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Gene Review

slo  -  slowpoke

Drosophila melanogaster

Synonyms: BK channel, BcDNA:GH10751, CG10693, Calcium-activated potassium channel slowpoke, Dmel\CG10693, ...
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High impact information on slo

  • Voltage-clamp analysis of Drosophila larval muscle revealed that ether à go-go (eag) mutations affected all identified potassium currents, including those specifically eliminated by mutations in the Shaker or slowpoke gene [1].
  • A dynamically regulated 14-3-3, Slob, and Slowpoke potassium channel complex in Drosophila presynaptic nerve terminals [2].
  • The open reading frames encode proteins ranging from 1154 to 1195 amino acids, and all possess significant identity with the slowpoke gene products in Drosophila and mouse [3].
  • Calcium-activated potassium channels were expressed in Xenopus oocytes by injection of RNA transcribed in vitro from complementary DNAs derived from the slo locus of Drosophila melanogaster [4].
  • 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 [5].

Biological context of slo

  • A mutation that eliminates slo expression prevents tolerance, whereas expression from an inducible slo transgene mimics tolerance in naive animals [6].
  • It is the sedative phase that stimulates slo gene expression and induces tolerance [6].
  • slo K(+) channel gene regulation mediates rapid drug tolerance [6].
  • During pupariation and embryogenesis, slo is expressed in muscles many hours prior to the appearance of functional channels [7].
  • BK channel activity underlies the fast afterhyperpolarization that follows an action potential and attenuates neurotransmitter and hormone secretion [8].

Anatomical context of slo

  • Fura-2-based imaging revealed in cultured embryonic neurons that the loss of either voltage-gated, inactivating Shaker channels or Ca(2+)-gated Slowpoke BK channels led to robust spontaneous Ca(2+) transients that preferentially occurred within the growth cone [9].
  • Interestingly, loss of Slowpoke currents strongly influenced tubulin regulation, enhancing the number of microtubule loop structures per growth cone [9].
  • Here we describe the effects of mutations in the slowpoke gene, which is the structural gene for a calcium activated potassium channel, on transmitter release at the neuromuscular junction in Drosophila melanogaster [10].
  • To date, five transcriptional promoters have been identified, which are responsible for slowpoke expression in neurons, midgut cells, tracheal cells, and muscle fibers [11].
  • Unlike native BK channels from rat skeletal muscle in which increasing internal Ca2+ concentration (Cai2+) in the range of 5 to 30 microM increases mean open time, increasing Cai2+ in this range for dSlo had little effect on mean open time [12].

Associations of slo with chemical compounds

  • We used Sh, slo and quinidine to remove specifically one or more K+ currents, so as to study physiological properties of these currents not previously characterized, and to examine their role in membrane excitability [13].
  • In Drosophila, a single sedation with the anesthetic benzyl alcohol changes the expression of the slo K(+) channel gene and induces rapid drug tolerance [6].
  • Mechanisms of Two Modulatory Actions of the Channel-binding Protein Slob on the Drosophila Slowpoke Calcium-dependent Potassium Channel [14].
  • The slowpoke gene is necessary for rapid ethanol tolerance in Drosophila [15].
  • Furthermore, the slowpoke mutation suppresses the striking increase in transmitter release that occurs following application of 4-aminopyridine to the ether a go-go mutant [10].

Physical interactions of slo

  • Direct application of Slob to the cytoplasmic face of detached membrane patches containing dSlo channels leads to an increase in channel activity [16].
  • Furthermore, the catalytically inactive PKAc mutant does bind to dSlo but does not modulate channel activity [17].

Regulatory relationships of slo

  • Slob binds to and modulates the Drosophila Slowpoke (dSlo) calcium-activated potassium channel and also recruits the ubiquitous signaling protein 14-3-3 to the channel regulatory complex [18].
  • Similarly, the slowpoke mutation significantly suppresses the increased transmitter release conferred either by a mutation in Shaker or by application of 4-aminopyridine, which blocks the Shaker-encoded potassium channel at the Drosophila nerve terminal [10].
  • Verification using real-time PCR shows that pan-neuronal expression of eve is sufficient to repress transcripts for both slo and nAcRalpha-96Aa [19].

Other interactions of slo

  • 3. Confocal fluorescence microscopy demonstrates that Slob and dSlo redistribute in cotransfected cells and are colocalized in large intracellular structures [16].
  • These data, taken together, suggest that monomeric D14-3-3zeta is capable of modulating dSlo channel activity in this regulatory complex [20].
  • Current-clamp recordings from normal, Sh, slo and the double-mutant Sh;slo fibers suggested that ICF plays a stronger role than IA in repolarization of the larval muscle membrane [13].
  • Anesthetic sensitivity was also examined in mutant strains of D.m. which express abnormalities either in other potassium channel conductances (eag, slo) or other ion conductances (para) [21].
  • The dSLIP1 and dSlo mRNAs are expressed coincidently throughout the Drosophila nervous system, the two proteins interact in vitro, and they may be coimmunoprecipitated from transfected cells [8].

Analytical, diagnostic and therapeutic context of slo

  • To further investigate this notion, we performed a sequence analysis of the alpha-subunit of cloned slowpoke KCa channels from Drosophila and mammals [22].
  • Cloned large conductance Ca2+-activated K+ channels (BK or maxi-K+ channels) from Drosophila (dSlo) were expressed in Xenopus oocytes and studied in excised membrane patches with the patch-clamp technique [23].


  1. Alteration of four identified K+ currents in Drosophila muscle by mutations in eag. Zhong, Y., Wu, C.F. Science (1991) [Pubmed]
  2. A dynamically regulated 14-3-3, Slob, and Slowpoke potassium channel complex in Drosophila presynaptic nerve terminals. Zhou, Y., Schopperle, W.M., Murrey, H., Jaramillo, A., Dagan, D., Griffith, L.C., Levitan, I.B. Neuron (1999) [Pubmed]
  3. Cloning, expression, and distribution of functionally distinct Ca(2+)-activated K+ channel isoforms from human brain. Tseng-Crank, J., Foster, C.D., Krause, J.D., Mertz, R., Godinot, N., DiChiara, T.J., Reinhart, P.H. Neuron (1994) [Pubmed]
  4. Calcium-activated potassium channels expressed from cloned complementary DNAs. Adelman, J.P., Shen, K.Z., Kavanaugh, M.P., Warren, R.A., Wu, Y.N., Lagrutta, A., Bond, C.T., North, R.A. Neuron (1992) [Pubmed]
  5. Impaired clock output by altered connectivity in the circadian network. Fernández, M.d.e. .L., Chu, J., Villella, A., Atkinson, N., Kay, S.A., Ceriani, M.F. Proc. Natl. Acad. Sci. U.S.A. (2007) [Pubmed]
  6. slo K(+) channel gene regulation mediates rapid drug tolerance. Ghezzi, A., Al-Hasan, Y.M., Larios, L.E., Bohm, R.A., Atkinson, N.S. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  7. Tissue-specific expression of a Drosophila calcium-activated potassium channel. Becker, M.N., Brenner, R., Atkinson, N.S. J. Neurosci. (1995) [Pubmed]
  8. dSLo interacting protein 1, a novel protein that interacts with large-conductance calcium-activated potassium channels. Xia, X., Hirschberg, B., Smolik, S., Forte, M., Adelman, J.P. J. Neurosci. (1998) [Pubmed]
  9. Sub-cellular Ca(2+) dynamics affected by voltage- and Ca(2+)-gated K(+) channels: Regulation of the soma-growth cone disparity and the quiescent state in Drosophila neurons. Berke, B.A., Lee, J., Peng, I.F., Wu, C.F. Neuroscience (2006) [Pubmed]
  10. Reduced transmitter release conferred by mutations in the slowpoke-encoded Ca2(+)-activated K+ channel gene of Drosophila. Warbington, L., Hillman, T., Adams, C., Stern, M. Invert. Neurosci. (1996) [Pubmed]
  11. Muscle-specific transcriptional regulation of the slowpoke Ca(2+)-activated K(+) channel gene. Chang, W.M., Bohm, R.A., Strauss, J.C., Kwan, T., Thomas, T., Cowmeadow, R.B., Atkinson, N.S. J. Biol. Chem. (2000) [Pubmed]
  12. Ca2+-dependent gating mechanisms for dSlo, a large-conductance Ca2+-activated K+ (BK) channel. Moss, B.L., Silberberg, S.D., Nimigean, C.M., Magleby, K.L. Biophys. J. (1999) [Pubmed]
  13. Properties of potassium currents and their role in membrane excitability in Drosophila larval muscle fibers. Singh, S., Wu, C.F. J. Exp. Biol. (1990) [Pubmed]
  14. Mechanisms of Two Modulatory Actions of the Channel-binding Protein Slob on the Drosophila Slowpoke Calcium-dependent Potassium Channel. Zeng, H., Weiger, T.M., Fei, H., Levitan, I.B. J. Gen. Physiol. (2006) [Pubmed]
  15. The slowpoke gene is necessary for rapid ethanol tolerance in Drosophila. Cowmeadow, R.B., Krishnan, H.R., Atkinson, N.S. Alcohol. Clin. Exp. Res. (2005) [Pubmed]
  16. Slob, a novel protein that interacts with the Slowpoke calcium-dependent potassium channel. Schopperle, W.M., Holmqvist, M.H., Zhou, Y., Wang, J., Wang, Z., Griffith, L.C., Keselman, I., Kusinitz, F., Dagan, D., Levitan, I.B. Neuron (1998) [Pubmed]
  17. Modulation of Drosophila slowpoke calcium-dependent potassium channel activity by bound protein kinase a catalytic subunit. Zhou, Y., Wang, J., Wen, H., Kucherovsky, O., Levitan, I.B. J. Neurosci. (2002) [Pubmed]
  18. Expression and function of variants of slob, slowpoke channel binding protein, in Drosophila. Jaramillo, A.M., Zeng, H., Fei, H., Zhou, Y., Levitan, I.B. J. Neurophysiol. (2006) [Pubmed]
  19. The homeobox transcription factor Even-skipped regulates acquisition of electrical properties in Drosophila neurons. Pym, E.C., Southall, T.D., Mee, C.J., Brand, A.H., Baines, R.A. Neural development (2006) [Pubmed]
  20. Monomeric 14-3-3 protein is sufficient to modulate the activity of the Drosophila slowpoke calcium-dependent potassium channel. Zhou, Y., Reddy, S., Murrey, H., Fei, H., Levitan, I.B. J. Biol. Chem. (2003) [Pubmed]
  21. Analysis of anesthetic action on the potassium channels of the Shaker mutant of Drosophila. Tinklenberg, J.A., Segal, I.S., Guo, T.Z., Maze, M. Ann. N. Y. Acad. Sci. (1991) [Pubmed]
  22. Hypothesis for a serine proteinase-like domain at the COOH terminus of Slowpoke calcium-activated potassium channels. Moss, G.W., Marshall, J., Moczydlowski, E. J. Gen. Physiol. (1996) [Pubmed]
  23. Wanderlust kinetics and variable Ca(2+)-sensitivity of dSlo [correction of Drosophila], a large conductance CA(2+)-activated K+ channel, expressed in oocytes. Silberberg, S.D., Lagrutta, A., Adelman, J.P., Magleby, K.L. Biophys. J. (1996) [Pubmed]
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