Carbon dioxide (CO 2 ) elicits different olfactory behaviors across species. In Drosophila, neurons that detect CO 2 are located in the antenna, form connections in a ventral glomerulus in the antennal lobe, and mediate avoidance. By contrast, in the mosquito these neurons are in the maxillary palps (MPs), connect to medial sites, and promote attraction. We found in Drosophila that loss of a microRNA, miR-279, leads to formation of CO 2 neurons in the MPs. miR-279 acts through downregulation of the transcription factor Nerfin-1. The ectopic neurons are hybrid cells. They express CO 2 receptors and form connections characteristic of CO 2 neurons, while exhibiting wiring and receptor characteristics of MP olfactory receptor neurons (ORNs). We propose that this hybrid ORN reveals a cellular intermediate in the evolution of species-specific behaviors elicited by CO 2 .In insects, both the position of CO 2 neurons and the behavior elicited by CO 2 differ among species. For example, olfactory detection of CO 2 through neurons positioned in or around the mouthparts of an insect, such as maxillary palps (MPs) and labial palps, correlates with feedingrelated behaviors. Indeed, in some blood-feeding insects such as mosquitoes and tsetse flies, these neurons are harbored in the MPs and are important in locating hosts via plumes of CO 2 that they emit (1-3). The hawkmoth, Manduca sexta, monitors nectar profitability of newly opened Datura wrightii flowers through CO 2 receptor neurons located in their labial palps (4,5). In these examples, CO 2 acts as an attractant. Conversely, in Drosophila CO 2 is a component of a stress-induced odor that triggers avoidance behavior (6). This repellent response is driven by antennal neurons expressing the CO 2 receptor complex 8). How did these diverse behavioral responses to CO 2 arise during insect evolution? We propose that this diversity emerged through multiple steps, including changes in cellular position (arising from elimination of CO 2 neurons in one appendage and generation of these neurons in another) and changes in circuitry.In the course of a genetic screen for mutants disrupting the organization of the olfactory system, we isolated a mutant (S0962−07) that resulted in the formation of ectopic Gr21a-expressing §To whom correspondence should be addressed.
In the fly visual system, each class of photoreceptor neurons (R cells) projects to a different synaptic layer in the brain. R1-R6 axons terminate in the lamina, while R7 and R8 axons pass through the lamina and stop in the medulla. As R cell axons enter the lamina, they encounter both glial cells and neurons. The cellular requirement for R1-R6 targeting was determined using loss-of-function mutations affecting different cell types in the lamina. nonstop (encoding a ubiquitin-specific protease) is required for glial cell development and hedgehog for neuronal development. Removal of glial cells but not neurons disrupts R1-R6 targeting. We propose that glial cells provide the initial stop signal promoting growth cone termination in the lamina. These findings uncover a novel function for neuron-glial interactions in regulating target specificity.
In the Drosophila visual system, photoreceptor neurons (R cells) extend axons towards glial cells located at the posterior edge of the eye disc. In gilgamesh (gish) mutants, glial cells invade anterior regions of the eye disc prior to R cell differentiation and R cell axons extend anteriorly along these cells. gish encodes casein kinase Igamma. gish, sine oculis, eyeless, and hedgehog (hh) act in the posterior region of the eye disc to prevent precocious glial cell migration. Targeted expression of Hh in this region rescues the gish phenotype, though the glial cells do not require the canonical Hh signaling pathway to respond. We propose that the spatiotemporal control of glial cell migration plays a critical role in determining the directionality of R cell axon outgrowth.
ABSTRACTcDNA clones encoding proteins of -18 kDa in which 83% of the amino acids are conserved relative to the published sequences of mammalian cyclophilin/rotamase (CyP) have been isolated from tomato, maize, and Brassica napus. In correspondence with the mammalian genes, but in contrast with the Neurospora gene and one yeast CyP gene, the plant CyP genes encode only mature proteins lacking transit peptides. RNA blot analyses demonstrate that CyP genes are expressed in all plant organs tested. Southern blots of genomic DNA indicate that there are small families (two to eight members) of CyP-related genes in maize and B. napus. A vector was constructed for expression of the tomato cDNA in E. coil. SDS/polyacrylamide gels show that extracts of appropriately induced cells harboring this vector contain nearly 40% of the protein as a single "18-kDa band. While the majority of this protein is sequestered in insoluble inclusion bodies, the soluble extracts have higher levels of peptidyl-prolyl cis-trans isomerase (rotamase) activity than extracts of wild-type cells. This additional activity is sensitive to inhibition by the cyclic undecapeptide cyciosporin A.
The R1-R6 subclass of photoreceptor neurons (R cells) in the Drosophila compound eye form specific connections with targets in the optic ganglia. In this paper, we report the identification of a gene, brakeless (bks), that is essential for R1-R6 growth cone targeting. In brakeless mutants, R1-R6 growth cones frequently fail to terminate migration in their normal target, the lamina, and instead project through it and terminate in the second optic ganglion, the medulla. Genetic mosaic analysis and transgene rescue experiments indicate that bks functions in R cells and not within the lamina target region. bks encodes a nuclear protein. We propose that it participates in a gene expression pathway regulating one or more growth cone components controlling R1-R6 targeting.N eurons form precise patterns of synaptic connections during development. Differentiating neurons extend axons that migrate along defined pathways toward their targets (1). The growth cone, a sensorimotor structure at the leading edge of the axon, plays a central role in axon guidance. It detects and integrates multiple signals (see, e.g., ref.2) and translates them into directed motility (see, e.g., ref.3). On reaching the target region, growth cone migration ceases and specific synapses are established. How growth cones select specific targets once they have reached the target region remains a central issue in developmental neurobiology.Considerable progress has been made in defining the molecular basis of targeting. In the chick visual system, for instance, the formation of a precise topographic map between retinal ganglion cells and tectal cells relies on the graded expression of the Ephrin ligands in the tectum and their receptors, the Ephs, on retinal ganglion cell growth cones (4). Antibody disruption experiments suggest that cadherins play an important role in subsequent steps in which retinal ganglion cells form specific connections in distinct laminae within the tectum (5). A large family of odorant receptors play an essential role in determining the precise patterns of connections made by olfactory neurons with their postsynaptic target cells (6). That targeting may rely on multiple signals, both attractive and repulsive in nature, is supported by the genetic analysis of motoneuron target specificity in the Drosophila embryo (2).Although targeting requires interactions between extracellular signals and receptors on the growth cone, the formation of neuronal connections also relies on the genetic programs that specify the precise spatial and temporal expression of these signaling molecules. Several transcription factors have been implicated in regulating axon guidance and target specificity (7-14). For instance, in Caenorhabditis elegans, a homeoboxcontaining protein UNC30 is required for normal pathfinding of a subset of axons suggesting that it may control the expression of specific guidance receptors; UNC-30 also controls genes necessary for other aspects of neuronal differentiation, including enzymes necessary for neurotransmitter metab...
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