Tissue-specific expression of a Drosophila calcium-activated potassium channel

Becker, Marie N.; Brenner, Robert; Atkinson, Nigel S.

doi:10.1523/jneurosci.15-09-06250.1995

Cited by 61 publications

(87 citation statements)

References 32 publications

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“…slo is highly regulated at the transcriptional level, employing several alternative promoters and splice variants (29)(30)(31). To distinguish between a neuronal and/or a muscular defect associated with the strong impairment observed in slo mutants, we evaluated locomotor activity in two transgenic lines that rescue predominantly neuronal [B52H;slo 4 (32)] or muscular [M131;slo 4 (30)] defects associated with the lack of SLO.…”

Section: Resultsmentioning

confidence: 99%

Impaired clock output by altered connectivity in the circadian network

Fernández

Chu

Villella

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Substantial progress has been made in elucidating the molecular processes that impart a temporal control to physiology and behavior in most eukaryotes. In Drosophila, dorsal and ventral neuronal networks act in concert to convey rhythmicity. Recently, the hierarchical organization among the different circadian clusters has been addressed, but how molecular oscillations translate into rhythmic behavior remains unclear. The small ventral lateral neurons can synchronize certain dorsal oscillators likely through the release of pigment dispersing factor (PDF), a neuropeptide central to the control of rhythmic rest-activity cycles. In the present study, we have taken advantage of flies exhibiting a distinctive arrhythmic phenotype due to mutation of the potassium channel slowpoke (slo) to examine the relevance of specific neuronal populations involved in the circadian control of behavior. We show that altered neuronal function associated with the null mutation specifically impaired PDF accumulation in the dorsal protocerebrum and, in turn, desynchronized molecular oscillations in the dorsal clusters. However, molecular oscillations in the small ventral lateral neurons are properly running in the null mutant, indicating that slo is acting downstream of these core pacemaker cells, most likely in the output pathway. Surprisingly, disrupted PDF signaling by slo dysfunction directly affects the structure of the underlying circuit. Our observations demonstrate that subtle structural changes within the circadian network are responsible for behavioral arrhythmicity.circadian circuitry ͉ Drosophila ͉ pigment dispersing factor ͉ potassium channels ͉ slowpoke R hythmicity in rest-activity cycles in Drosophila is under control of the circadian clock, which is based on selfsustaining, cell-autonomous transcriptional negative feedback loops. These feedback loops ultimately give rise to rhythms in the abundance, phosphorylation state, and nuclear localization of key intracellular proteins, such as period (PER) and timeless (TIM) (1). To date, several neuronal clusters have been shown to include a molecular oscillator. The one best understood encompasses the small ventral lateral neurons (LNvs), comprised of five cells, of which four rhythmically release the neuropeptide pigment dispersing factor (PDF) at their dorsal terminals. Other oscillators within the fly brain include the dorsal lateral neurons (LNds) together with the dorsal neurons (DN1-3) (2). Ablation of all LNvs by overexpression of proapoptotic genes, as well as null mutations on the pdf gene or its receptor, cause behavioral arrhythmicity a few days upon transfer to constant conditions (3-6) likely through the gradual loss of synchronization among the components of the small LNv cluster (7).The question of how the intracellular molecular oscillations taking place within specific neuronal clusters ultimately drive rhythmic locomotor activity has only recently been approached in Drosophila (7-11). Molecular oscillations must be somehow transduced into neuronal function to...

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Section: Resultsmentioning

confidence: 99%

Impaired clock output by altered connectivity in the circadian network

Fernández

Chu

Villella

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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“…Surprisingly, there have been only two reports in the literature on the immunolocalization of K ϩ -channels in Drosophila (Schwarz et al, 1990;Becker et al, 1995). The shortage of experimental results in such an active field of research probably reflects the lack of high-affinity antisera for elucidating this important matter.…”

Section: K-channel Expression; K-channel Localization; K-channel Distmentioning

confidence: 99%

Diverse Expression and Distribution ofShakerPotassium Channels during the Development of theDrosophilaNervous System

1997

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The spatio-temporal expression ofShaker(Sh) potassium channels (Kch) in the developing and adult nervous system ofDrosophilahas been studied at the molecular and histological level using specific antisera.ShKch are distributed in most regions of the nervous system, but their expression is restricted to only certain populations of cells.ShKch have been found in the following three locations: in synaptic areas of neuropile, in axonal fiber tracks, and in a small number of neuronal cell bodies. This wide subcellular localization, together with a diverse distribution, implicatesShKch in multiple neuronal functions.Experiments performed withShmutants that specifically eliminate a few of theShKch splice variants clearly demonstrate an abundant differential expression and usage of the wide repertoire ofShisoforms, but they do not support the idea of extensive segregation of these isoforms among different populations of neurons.ShKch are predominantly expressed at late stages of postembryonic development and adulthood. Strikingly, wide changes in the repertoire ofShsplice isoforms occur some time after the architecture of the nervous system is complete, indicating that the expression ofShKch contributes to the final refinements of neuronal differentiation. These late changes in the expression and distribution ofShKch seem to correlate with activity patterns suggesting thatShKch may be involved in adaptative mechanisms of excitability.

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“…The cDNA H13 was isolated from an adult head cDNA library (a kind gift from Thomas Schwarz, Stanford University School of Medicine) and has been described previously (Atkinson et al, 1991;Becker et al, 1995). The M131 transgene was constructed in pCaSperAUG␤gal (Thummel et al, 1988).…”

Section: Construction Of Transgene M131mentioning

confidence: 99%

“…In this vector, the insert is flanked by P-element ends and can be used to transform Drosophila. The cloned slowpoke transcriptional control region (KpnI to ApaI; plasmid 125) was fused, in translational frame, to the cDNA H13 (Becker et al, 1995). Plasmid 185 contains the full-length H13 cDNA followed by an HSV epitope tag (QPELAPEDPED) and a stop codon (Novagen, Inc., Madison, WI, U.S.A.).…”

Section: Construction Of Transgene M131mentioning

confidence: 99%

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Complementation of Physiological and Behavioral Defects by a Slowpoke Ca²⁺ ‐Activated K⁺ Channel Transgene

Brenner

Srinivasan

et al. 2000

Journal of Neurochemistry

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Abstract:The Drosophila slowpoke gene encodes a large conductance calcium-activated potassium channel used in neurons, muscle, and some epithelial cells. Tissuespecific transcriptional promoters and alternative mRNA splicing generate a large array of transcripts. These distinct transcripts are thought to tailor the properties of the channel to the requirements of the cell. Presumably, a single splice variant cannot satisfy the specific needs of all cell types. To test this, we examined whether a single slowpoke splice variant was capable of complementing all slowpoke behavioral phenotypes. Null mutations in slowpoke cause animals to be semiflightless and to manifest an inducible "sticky-feet" phenotype. The well-characterized slowpoke transcriptional control region was used to direct the expression of a single slowpoke splice variant (cDNA H13) in transgenic flies. The endogenous gene in these flies had been inactivated by the slo 4 mutation. Action-potential recordings and voltage-clamp recordings demonstrated the production of functional channels from the transgene. The transgene completely complemented the flight defect, but not the sticky-feet phenotype. We conclude that distinct slowpoke channel isoforms, produced by alternative splicing, are not interchangeable and are required for proper function of different cell types. Key Words: Potassium channel-slowpoke-Drosophila-mRNA splicing-Behavior-Voltage clamp.

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Tissue-specific expression of a Drosophila calcium-activated potassium channel

Cited by 61 publications

References 32 publications

Impaired clock output by altered connectivity in the circadian network

Impaired clock output by altered connectivity in the circadian network

Diverse Expression and Distribution ofShakerPotassium Channels during the Development of theDrosophilaNervous System

Complementation of Physiological and Behavioral Defects by a Slowpoke Ca²⁺ ‐Activated K⁺ Channel Transgene

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Tissue-specific expression of a Drosophila calcium-activated potassium channel

Cited by 61 publications

References 32 publications

Impaired clock output by altered connectivity in the circadian network

Impaired clock output by altered connectivity in the circadian network

Diverse Expression and Distribution ofShakerPotassium Channels during the Development of theDrosophilaNervous System

Complementation of Physiological and Behavioral Defects by a Slowpoke Ca2+ ‐Activated K+ Channel Transgene

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Complementation of Physiological and Behavioral Defects by a Slowpoke Ca²⁺ ‐Activated K⁺ Channel Transgene