A<i>Drosophila</i>KCNQ Channel Essential for Early Embryonic Development

Hua, Wen; Weiger, Thomas; Ferguson, Tanya S; Shahidullah, Mohammad; Scott, Samae S.; Levitan, Irwin B.

doi:10.1523/jneurosci.3086-05.2005

Cited by 24 publications

(34 citation statements)

References 54 publications

(66 reference statements)

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“…8). KCNQ and Na V orthologs were present in numerous invertebrate genomes as shown previously (Plummer and Meisler, 1999;Goldin, 2002;Yu and Catterall, 2004;Wei et al, 2005;Wen et al, 2005). However, we found no examples of invertebrate KCNQ or Na V channels possessing the ankyrin-G binding motif.…”

Section: Ankyrin-g Coexpression Has Slight Effects On Kcnq2/kcnq3 Chasupporting

confidence: 76%

A Common Ankyrin-G-Based Mechanism Retains KCNQ and Na_VChannels at Electrically Active Domains of the Axon

et al. 2006

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KCNQ (K V 7) potassium channels underlie subthreshold M-currents that stabilize the neuronal resting potential and prevent repetitive firing of action potentials. Here, antibodies against four different KCNQ2 and KCNQ3 polypeptide epitopes show these subunits concentrated at the axonal initial segment (AIS) and node of Ranvier. AIS concentration of KCNQ2 and KCNQ3, like that of voltage-gated sodium (Na V ) channels, is abolished in ankyrin-G knock-out mice. A short motif, common to KCNQ2 and KCNQ3, mediates both in vivo ankyrin-G interaction and retention of the subunits at the AIS. This KCNQ2/KCNQ3 motif is nearly identical to the sequence on Na V ␣ subunits that serves these functions. All identified Na V and KCNQ genes of worms, insects, and molluscs lack the ankyrin-G binding motif. In contrast, vertebrate orthologs of Na V ␣ subunits, KCNQ2, and KCNQ3 (including from bony fish, birds, and mammals) all possess the motif. Thus, concerted ankyrin-G interaction with KCNQ and Na V channels appears to have arisen through convergent molecular evolution, after the division between invertebrate and vertebrate lineages, but before the appearance of the last common jawed vertebrate ancestor. This includes the historical period when myelin also evolved.

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Section: Ankyrin-g Coexpression Has Slight Effects On Kcnq2/kcnq3 Chasupporting

confidence: 76%

A Common Ankyrin-G-Based Mechanism Retains KCNQ and Na_VChannels at Electrically Active Domains of the Axon

et al. 2006

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“…In the tormogen, it is the apical membrane that is highly infolded, and the more likely site of the ion pump. Further, the TEP is insensitive to the Na + /K + ATPase inhibitor ouabain [87], and mutants lacking the only Drosophila KCNQ channel show no evidence of mechanosensory defects [101]. K + transport by the tormogen more likely involves the coupled activity of a proton-exporting V-ATPase and a H + /K + exchanger (as yet unidentified in Drosophila [33]), which energizes the apical surfaces of insect gut, excretory, and salivary gland cells [102].…”

Section: Ion Transport and Transduction In Es Organsmentioning

confidence: 99%

Mechanotransduction and auditory transduction in Drosophila

Kernan

2007

Pflugers Arch - Eur J Physiol

168

167

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Insects are utterly reliant on sensory mechanotransduction, the process of converting physical stimuli into neuronal receptor potentials. The senses of proprioception, touch, and hearing are involved in almost every aspect of an adult insect's complex behavioral repertoire and are mediated by a diverse array of specialized sensilla and sensory neurons. The physiology and morphology of several of these have been described in detail; genetic approaches in Drosophila, combining behavioral screens and sensory electrophysiology with forward and reverse genetic techniques, have now revealed specific proteins involved in their differentiation and operation. These include three different TRP superfamily ion channels that are required for transduction in tactile bristles, chordotonal stretch receptors, and polymodal nociceptors. Transduction also depends on the normal differentiation and mechanical integrity of the modified cilia that form the neuronal sensory endings, the accessory structures that transmit stimuli to them and, in bristles, a specialized receptor lymph and transepithelial potential. Flies hear near-field sounds with a vibration-sensitive, antennal chordotonal organ. Biomechanical analyses of wild-type antennae reveal non-linear, active mechanical properties that increase their sensitivity to weak stimuli. The effects of mechanosensory and ciliary mutations on antennal mechanics show that the sensory cilia are the active motor elements and indicate distinct roles for TRPN and TRPV channels in auditory transduction and amplification.

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“…There is only one copy of the KCNQ gene found in Drosophila genome (Wen et al 2005) and deletion mutants of the single Drosophila KCNQ gene are viable but show a 3-fold higher than normal susceptibility to pacing-induced heart failure [see below; and (Ocorr et al 2007)]. Recent investigation of the heart rhythm of KCNQ mutants revealed that Drosophila, the only invertebrate genetic model organism with a heart (Bier and Bodmer 2004), may also be a surprisingly good model for studying the genetics of arrhythmias, as a result of both mutations and aging.…”

Section: Modulation Of the Heart Rhythmmentioning

confidence: 99%

Genetic Control of Heart Function and Aging in Drosophila

Ocorr¹,

Perrin²,

Lim³

et al. 2007

Trends in Cardiovascular Medicine

123

101

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Why is Drosophila a good model of cardiac physiology?The fly heart has been an excellent model of cardiovascular development for over a decade. Since the discovery of the homeobox transcription factor tinman (Azpiazu and Frasch 1993, Bodmer 1993, Bodmer et al. 1990) and the recognition that it is conserved in vertebrates [reviewed in (Bodmer 1995, Harvey 1996], more and more evidence has corroborated the idea that much of the regulatory genetic network controlling the specification and differentiation of the heart is conserved from flies to mammals [reviewed in (Bodmer and Frasch 1999, Bodmer et al. 2005, Cripps and Olson 2002, Zaffran and Frasch 2002 ], laying the ground work for molecular models of congenital heart disease in humans [reviewed in (Chien and Olson 2002, Prall et al. 2002, Seidman and Seidman 2002, Olson 2004, Srivastava 2006]. Given the remarkable conservation of molecular and embryological mechanisms underlying cardiogenesis in the animal kingdom, it seems plausible that the genetic control of heart function may also be conserved. Clearly, many proteins that carry out cardiac function, such as ion channels and contractile proteins, are highly conserved (reviewed in Bodmer et al. 2005): contributors to excitation-contraction coupling, such as the ryanodine receptor, SERCA, myosin, troponin, and ion channels likely to be involved in pacemaking, such as Ih/HCN (Monier et al. 2005), are all present in fly cardiomyocytes. Also, plasma membrane invag inations forming T tubules have been observed in the fly's heart, much like in vertebrates, and the mononucleate cardiomyocytes that comprise the heart tube are electrically connected by GAP junctions formed by innexin proteins in invertebrates. Thus, it is conceivable that the way these conserved proteins function within the mature heart to ensure a normal heartbeat has also evolved from a common evolutionary design that was in place prior to the invertebratevertebrate split.In the following we review recent advances in elucidating the genetics of cardiac function and aging in Drosophila and propose that the control of the cardiac physiology and rhythmicity is conserved between in many ways vertebrates and invertebrates. As a consequence, the fly heart is a potentially useful genetic model not only for understanding congenital heart disease that Correspondence: R. Bodmer (rolf@burnham.org) and X. Wu

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ADrosophilaKCNQ Channel Essential for Early Embryonic Development

Cited by 24 publications

References 54 publications

A Common Ankyrin-G-Based Mechanism Retains KCNQ and Na_VChannels at Electrically Active Domains of the Axon

A Common Ankyrin-G-Based Mechanism Retains KCNQ and Na_VChannels at Electrically Active Domains of the Axon

Mechanotransduction and auditory transduction in Drosophila

Genetic Control of Heart Function and Aging in Drosophila

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ADrosophilaKCNQ Channel Essential for Early Embryonic Development

Cited by 24 publications

References 54 publications

A Common Ankyrin-G-Based Mechanism Retains KCNQ and NaVChannels at Electrically Active Domains of the Axon

A Common Ankyrin-G-Based Mechanism Retains KCNQ and NaVChannels at Electrically Active Domains of the Axon

Mechanotransduction and auditory transduction in Drosophila

Genetic Control of Heart Function and Aging in Drosophila

Contact Info

Product

Resources

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A Common Ankyrin-G-Based Mechanism Retains KCNQ and Na_VChannels at Electrically Active Domains of the Axon

A Common Ankyrin-G-Based Mechanism Retains KCNQ and Na_VChannels at Electrically Active Domains of the Axon