John de Belle

... The species with the greatest use of their forepaws had the largest area devoted to forepaw control ([Butler and Hodos, 1996] and [Radinsky, 1968]). Many brain structures found in vertebrates and invertebrates have similar connectivity and organization. ...

A role for Notch in the elaboration of existing neural processes is emerging that is distinct from the increasingly well understood function of this gene in binary cell-fate decisions. Several research groups, by using a variety of organisms, have shown that Notch is important in the development of neural ultrastructure. Simultaneously, Presenilin ( Psn ) was identified both as a key mediator of Notch signaling and as a site of genetic lesions that cause early-onset Alzheimer's disease. Here we demonstrate that Notch loss of function produces memory deficits in Drosophila melanogaster . The effects are specific to long-term memory, which is thought to depend on ultrastructural remodeling. We propose that Notch plays an important role in the neural plasticity underlying consolidated memory.

Associative conditioning in Drosophila melanogaster has been well documented for several decades. However, most studies report only simple associations of conditioned stimuli (CS, e.g., odor) with unconditioned stimuli (US, e.g., electric shock) to measure learning or establish memory. Here we describe a straightforward second-order conditioning (SOC) protocol that further demonstrates the flexibility of fly behavior. In SOC, a previously conditioned stimulus (CS1) is used as reinforcement for a second conditioned stimulus (CS2) in associative learning. This higher-order context presents an opportunity for reassessing the roles of known learning and memory genes and neuronal networks in a new behavioral paradigm.

The central complex (CC) is a prominent component of the adult insect brain. In Drosophila melanogaster, mutations which alter CC structure also impair adult locomotion. This has led to the suggestion that the CC functions as a higher organizer of adult locomotor patterns (Strauss and Heisenberg, 1993). In the present study, we describe altered larval behavior resulting from mutations in six CC structural genes. Differences from the control strain were found for larvae from each CC mutant strain in at least one of three assays. central body defect1 (cbd1), central complex deranged1 (ccd1), central brain deranged1 (ceb1) and central complex1 (cex1) larvae all had general defects in locomotion (on a non-nutritive agar surface). Both ellipsoid body open2 (ebo2) and no bridge1 (nob1) had larval foraging behavior defects (on a nutritive yeast surface). Only cex1 larvae required significantly longer time in a roll over assay of muscle tone. Genetic analysis suggested that nob1 interacts additively with two other genes influencing larval foraging behavior, foraging (for) and Chaser (Csr). for also had an influence on adult foraging, whereas here we found that Csr did not. We did not include adult foraging behavior tests of the CC mutants due to general locomotion defects in these flies (Strauss and Heisenberg, 1993).

The central body (or central complex, CCX) and the mushroom bodies (MBs) are brain structures in most insect phyla that have been shown to influence aspects of locomotion. The CCX regulates motor coordination and enhances activity while MBs have, thus far, been shown to suppress motor activity levels measured over time intervals ranging from hours to weeks. In this report, we investigate MB involvement in motor behavior during the initial stages (15 minutes) of walking in Buridan's paradigm. We measured aspects of walking in flies that had MB lesions induced by mutations in six different genes and by chemical ablation. All tested flies were later examined histologically to assess MB neuroanatomy. Mutant strains with MB structural defects were generally less active in walking than wild-type flies. Most mutants in which MBs were also ablated with hydroxyurea (HU) showed additional activity decrements. Variation in measures of velocity and orientation to landmarks among wild-type and mutant flies was attributed to pleiotropy, rather than to MB lesions. We conclude that MBs upregulate activity during the initial stages of walking, but suppress activity thereafter. An MB influence on decision making has been shown in a wide range of complex behaviors. We suggest that MBs provide appropriate contextual information to motor output systems in the brain, indirectly fine tuning walking by modifying the quantity (i.e., activity) of behavior.

The rover/sitter polymorphism in Drosophila melanogaster larval behaviour is a unique example of a genetically determined, naturally occurring behavioural polymorphism. Allelic variation at the foraging locus (for) accounts for the rover (long foraging paths) and sitter (short foraging paths) phenotypes. We previously developed lethal tagging and used deficiency mapping to place for in the 24A3-C5 interval on the polytene chromosome map, thereby defining the for microregion. Here, we subjected this microregion to mutational analysis to (i) isolate putative lethal foraging mutations and characterize their behavioural phenotypes to assess whether or not for is a vital locus, (ii) generate cytologically detectable chromosome rearrangements with breakpoints in or near for for more precise localization and for future molecular analysis of the for gene, and (iii) identify other gene loci in the immediate vicinity of the for locus. We recovered 10 gamma-induced and 33 ethyl methanesulfonat...

Mutations in 12 genes regulating Drosophila melanogaster mushroom body (MB) development were each studied in two genetic backgrounds. In all cases, brain structure was qualitatively or quantitatively different after replacement of the "original" genetic background with that of the Canton Special wild-type strain. The mushroom body miniature gene (mbm) was investigated in detail. mbm supports the maintenance of MB Kenyon cell fibers in third instar larvae and their regrowth during metamorphosis. Adult mbm1 mutant females are lacking many or most Kenyon cell fibers and are impaired in MB-mediated associative odor learning. We show here that structural defects in mbm1 are apparent only in combination with an X-linked, dosage-dependent modifier (or modifiers). In the Canton Special genetic background, the mbm1 anatomical phenotype is suppressed, and MBs develop to a normal size. However, the olfactory learning phenotype is not fully restored, suggesting that submicroscopic def...