals using low-noise circuits. One of the chips also digitizes three acceleration signals from an off-chip microelectromechanical-system accelerometer. All information is transmitted over a wireless ~ 900-MHz telemetry link. The first unit, using a custom chip fabricated in a 0.6- μm BiCMOS process, weighs 0.79 g and runs for two hours on two small batteries. We have used this system to monitor neural and EMG signals in jumping and flying locusts as well as transdermal potentials in weakly swimming electric fish. The second unit, using a custom chip fabricated in a 0.35-μ m complementary metal-oxide semiconductor CMOS process, weighs 0.17 g and runs for five hours on a single 1.5-V battery. This system has been used to monitor neural potentials in untethered perching dragonflies.

Wiring economy has successfully explained the individual placement of neurons in simple nervous systems like that of Caenorhabditis elegans [1-3] and the locations of coarser structures like cortical areas in complex vertebrate brains [4]. However, it remains unclear whether wiring economy can explain the placement of individual neurons in brains larger than that of C. elegans. Indeed, given the greater number of neuronal interconnections in larger brains, simply minimizing the length of connections results in unrealistic configurations, with multiple neurons occupying the same position in space. Avoiding such configurations, or volume exclusion, repels neurons from each other, thus counteracting wiring economy. Here we test whether wiring economy together with volume exclusion can explain the placement of neurons in a module of the Drosophila melanogaster brain known as lamina cartridge [5-13]. We used newly developed techniques for semiautomated reconstruction from serial electron microscopy (EM) [14] to obtain the shapes of neurons, the location of synapses, and the resultant synaptic connectivity. We show that wiring length minimization and volume exclusion together can explain the structure of the lamina microcircuit. Therefore, even in brains larger than that of C. elegans, at least for some circuits, optimization can play an important role in individual neuron placement.

The placement of neuronal cell bodies relative to the neuropile differs among species and brain areas. Cell bodies can be either embedded as in mammalian cortex or segregated as in invertebrates and some other vertebrate brain areas. Why are there such different arrangements? Here we suggest that the observed arrangements may simply be a reflection of wiring economy, a general principle that tends to reduce the total volume of the neuropile and hence the volume of the inclusions in it. Specifically, we suggest that the choice of embedded versus segregated arrangement is determined by which neuronal component - the cell body or the neurite connecting the cell body to the arbor - has a smaller volume. Our quantitative predictions are in agreement with existing and new measurements.

We pursue the hypothesis that neuronal placement in animals minimizes wiring costs for given functional constraints, as specified by synaptic connectivity. Using a newly compiled version of the Caenorhabditis elegans wiring diagram, we solve for the optimal layout of 279 nonpharyngeal neurons. In the optimal layout, most neurons are located close to their actual positions, suggesting that wiring minimization is an important factor. Yet some neurons exhibit strong deviations from "optimal" position. We propose that biological factors relating to axonal guidance and command neuron functions contribute to these deviations. We capture these factors by proposing a modified wiring cost function.

Wiring a brain presents a formidable problem because neural circuits require an enormous number of fast and durable connections. We propose that evolution was likely to have optimized neural circuits to minimize conduction delays in axons, passive cable attenuation in dendrites, and the length of "wire" used to construct circuits, and to have maximized the density of synapses. Here we ask the question: "What fraction of the volume should be taken up by axons and dendrites (i.e., wire) when these variables are at their optimal values?" The biophysical properties of axons and dendrites dictate that wire should occupy 3/5 of the volume in an optimally wired gray matter. We have measured the fraction of the volume occupied by each cellular component and find that the volume of wire is close to the predicted optimal value.

Many animals rely on acoustic cues to decide what action to take next. Unraveling the wiring patterns of the auditory neural pathways is prerequisite for understanding such information processing. Here we reconstructed the first step of the auditory neural pathway in the fruit fly brain, from primary to secondary auditory neurons, at the resolution of transmission electron microscopy. By tracing axons of two major subgroups of auditory sensory neurons in fruit flies, low-frequency tuned Johnston's organ (JO)-B neurons and high-frequency tuned JO-A neurons, we observed extensive connections from JO-B neurons to the main second-order neurons in both the song-relay and escape pathways. In contrast, JO-A neurons connected strongly to a neuron in the escape pathway. Our findings suggest that heterogeneous JO neuronal populations could be recruited to modify escape behavior whereas only specific JO neurons contribute to courtship behavior. We also found that all JO neurons have postsynaptic sites at their axons. Presynaptic modulation at the output sites of JO neurons could affect information processing of the auditory neural pathway in flies. This article is protected by copyright. All rights reserved.

A complex brain consists of multiple intricate neural networks assembled from distinct sets of input and output neurons as well as region-specific local interneurons. Within a given anatomical set, there exist diverse neuronal types that can vary in morphology, neural physiology, and modes of neurotransmission. The genetic programs that guide specification of neuronal types during neurogenesis preconfigure the brain. This is best demonstrated in the Drosophila central brain, which is composed of ∼100 pairs of individually tailored neuronal lineages. Each neuronal lineage (the neurons/glia produced from a single stem cell) can contain multiple morphological classes of neurons that can consist of many analogous neuronal types. The detailed patterns of neuronal diversification are lineage-specific and can differ drastically even among neighboring neuronal lineages. Furthermore, the interrelationships between neuronal lineages and neural networks are complex. These phenomena underscore the importance of tracking all neuronal lineages in understanding brain development and evolution.

Axon pruning by degeneration remodels exuberant axonal connections and is widely required for the development of proper circuitry in the nervous system from insects to mammals. Developmental axon degeneration morphologically resembles injury-induced Wallerian degeneration, suggesting similar underlying mechanisms. As previously reported for mice, we show that Wlds protein substantially delays Wallerian degeneration in flies. Surprisingly, Wlds has no effect on naturally occurring developmental axon degeneration in flies or mice, although it protects against injury-induced degeneration of the same axons at the same developmental age. By contrast, the ubiquitin-proteasome system is intrinsically required for both developmental and injury-induced axon degeneration. We also show that the glial cell surface receptor Draper is required for efficient clearance of axon fragments during developmental axon degeneration, similar to its function in injury-induced degeneration. Thus, mechanistically, naturally occurring developmental axon pruning by degeneration and injury-induced axon degeneration differ significantly in early steps, but may converge onto a common execution pathway.

Understanding the diverse activities of the multisubunit core promoter recognition complex TFIID in vivo requires knowledge of how individual subunits contribute to overall functions of this TATA box-binding protein (TBP)/TBP-associated factor (TAF) complex. By generating altered holo-TFIID complexes in Drosophila we identify the ETO domain of TAF4 as a coactivator domain likely targeted by Pygopus, a protein that is required for Wingless-induced transcription of naked cuticle. These results establish a coactivator function of TAF4 and provide a strategy to dissect mechanisms of TFIID function in vivo.