Polytene chromosomes normal.
slo1 animals exhibit defects in mitochondrial functional integrity (significantly increased levels of reactive oxygen species (DHE staining)); young adults exhibit hallmarks of the early aging phenotype (mitochondrial swirls (which are observed only in very old controls) and increased number of vacuoles); old adults exhibit fewer and larger mitochondria with swollen appearance, loss of continuous inner mitochondrial membrane and severe defects in cristae arrangement in the indirect flight muscles when compared to controls.
slo1 adults do not exhibit a difference in their short life span between genders or culturing conditions (genders separately or together).
slo1 adults exhibit following aging defects: a dramatic reduction in locomotion (negative geotaxis, both in males and females), a significant increase in protein aggregates (Ubiquitin staining) and a fluorescent dye leakage through the gut perforations both at young and old ages when compared to controls.
slo1 adults adults are more susceptible to oxidative stress (induced by feeding with paraquat) compared to controls.
Air puff-triggered flight initiation success is dramatically reduced in slo1 mutants.
Homozygous third instar larvae show a significant increase in bouton size at the neuromuscular junction compared to controls.
The excitatory junctional current amplitude at the neuromuscular junction is reduced in mutants compared to controls. The EJC response of mutant neuromuscular junctions under low conditions (pH 6.1) is not different to wild-type.
slo1 mutants display abundant small boutons, termed 'satellites', budding from the larger primary boutons along the branch axis. Such aberrant outgrowth is found at both type Ib and Is neuromuscular junctions in different muscles, e.g. 6/7 and 4. Upon closer examination, two distinct types of satellites are observed, one without a clear constriction between satellites and primary boutons, resembling yeast budding (type B satellites) and the other with a short but clear constriction or 'neck' (type M satellites). Type B satellites are more abundant than type M satellites in these mutants. There is also an overall increase in synaptic bouton number and terminal branching in these mutants.
Exposure to high temperatures (29[o]C) for 2 hours during development fails to induce significant morphological changes in synaptic growth in slo1 mutants. However, numbers of both B- and M-type satellites are drastically reduced after 5 hours of high temperature. Wild-type synapses do not exhibit this behaviour. 5 hour heat treatment also increases the number of branches seen in slo1 mutants.
Larvae heterozygous for slo1 show increases in the numbers of type-B and -M satellites, mature boutons, and branch segments, comparable to homozygous mutants.
The rate of habituation of the giant fiber escape pathway is markedly reduced in slo1 flies compared to wild-type. The refractory period of the long-latency response is shorter than normal. The short-latency response of the tergotrochanteral muscle is delayed.
Homozygous males produce very low amplitude courtship songs with long interpulse intervals, and low interpulse frequency and cycles per pulse values compared to wild-type males. Isolated putative pulses, usually monocyclic signals, often occur. Males show many courtship wing extensions without actually producing audible sound. The interpulse frequency of heterozygous males is significantly lower than in wild-type males at 25oC, although other courtship song parameters of heterozygous males are normal. slo1/Df(3R)slo3 males show an intermediate courtship song phenotype between slo1 and Df(3R)slo3 homozygous males.
Homozygotes show increased sensitivity to halothane, chloroform and trichloroethylene in an inebriometer assay (an assay of geotactic and postural behaviour) compared to wild-type flies.
In combination with DAP or Sh14, electrotonically evoked synaptic currents show delay before transmitter release and decrease in onset slope when assayed in third instar larvae.
The Ca2+-activated fast K+ current (ICF) is eliminated in larval muscle fibres.
slo1 has short lived phenotype, suppressible by Scer\GAL4da.PU/Sod2UAS.cUa
slo1 has abnormal neuroanatomy phenotype, suppressible by dlg1WT.UAS.EGFP/Scer\GAL4Mef2.247
slo1 has abnormal neuroanatomy phenotype, suppressible by rut1
slo1 has abnormal neuroanatomy phenotype, suppressible by dncM14
slo1 has abnormal neuroanatomy phenotype, suppressible by dncUAS.cCa/Scer\GAL4C164
slo1 has abnormal neuroanatomy phenotype, suppressible by sei1
slo1 has abnormal neuroanatomy phenotype, suppressible by Ca-α1DAR66
slo1 has abnormal neuroanatomy phenotype, non-suppressible by dlg17
slo1 has abnormal neuroanatomy phenotype, non-suppressible by mlenap-ts1
slo1 has abnormal neuroanatomy phenotype, non-suppressible by Scer\GAL4elav-C155/dncUAS.cCa
slo1 has NMJ bouton | increased number phenotype, suppressible by sei1
slo1 has neuromuscular junction phenotype, suppressible by sei1
slo1 has NMJ bouton | increased number phenotype, suppressible by Fas2e76
slo1 has NMJ bouton | increased number phenotype, suppressible by dlg17
slo1 has neuromuscular junction phenotype, suppressible by dlg17
slo1 has NMJ bouton | increased number phenotype, suppressible by Ca-α1DAR66
slo1 has neuromuscular junction phenotype, suppressible by Ca-α1DAR66
slo1 has NMJ bouton | increased number phenotype, suppressible by dlg1WT.UAS.EGFP/Scer\GAL4Mef2.247
slo1 has neuromuscular junction phenotype, suppressible by dlg1WT.UAS.EGFP/Scer\GAL4Mef2.247
slo1 has NMJ bouton | increased number phenotype, suppressible by rut1
slo1 has neuromuscular junction phenotype, suppressible by rut1
slo1 has NMJ bouton | increased number phenotype, suppressible by dncM14
slo1 has neuromuscular junction phenotype, suppressible by dncM14
slo1 has NMJ bouton | increased number phenotype, suppressible by dncUAS.cCa/Scer\GAL4C164
slo1 has neuromuscular junction phenotype, suppressible by dncUAS.cCa/Scer\GAL4C164
slo1 has neuromuscular junction phenotype, non-suppressible by Fas2e76
slo1 has NMJ bouton | increased number phenotype, non-suppressible by mlenap-ts1
slo1 has neuromuscular junction phenotype, non-suppressible by mlenap-ts1
slo1 has NMJ bouton | increased number phenotype, non-suppressible by Scer\GAL4elav-C155/dncUAS.cCa
slo1 has neuromuscular junction phenotype, non-suppressible by Scer\GAL4elav-C155/dncUAS.cCa
When compared with single mutants, the combined mutational effects of sei1/slo1 are not simply additive, with a further enhancement of some slo, but not sei phenotypes. Satellite abundance is less extreme in sei1/slo1 double mutants compared to sei1 mutants. There is a slight, but not significant, reduction in the numbers of both types B and M satellites. In contrast, the numbers of type M (but not type B) satellites and mature boutons are significantly greater in double mutants compared to slo single mutants.
The frequency of satellite formation in Fas2e76; slo1 double mutants is comparable to slo1 single mutants. Overall bouton number is slightly reduced in these double mutants. However, a similar reduction is seen in Fas2e76 mutants.
dlg17/slo1 mutants exhibit reduced levels of type B and type M satellites, close to wild-type levels, compared to slo1 single mutants. This reduction correlates with reduced levels of mature boutons and with simpler branching patterns.
A Ca-α1DAR66 mutant background suppresses both type B and type M satellites in Ca-α1DAR66; slo1 double mutants nearly to wild-type levels. Such suppression in satellite formation leads to the morphology of these double mutants to resemble Ca-α1DAR66 single mutants.
Overexpression of dlg1WT.Scer\UAS.T:Avic\GFP-EGFP in the developing muscle under the control of Scer\GAL4Mef2.247 induces a more pronounced reduction in type B satellites (small boutons) in slo1 mutants. As a result, the numbers of remaining type B and type M satellites becomes similar, and there are fewer satellites in total. The number of mature boutons is significantly enhanced in slo1 larvae expressing post-synaptic dlg1WT.Scer\UAS.T:Avic\GFP-EGFP.
Despite their abundance in slo1 single mutants, levels of both type B and type M satellites are suppressed in rut1; slo1 double mutants to wild-type levels, along with a slight reduction in mature bouton number.
A mlenap-ts1 mutant background does not affect synaptic satellite growth in slo1 mutants.
A dncM14 mutant background severely suppresses the frequency of type B and type M satellites (small boutons) in dncM14; slo1 double mutants.
Pre-synaptic expression of dncScer\UAS.cCa (under the control of Scer\GAL4elav-C155 in a slo1 background does not influence satellite bouton number.
Post-synaptic expression of dncScer\UAS.cCa (under the control of Scer\GAL4C164 in a slo1 background suppresses the number of both type M and type B satellites. However, the number of mature boutons remains higher in these mutants.
The physiological properties and role in membrane excitability of ICF, the voltage-activated fast K+ current (IA) and the voltage-activated delayed K+ current (IK) have been investigated using Sh14 and slo1 mutant larval muscle fibres and quinidine (which blocks IK). Current-clamp recordings from wild-type, Sh14, slo1 and Sh14 slo1 double mutant larval muscle fibres suggest that ICF plays a stronger role than IA in repolarisation of the larval muscle membrane.
Eliminate the ICF, fast Ca2+ activated K+ current.