adherens junction & embryonic dorsal trunk, with Scer\GAL4btl.B123
adherens junction & embryonic dorsal trunk, with Scer\GAL4btl.PS
wing, with Scer\GAL4T80
wing vein, with Scer\GAL4A9
wing vein | ectopic, with Scer\GAL4A9
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4esg.PU, Scer\GAL4dsx.KI or Scer\GAL4spi-NP0261 (in combination with Gal80[ts] for the temporal regulation of expression) leads to a significant decrease in the relative and absolute size of secondary cell nuclei compared to neighboring main cells and wild-type controls; adulthood-only expression under the combined control of Scer\GAL4esg.PU and Gal80[ts] does not affect the size of main cell nuclei compared to controls. The adulthood-only expression under the control of Scer\GAL4dsx.KI (and Gal80[ts]) leads to a significant increase in the number of secretory vesicles, associated with a significant increase in the size of the largest multivesicular body/lysosome, within accessory gland secondary cells compared to controls; there is also a severe decrease in the secretion of (CD63-positive) exosomes into the accessory gland lumen. The adulthood-only expression under the control of Scer\GAL4spi-NP0261 (and Gal80[ts]) leads to a significant increase in the size of the largest multivesicular body/lysosome within accessory gland secondary cells, as compared to controls.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 driven by Scer\GAL4elav.PU does not lead to significant increases in satellite bouton number at the neuromuscular junction of third instar larvae.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4dsx.KI results in hypertrophy of the male accessory gland secondary cells. Secondary cells expressing tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4spi-NP0261 contain fewer, but much larger, maturing multivesicular bodies or lysosomes (mMVBLs) compared to controls. The number of immature late endosomes (iLEs) per secondary cell is increased and more of these cells than controls contain multiple secretory vacuoles (SVs) clustered around the enlarged mMVML.
The amplitude of miniature excitatory junctional currents (mEJCs) is normal at the neuromuscular junction (NMJ) in larvae expressing tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4BG380, but the evoked EJC shows an increase in amplitude compared to wild type, resulting in an increase in quantal content at the mutant NMJ.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 in the wing discs under the control of Scer\GAL4T80 leads to ectopic wing vein formation.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4A9 results in small wings that are highly pigmented with excess vein tissue.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 in the wing with Scer\GAL4ptc-559.1 induces patterning abnormalities including extensive ectopic vein, fusion of longitudinal veins, and loss of intervein regions.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4BG380 does not significantly alter the number of boutons per muscle surface area at the neuromuscular junction of third instar larvae.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4elav.PH in clones induced by FLP/FRT mediated recombination (to activate the Scer\GAL4elav.PH driver) results in an increase in the number of type 1b boutons at muscle 13 compared to wild type.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4elav.PU does not affect synaptic growth at the larval neuromuscular junction (the average number of satellite boutons is not significantly different from wild type).
Expression of two copies of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4elav-C155 results in an increase in both the total number of boutons and the number of satellite boutons at the larval neuromuscular junction.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Mhc.PW results in the ratio of import/export rates being higher than in control muscles (7.4 compared to 3.6). This difference in the import/export ratio explains the net accumulation of nuclear Mad in tkvQ199D.Scer\UAS.T:Ivir\HA1 muscles above the levels of control in steady state. The effective import rate does not increase, but decreases slightly upon constitutive signalling (1.6 times smaller in tkvQ199D.Scer\UAS.T:Ivir\HA1 than in controls), while it is the effective export rate that significantly decreases (3.4 times smaller in
tkvQ199D.Scer\UAS.T:Ivir\HA1).
Constitutive signalling caused by expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Mhc.PW leads to an increase by an order of magnitude (67%) of the immobile pool of Mad in the nucleus.
100% of wings are overgrown and have numerous ectopic veins in flies expressing tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4A9.
Expression of tkvQ199D.UAS.Tag:HA in presynaptic cholinergic neurons, driven by Scer\GAL4ChAT.7.4, is sufficient to produce a large and significant increase in synaptic current amplitude in aCC/RP2 neurons compared to controls. tkvQ199D.UAS.Tag:HA expression in postsynaptic neurons, driven by Scer\GAL4eve.RN2, has no effect on synaptic current amplitude.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4elav.PLu or Scer\GAL4OK6 in a wild-type background does not result in a significant increase in the number of neuromuscular junction synaptic boutons.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4btl.PS in the tracheal system results in the formation of fine dorsal trunks containing stretches of autocellular adherens junctions. Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4btl.B123 in single cells or groups of cells in the dorsal trunk results in the formation of ectopic autocellular adherens junctions, although at a low frequency.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4A9 causes a wing phenotype.
Flies expressing tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4A9 have small wings which are blistered due to lack of adhesion of the dorsal and ventral compartments. Intervein cells express vein-specific hairs and the marginal triple row bristles are transformed into the oversized double row bristles normally seen at more distal positions along the wing margin. The wings are darkly pigmented.
Scer\GAL4BG380, saxA.UAS.cBa, tkvQ199D.UAS.Tag:HA has abnormal neurophysiology | third instar larval stage phenotype, suppressible by trio6A/trioS137203
Scer\GAL4elav-C155, tkvQ199D.UAS.Tag:HA has abnormal neuroanatomy | larval stage phenotype, suppressible by Scer\GAL4elav-C155/nwkUAS.cCa
Scer\GAL4elav-C155, tkvQ199D.UAS.Tag:HA has abnormal neuroanatomy | larval stage phenotype, suppressible by Dap160UAS.cKa, Scer\GAL4elav-C155
Scer\GAL4A9, tkvQ199D.UAS.Tag:HA has visible phenotype, suppressible by SnooUAS.cTa/Scer\GAL4A9
Scer\GAL4elav-C155/tkvQ199D.UAS.Tag:HA is an enhancer of abnormal neuroanatomy | larval stage phenotype of Scer\GAL4elav-C155, Snx163A.UAS.GFP
Scer\GAL4elav.PU/tkvQ199D.UAS.Tag:HA is an enhancer of abnormal neuroanatomy | larval stage phenotype of nwk2
tkvQ199D.UAS.Tag:HA/Scer\GAL4elav.PLu is an enhancer of abnormal neuroanatomy phenotype of hiwEMS
Scer\GAL4BG380/tkvQ199D.UAS.Tag:HA is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of nmounspecified
Snx163A.UAS.GFP/tkvQ199D.UAS.Tag:HA, Scer\GAL4VGlut1.PD is a non-suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Hsap\TARDBPUAS.cHa, Scer\GAL4VGlut1.PD
Snx163A.UAS.GFP/tkvQ199D.UAS.Tag:HA, Scer\GAL4VGlut1.PD is a non-suppressor of abnormal locomotor behavior | third instar larval stage phenotype of Hsap\TARDBPUAS.cHa, Scer\GAL4VGlut1.PD
kek5UAS.GFP, tkvQ199D.UAS.Tag:HA has visible | recessive phenotype
tkvQ199D.UAS.Tag:HA has wing cell phenotype, enhanceable by kek5UAS.GFP
tkvQ199D.UAS.Tag:HA has wing vein phenotype, enhanceable by kek5UAS.GFP
Scer\GAL4A9, tkvQ199D.UAS.Tag:HA has wing phenotype, non-enhanceable by Scer\GAL4A9/sogsupersog1.UAS
Scer\GAL4T80, tkvQ199D.UAS.Tag:HA has wing phenotype, suppressible by Scer\GAL4T80, tkvQ199D.UAS.Tag:HA
Scer\GAL4elav-C155, tkvQ199D.UAS.Tag:HA has NMJ bouton | increased number | larval stage phenotype, suppressible by Scer\GAL4elav-C155/nwkUAS.cCa
Scer\GAL4elav-C155, tkvQ199D.UAS.Tag:HA has NMJ bouton | increased number | larval stage phenotype, suppressible by Dap160UAS.cKa, Scer\GAL4elav-C155
Scer\GAL4A9, tkvQ199D.UAS.Tag:HA has wing phenotype, suppressible by SnooUAS.cTa/Scer\GAL4A9
Scer\GAL4A9, tkvQ199D.UAS.Tag:HA has wing vein | ectopic phenotype, suppressible by SnooUAS.cTa/Scer\GAL4A9
Scer\GAL4A9, tkvQ199D.UAS.Tag:HA has wing phenotype, non-suppressible by Scer\GAL4A9/sogsupersog1.UAS
Scer\GAL4elav-C155/tkvQ199D.UAS.Tag:HA is an enhancer of NMJ bouton | larval stage | increased number phenotype of Scer\GAL4elav-C155, Snx163A.UAS.GFP
Scer\GAL4elav.PU/tkvQ199D.UAS.Tag:HA is an enhancer of NMJ bouton | larval stage | increased number phenotype of nwk2
tkvQ199D.UAS.Tag:HA/Scer\GAL4elav.PLu is an enhancer of bouton | increased number phenotype of hiwEMS
tkvQ199D.UAS.Tag:HA/Scer\GAL4elav.PLu is an enhancer of neuromuscular junction phenotype of hiwEMS
Scer\GAL4T80, tkvQ199D.UAS.Tag:HA is a suppressor of wing phenotype of Scer\GAL4T80, tkvQ199D.UAS.Tag:HA
Scer\GAL4VP16.nanos.UTR/tkvQ199D.UAS.Tag:HA is a suppressor of wing vein phenotype of mague00439/maguf02256
Scer\GAL4VP16.nanos.UTR/tkvQ199D.UAS.Tag:HA is a suppressor of testis phenotype of mague00439/maguf02256
Scer\GAL4VP16.nanos.UTR/tkvQ199D.UAS.Tag:HA is a suppressor of male germline stem cell | third instar larval stage phenotype of mague00439/maguf02256
Scer\GAL4BG380/tkvQ199D.UAS.Tag:HA is a suppressor of NMJ bouton | third instar larval stage phenotype of nmounspecified
tkvQ199D.UAS.Tag:HA/Scer\GAL4hs.PB is a suppressor of embryonic dorsal epidermis | germline clone | rescuable maternal effect phenotype of Cka05836
Scer\GAL4LE/tkvQ199D.UAS.Tag:HA is a suppressor of embryonic epidermis | dorsal phenotype of arm3
Scer\GAL4pnr-MD237/tkvQ199D.UAS.Tag:HA is a suppressor of embryonic dorsal epidermis phenotype of Jra76-19
Snx163A.UAS.GFP/tkvQ199D.UAS.Tag:HA, Scer\GAL4VGlut1.PD is a non-suppressor of NMJ bouton | third instar larval stage phenotype of Hsap\TARDBPUAS.cHa, Scer\GAL4VGlut1.PD
tkvQ199D.UAS.Tag:HA/Scer\GAL4T80 is a non-suppressor of wing phenotype of Scer\GAL4T80, fussUAS.cTa
Scer\GAL4VGlut1.PD, Snx163A.UAS.GFP, tkvQ199D.UAS.Tag:HA has NMJ bouton | third instar larval stage phenotype
DIP-γMI03222, Scer\GAL4elav.PU, tkvQ199D.UAS.Tag:HA has NMJ bouton | increased number | third instar larval stage phenotype
Scer\GAL4elav.PU, dpr11MI02231, tkvQ199D.UAS.Tag:HA has NMJ bouton | increased number | third instar larval stage phenotype
Third instar larvae expressing tkvQ199D.Scer\UAS.T:Ivir\HA1 and Snx163A.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4VGlut.PD display increased number of boutons on neuromuscular junctions.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 driven by Scer\GAL4elav.PU in a dpr11MI02231/+ or DIP-γMI03222/+ background leads to extra satellite boutons at the neuromuscular junction (NMJ) of third instar larvae.
Over-activation of the BMP pathway, by co-expressing tkvQ199D.Scer\UAS.T:Ivir\HA1 and saxQ263D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4nos.UTR.T:Hsim\VP16, leads to an increase of early somatic cells in the male gonad, but no increase in somatic cell proliferation.
Co-expression of CORLScer\UAS.cTa in the wing disc under the control of Scer\GAL4T80 suppresses ectopic wing vein formation from CORLScer\UAS.cTa expression. These wings exhibit a few ectopic veins and truncations of L2, L4 and L5 wing veins.
Co-expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 dramatically enhances the increase in satellite bouton number at the neuromuscular junction which is seen in larvae expressing Snx163A.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4elav-C155.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 using the germ cell driver Scer\GAL4nos.UTR.T:Hsim\VP16 raises the fraction of testes with germline stem cells from 63% to 100% in a mague00439/maguf02256 background. The median germline stem cell number also doubles compared to that observed in mutants.
Co-expression of saxA.Scer\UAS.cBa and tkvQ199D.Scer\UAS.T:Ivir\HA1 in motor neurons under the control of Scer\GAL4BG380 produces increased mean evoked excitatory junctional potentials (EJPs) and quantal content compared to controls. The size of miniature excitatory junctional potentials (mEJPs) does not differ from controls.
trioS137203/trio6A suppresses the increase in evoked excitatory junctional potential (EJPs) and quantal content seen when saxA.Scer\UAS.cBa and tkvQ199D.Scer\UAS.T:Ivir\HA1 are expressed in motor neurons under the control of Scer\GAL4BG380.
The wing patterning phenotypes resulting from the expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 with Scer\GAL4ptc-559.1 are enhanced by the co-expression of kek5Scer\UAS.T:Avic\GFP, and there is an additional decrease in wing size.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4BG380 significantly suppresses the reduction in the number of boutons per muscle surface area which is seen at the neuromuscular junction in nmounspecified third instar larvae.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4elav.PH in ewg2 motorneurons (these motorneurons have been obtained by using FLP/FRT mediated recombination to inactivate the ewgelav.PH rescuing transgene and simultaneously activate the Scer\GAL4elav.PH driver in a ewg2 background) results in intermediate numbers of boutons at the larval neuromuscular junction compared to wild-type and ewg2 motorneurons.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4elav.PU enhances the increase in the average number of satellite boutons at the neuromuscular junction that is seen in nwk2 larvae.
Co-expression of nwkScer\UAS.cCa suppresses the increase in the total number of boutons and in the number of satellite boutons at the neuromuscular junction that is seen in larvae expressing two copies of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4elav-C155.
Expression of one copy of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4elav-C155 in a Dap160Δ1/+ background results in an increase in both the total number of boutons and the number of satellite boutons at the larval neuromuscular junction compared to wild type.
Co-expression of Dap160Scer\UAS.cKa suppresses the increase in the total number of boutons and in the number of satellite boutons at the neuromuscular junction that is seen in larvae expressing two copies of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4elav-C155.
The wing phenotypes caused by expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4A9 are suppressed by co-expression of SnooScer\UAS.cTa; the wing in the co-expressing flies appears similar to the phenotype seen in flies expressing SnooScer\UAS.cTa alone under the control of Scer\GAL4A9.
Expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4elav.PLu in a hiwEMS background results in a 30% increase in the number of boutons per muscle surface area at the neuromuscular junction compared to hiwEMS single mutants.
The dorsal open phenotype seen in homozygous Cka05836 embryos derived from females carrying homozygous Cka05836 germ-line clones is substantially rescued by expression of tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.PB using heat shock.
Scer\GAL4pnr-MD237-mediated expression in Jra76-19 embryos rescues the dorsal open phenotype.
Similar dominant wing phenotypes are observed in flies expressing dppScer\UAS.cHa and tkvQ199D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4unspecified that are not observed in flies expressing tkvScer\UAS.cHa under the control of Scer\GAL4unspecified.
The reduced number of boutons on neuromuscular junctions as well as crawling defects observed in third instar larvae expressing Hsap\TARDBPScer\UAS.cHa under the Scer\GAL4VGlut.PD driver cannot be restored by either by simultaneous co-expression of Snx163A.Scer\UAS.T:Avic\GFP and tkvQ199D.Scer\UAS.T:Ivir\HA1. Co-expressing Rab5S43N.Scer\UAS also fails to restore the neuromuscular junction growth defects.
Constitutively active.