|Feature type||allele||Associated gene||Dmel\tkv|
|Also Known As||tkvstrII, tkvstr-II, tkv-, tkvIIB, tkvIIB09|
|Map ( GBrowse )|
|Allele class||loss of function allele, amorphic allele - genetic evidence|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: C144@. The predicted product terminates immediately N-terminal to the conserved cysteine cluster in the extracellular domain.
|Phenotype Manifest In|
adult head & cuticle | somatic clone
visceral mesoderm & parasegment 7
Clones of tkv-mutant cells cause premature differentiation of the adult midgut precursor cells into large, polyploid, enterocyte-like cells compared with wild-type cells.
Clones of tkv homozygous cells in the pupal retina have defects in the apical profiles and packing of secondary pigment cells relative to tertiary pigment cells. Single, isolated tkv homozygous secondary pigment cells in the pupal retina have a restricted apical profile compared to neighbouring wild-type inter-ommatidial cells which expand apically to fill the unoccuppied space.
tkv8 mutant embryos show a delay in dorsal closure and rapture of the dorsal epidermis-peripheral amnioserosa interface, along with discontinuation of F-actin accumulation in the leading edge. The mutants also exhibit rupture of the amino serosa-dorsal epidermis interface. In tkv8 mutants the F-actin cable is absent in the peripheral amnioserosa, suggesting that specification is incomplete. Time-lapse recording reveals that the progression and removal of the peripheral amnioserosa is delayed.
Somatic clones of tkv homozygous cells in the late third instar eye disc are much smaller than wild-type twin spots. However, many of the cells in these clones go on to express neuronal differentiation markers. Mutant cells enter the S phase in the second mitotic wave, but the G2/M transition of this mitosis is disrupted.
When neutral marked clones are induced in the ovary, the proportion of germaria carrying marked somatic stem cells 3 weeks after clone induction is around 70% of that seen one week after clone induction. For tkv8 homozygous clones, the equivalent figure is around 25%. However, the number of resulting clones in the ovarian follicle cells is only slightly reduced compared to controls and these clones have no fewer cells than their twin-spots.
Clones of male tkv8 homozygous germline stem cells are still present in only 1.3X% of testes one week after clone induction and none are present two weeks after clone induction. This is in contrast to wild-type control clones, which are present in 82% of testes one week after clone induction and 64% two weeks after clone induction.
tkv1/tkv8 animals show a significant reduction in neuromuscular junction (NMJ) size compared to wild type; the number of synaptic boutons/muscle surface area at muscle 6/7 is 71.6 +/- 1.9% of wild type. The evoked excitatory junctional potential (EJP) (measured at muscle 6 of segment A3) shows a decrease in amplitude in tkv1/tkv8 animals compared to wild type. Quantal content is reduced compared to wild type.
R8 photoreceptor differentiation is normal in somatic clones of tkv8 mutant cells.
Only 2.5% of ovarioles carry mutant tkv8 germline stem cell (GSC) clones, compared to 11.2% of ovarioles carrying wild-type GSC clones, and many tkv8 GSCs are lost before adulthood.
Homozygous clones in the adult abdomen do not show any effect on polarity.
Mutant embryos have a "dorsal open" cuticle phenotype.
Wing discs are lost completely and the number of proximal leg disc cells is reduced in mutant embryos. The leg phenotype is sometimes variable.
The dorsal branches of the tracheal system do not develop in homozygous embryos, and the more ventral branches are absent or severely affected. Some tracheal cells invaginate in stage 12 embryos but others remain in an intermediate position between the epidermis and the branches that are formed.
Homozygous embryos show a dorsal-open phenotype, with severe head defects and large holes in the dorsal cuticle.
Clonal analysis in the germarium reveals that mutant stem cells are lost more rapidly than wild type, though there is no effect on the formation of 16 cell cysts or their subsequent development. Stem cell half life is 0.69 weeks (wild type being 4.6 weeks). Stem cell division rate relative to control is 0.29.
tkv1/tkv8 flies have variable thickening of the wing veins, particularly in regions close to the cross veins and at the distal ends of all longitudinal veins.
Tracheal tree defects consisting mainly of a failure to develop some particular branches in the dorsoventral axis. Other tracheal branches form in the anteroposterior axis, though they display an occasional gap.
Embryos exhibit a partial dorsal closure phenotype, leading edge cells are extremely elongated but adjacent more ventral epithelial cells fail to stretch. Most dorsal cuticle is turned inwards and the mouth hooks are retained inside the embryo.
Dorsal branches of the tracheal system are lacking and ganglion branches and the lateral trunk are severely affected.
Mutant embryos show absence of the dorsal branch and lateral trunks. The visceral branch forms normally.
Small homozygous clones are observed in the adult eye; photoreceptor differentiation occurs relatively normally, 25% ommatidia are missing one or more photoreceptor cell and the normal precise hexagonal array of the ommatidia is disrupted in the clone and surrounding wild type tissue. Eye is significantly reduced in size or completely missing and the surrounding head cuticle is missing (loss of head cuticle is not caused by put clones).
Dorsal clones induced in second instar larvae in the tarsus convert dorsal cells to ventral or ventrolateral cell fates. Clones often produce outgrowths that include normal neighbours, some of which have been respecified to ventral fates. Ventral clones induced in second instar larvae in the tarsus produce excessive ventral-most structures (peg-like bristles). Tarsal clones cause polarity disruptions in neighbouring normal cells.
Thickened vein mutant.
Embryos show a dorsal hole. Parts of the dorsal hypoderm in the trunk region are missing. Cephalopharyngeal skeleton is severely disrupted or absent and its remains are forced out of the body cavity. Embryos fail to form the second midgut constriction, and later the gastric caeca are missing. Visceral mesoderm of parasegment 7 is absent. Tracheal system shows a complete absence of dorsally directed trachea, ganglionic branches and lateral trunk. The remaining tracheal lumen is only established in a rudimentary fashion.
Homozygotes display dorsally open cuticle, severe defective head and contracted epidermis giving the cuticle a rounded appearance. Lethal when heterozygous with tkv6. Female transheterozygotes with tkv1 are viable and display a wing phenotype, wing veins are very thick and short along the proximal distal axis, transheterozygotes with Df(2L)tkv3 display extremely thickened wing veins. Adult Df(2L)tkv3/tkv8 females are very weak, possess atrophic ovaries and do not lay eggs in the few days they survive beyond eclosion.
Nondefective in gonad assembly.
|NOT Enhanced by|
|Phenotype Manifest In|
tkv8/tkv[+] is an enhancer of inter-ommatidial precursor cell | supernumerary | pupal stage phenotype of Scer\GAL4GMR.PF, pyd3.dsRNA.Scer\UAS
One copy of tkv strongly enhances the increase in inter-ommatidial precursor cell number seen when pyd[3.dsRNA.Scer\UAS] is expressed under the control of Scer\GAL4[GMR.PF].
tkv/+ almost completely suppresses the abberant arrangement of inter-ommatidial cells seen in the pupal and adult retinas of In(1)rst/Y animals. The retinas of tkv/+ or shg[R69]/+ animals at 42 hours APF have only very occasional inter-ommatidial patterning defects (the occasional extra or misplaced cell). This phenotype is dramatically enhanced in tkv/shg[R69] transheterozygotes.
Marker analysis shows that some photoreceptor differentiation begins in some fraction of the cells in smo tkv double homozygous cones in the late third instar eye disc.
In smo, tkv double mutant eye disc clones, BrdU incorporation, a marker of S phase, is abolished in the second mitotic wave.
The number of synaptic boutons/muscle surface area at muscle 6/7 in tkv8/witHA3 double heterozygotes is 88.8 +/- 2.4 % of wild type.
R8 photoreceptor differentiation fails in tkv8; smo3 double mutant clones, whereas it is only delayed in smo3 single mutant clones.
Ommatidial clusters situated posterior to smo3; tkv8 double mutant clones differentiate properly, but over-rotate at a much higher frequency than those situated in other regions of the same eye disc, with many of them reaching 110o-120o.
The tkv8 "dorsal open" cuticle phenotype is rescued in brkXH ; tkv8 double mutant embryos. These double mutant larvae differentiate a contiguous dorsal epidermis, but the Filzkorper are reduced and are more ventralised than brkXH single mutant embryos.
The disc phenotype of tkv8 Egfrf6 and tkv8 ; rho6 double mutant embryos is a simple addition of each single mutant phenotype, in which wing discs are lost completely and leg discs are severely reduced.
When wgScer\UAS.cLa is expressed under the control of Scer\GAL4btl.PS in a tkv8 background a huge dorsal trunk is formed and no other tracheal branches are usually formed. The formation of all tracheal branches except the transverse connective and visceral branch is impaired in arm2 ; tkv8 double mutants.
At 25oC, Chc1/+, tkv8/+ double heterozygotes show thickened veins and wing reduction phenotypes. At 29oC only wing remnants develop.
The dpp shortvein phenotype is strongly enhanced, and the tkv phenotype is suppressed, in dpps4 tkv1/dpps8 tkv8 double mutant flies. rhove-1 suppresses the differentiation of thicker veins seen in tkv1/tkv8 flies. The differentiation of thicker veins seen in rhohs.PSt flies is strongly increased in combination with tkv1/tkv8. The ectopic vein phenotype of Ras64BAct5C.PC flies is increased in combination with tkv1/tkv8. tkv1/tkv8 NAx-1 double mutant flies show pronounced wing vein loss. The thickening of veins seen in tkv1/tkv8 flies is strongly enhanced in combination with Nnd-3 and is suppressed in combination with NAx-1.
|Complementation & Rescue Data|
Allelism with tkv indicated by location, failure to complement lethal and viable tkv alleles and thick vein and abnormal thorax phenotype over Tp(2;3)tkv (Szidonya and Reuter, 1988).
|Stocks ( 1 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 11 )|
|Secondary FlyBase IDs|
|References ( 62 )|
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|Recent research papers (0)|
|All research papers listed in FlyBase were published before 2011|