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Flies lacking all synapsins are unexpectedly healthy but are impaired in complex behaviour (2004)

Godenschwege, Tanja A. ; Reisch, Dietmar ; Diegelmann, Sören ; [et al.]

Oxford, UK : Blackwell Science Ltd

European journal of neuroscience 20 (2004), S. 0

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ISSN: 1460-9568

Source: Blackwell Publishing Journal Backfiles 1879-2005

Topics: Medicine

Notes: Vertebrate synapsins are abundant synaptic vesicle phosphoproteins that have been proposed to fine-regulate neurotransmitter release by phosphorylation-dependent control of synaptic vesicle motility. However, the consequences of a total lack of all synapsin isoforms due to a knock-out of all three mouse synapsin genes have not yet been investigated. In Drosophila a single synapsin gene encodes several isoforms and is expressed in most synaptic terminals. Thus the targeted deletion of the synapsin gene of Drosophila eliminates the possibility of functional knock-out complementation by other isoforms. Unexpectedly, synapsin null mutant flies show no obvious defects in brain morphology, and no striking qualitative changes in behaviour are observed. Ultrastructural analysis of an identified ‘model’ synapse of the larval nerve muscle preparation revealed no difference between wild-type and mutant, and spontaneous or evoked excitatory junction potentials at this synapse were normal up to a stimulus frequency of 5 Hz. However, when several behavioural responses were analysed quantitatively, specific differences between mutant and wild-type flies are noted. Adult locomotor activity, optomotor responses at high pattern velocities, wing beat frequency, and visual pattern preference are modified. Synapsin mutant flies show faster habituation of an olfactory jump response, enhanced ethanol tolerance, and significant defects in learning and memory as measured using three different paradigms. Larval behavioural defects are described in a separate paper. We conclude that Drosophila synapsins play a significant role in nervous system function, which is subtle at the cellular level but manifests itself in complex behaviour.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1111/j.1460-9568.2004.03527.x

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Wide distribution of the cysteine string proteins in Drosophila tissues revealed by targeted mutagenesis (1998)

Eberle, Kai K. ; Zinsmaier, K. E. ; Buchner, Sigrid ; [et al.]

Springer

Cell & tissue research 294 (1998), S. 203-217

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ISSN: 1432-0878

Keywords: Key words Exocytosis ; “J” domain ; Gene knock-out ; Temperature-sensitive paralysis ; Chaperone ; Calcium channel ; Drosophila melanogaster (Insecta)

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Medicine

Notes: Abstract The “cysteine string protein” (CSP) genes of higher eukaryotes code for a novel family of proteins characterized by a “J” domain and an unusual cysteine-rich region. Previous studies had localized the proteins in neuropil and synaptic terminals of larval and adult Drosophila and linked the temperature-sensitive paralysis of the mutants described here to conditional failure of synaptic transmission. We now use the null mutants as negative controls in order to reliably detect even low concentrations of CSPs by immunohistochemistry, employing three monoclonal antibodies. In wild-type flies high levels of cysteine string proteins are found not only in apparently all synaptic terminals of the embryonic, larval, and adult nervous systems, but also in the “tall cells” of the cardia, in the follicle cells of the ovary, in specific structures of the female spermatheca, and in the male testis and ejaculatory bulb. In addition, low levels of CSPs appear to be present in all tissues examined, including neuronal perikarya, axons, muscles, Malpighian tubules, and salivary glands. Western blots of isolated tissues demonstrate that of the four isoforms expressed in heads only the largest is found in non-neural organs. The wide expression of CSPs suggests that at least some of the various phenotypes of the null mutants observed at permissive temperatures, such as delayed development, short adult lifespan, modified electroretinogram, and optomotor behavior, may be caused by the lack of CSPs outside synaptic terminals.