A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\stanE59

General Information
SymbolDmel\stanE59SpeciesD. melanogaster
NameFlyBase IDFBal0101421
Feature typealleleAssociated geneDmel\stan
Also Known AsfmiE59
Map ( GBrowse ) GBrowse View Helpdetailed view FBal0177634 FBal0137082 FBal0101421 FBal0101422 FBal0102372
Allele classloss of function allele
Mutagenethyl methanesulfonate
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Description
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FB2013_03
FB2013_02
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hide Nature of the Allele
Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
References
point mutation
comment=Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
evidence=experimental
na_change=C6599613T
pr_change=Q1837@|stan-PA
reported_pr_change=Q1838@
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Amino acid replacement: Q1838@. Has a nonsense mutation in the ectodomain.
Cytology
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2nd posterior cell & wing hair
axon & photoreceptor cell R8 | somatic clone
microchaeta & scutum
photoreceptor cell & axon
photoreceptor cell R8 & axon
photoreceptor cell R8 & axon & growth cone
trichome & abdominal tergite (with stan3)
trichome & pleural membrane | somatic clone
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Statement
Reference
Axons of homozygous single cell R8 photoreceptor clones show targeting defects and stop abnormally at the M1 layer in the adult medulla.
stan[E86]/stan[E59] transheterozygotes survive until wandering third larval instar stages and even up to the adult stage. The branches of the ddaC class IV neurons show a four-fold increase in the crossing index within the dorsal region of the arbor in stan[E86]/stan[E59] third instar larvae compared to wild type, although the cumulative branch length of the dendrites is unchanged in the mutant larvae. The class IV neurons also show occasional axon misrouting and stalling of growth cones.
stan[192]/stan[E59] stage 16 embryos have longer dorsal trunks than normal.
Of the mutant larvae of the genotype stan[E59]/Df(2R)stan2, roughly 7.6% of the 1st instar larvae live to the third instar stage but die either at this stage or during pupation. Mutant larvae surviving to 3rd instar are smaller compared to similar aged controls. These animals do not grow into mature 3rd instar larvae for another 4-7 days and become slightly larger than wildtype wandering 3rd instar. Compared to wildtype, these mutant larvae are sluggish in locomotion either spontaneously or in response to a gentle poke. Their average speed is 0.14mm/s compared to 0.79mm/sec for controls. Approximately 27% of muscle 12 in stan[E59]/Df(2R)stan2, and 21% of stan[E59]/stan[72] larvae have ectopic type 1 synapses, compared to 1.5% in controls. Approximately 12.1% of stan[E59]/Df(2R)stan2 and 14.8% of stan[E59]/stan[72] larval muscle 13 have ectopic type 1 synapses. 73.3% of stan[E59]/Df(2R)stan2, and 70.5% of stan[E59]/stan[72] muscle 4 are ectopically innervated by type II motorneurons, compared to 15.4% of controls. Larval synapses of stan[E59]/Df(2R)stan2 and stan[E59]/stan[72] found on muscle 2, and to a lesser extent on muscle 3, exhibit abnormal, but functionally active synaptic bouton-like varicosities located along the intersegmental nerve tract. These varicosities are typically larger than wildtype synapses, and are found randomly at a low rate (3-5 per larvae) throughout all checked segments. 6.58% of segmental nerves from 3rd instar stan[E59]/Df(2R)stan2, and 6.75% of segmental nerves from 3rd instar stan[E59]/stan[72], show these axonal varicosities. 15.5% of muscle 12, 8.7% of muscle 13, and 7% of muscles 6/7 of 3rd instar stan[E59]/Df(2R)stan2 have completely lost their neuromuscular junctions. 8.6% of muscle 12, 4.7% of muscle 13, and 2% of muscles 6/7 of 3rd instar stan[E59]/stan[72] do not have any synaptic innervation. In stan[E59]/Df(2R)stan2 second instar larvae, 4.5% of muscle 12s observed show loss of synapses. Mutants display variable excitatory junction potential (EJP) defects, with some 3rd instar muscles showing a dramatic reduction in EJP and others showing no synaptic potentials when evoked by stimulation of the segmental nerve. Electron micrographs from segmental nerves of stan[E59]/Df(2R)stan2 show a reduced average diameter and cross-sectional area compared to controls. Gaps and signs of microtubule loss and axonal membrane breakup are seen in the mutants. Fewer axons are present in mutants (30.6) compared to controls (81.7). The peripheral glial sheath surrounding the segmental nerve is thicker in the mutant larvae compared to controls, and the average area of glial processes is significantly reduced. The ratio of glial area to nerve area was reduced from 0.49 in controls to 0.33 in stan[E59]/Df(2R)stan2. The average area of the segmental nerve of stan[E59]/Df(2R)stan2 animals, in which stan[Scer\UAS.cUa] is driven by Scer\GAL4[elav-C155], is significantly larger than in wildtype controls or in the stan[E59]/Df(2R)stan2 mutants. A small number of axons (2-3 per segmental nerve) axons have large vacuoles. The rescued segmental nerves contain more axons (113) than the mutants or the wildtype controls, and show a rescue of the thickness of the peripheral glial sheath surrounding the segmental nerve compared to mutants. The average number of sensory cells (multidendritic neurons and external sensory cells) in the dorsal cluster is 10.97 in stan[E59]/Df(2R)stan2, compared to 9.89 in controls, which, although small, is statistically significant.
Clones of stanE59 in the lamina target neurons result in R8 axon guidance defects.
stan3/stanE59 flies have almost normal hair polarities in the tergite, apart from near the front and near the rear of the anterior compartment.
The hexagonal packing of intervein cells, which usually occurs between wing development stage P2B (when the first morphological signs of veins appear (FBrf0005070), and the middle of P2C (before hair formation (FBrf0005070)) is disrupted in stanE59/stanE59 flies. This phenotype is also seen in somatic clones of stanE59/stanE59 cells in the developing intervein, but this effect is cell-autonomous.
Large somatic clones of stanE59 homozygous cells in the wing have largely normal planar polarity. However, when these clones fall in the ventral pleura of the abdomen they have a disheveled planar polarity phenotype. These clones show occasional local non-autonomy, disturbing the polarity of hairs here and there in front of the clone.
Mutant mushroom body neuroblast clones have a significant reduction in cell number compared to control clones and overextend processes from the mushroom body calyx. Overextended processes from the calyx are also seen in the adult.
When stanE59 clones are made in the developing eye, R axons terminate in a highly disorganised pattern, when compared to wild-type, particularly within the medulla. R1-R6 axons correctly target the lamina, and R7 axons generally appear to select their correct target although their termini are slightly disorganised. When single cell clones are made in R7 axons, they always target normally. However R8 axons are highly disorganised and although they initially reach their correct target layer in the medulla it appears they later retract to more superficial layers. The R8 growth cones are irregularly spaced and have a 'club-like' morphology, but they have many elaborate fine processes. the processes of individual R8 growth cones often overlap intensively. Despite this irregular spacing, the entire target field appears to be filled and there does not appear to be any dramatic misrouting of axons within the optic lobe. The ommatidial fascicles within the optic stalk are basically wild-type though there is a 5% increase in the number of fascicles comprising more than 8 R axons.
Mutants show no significant disruption of ovarian morphology.
Somatic clones of stanE59 in the eye display defects in ommatidial chirality (random chirality and symmetrical clusters) and rotation. In these clones, apical-basal polarity, cell subtype specification and cell survival all appear to be normal, but approximately 20% of ommatidia have reduced numbers of photoreceptors. In mosaic ommatidia, chirality of the whole ommatidium is dependent on the genotype of R3 and R4 photoreceptors: If R3 and R4 are wild-type then ommatidial chirality is normal. If either or both fall within a stanE59 somatic clone then the ommatidium has random chirality or stays symmetrical.
Most single-cell clone stanE59 da neurons terminate their dendritic fields at normal locations at the lateral margin and segment border (where they meet or approach the like dendrites of adjacent neurons). However, in a few cases, the mutant neurons have sparsely branched processes which extend beyond these territories.
36.8% of ommatidia in stanE45/stanE59 mutant somatic clones in the eye are normal. 20.2% have rotated ommatidia, 26.1% have chirality defects, 15.9% are achiral (1% unscorable).
Single homozygous dorsal cluster multiple dendritic (MD) neurons (in an otherwise wild-type background) overextend one or more dendritic processes towards the dorsal midline in about 15% of cases. The basic architecture of the dendritic branching pattern is not altered. 10% of single mutant MD neurons (in an otherwise wild-type background) do not extend their axons fully to the central nervous system. Multiple dendritic (MD) neuron dorsal dendritic processes have already extended in 74% of hemisegments in homozygous embryos 11-12 hours after egg laying (in contrast to wild-type embryos where the dorsal dendrites of the MD neurons have not yet extended at this stage). Axonal break points are seen in the axon bundles of dorsal cluster MD neurons. The axons of the PNS neurons fail to fasciculate as tightly as in wild type.
Homozygous mutant somatic clones in the eye, lead to dramatic polarity defects. These include aberrant rotation and a lack of distinct R3/R4 fates.
When trans-heterozygous with stan72, exhibits excessive dorsal branch outgrowth and misrouting in the dorsal cluster of embryonic dendrites.
The bristles on the notum of stanE59/stan71 flies show disorganised polarity and point towards different directions. Over 50% of the posterior, left lateral and right lateral bristles showed polarity defects, whereas only about 10% of the anterior and dorsocentral bristles showed defects. Homozygous stanE59 clones on the notum show disrupted planar polarity of bristles in a cell autonomous fashion, with cells outside the clone only rarely being affected.
Mutants show local disconnection of longitudinal axon fascicles in the central nervous system. stanE45/stanE59 mutants partially rescued by stanScer\UAS.cUa driven by Scer\GAL41407 have planar polarity defects in ommatidia, sensory bristles and wing hairs. In region D (2nd posterior cell) of the wing, hairs are deflected from the proximo-distal axis and oriented towards the posterior wing margin. In somatic clones in the wing, polarity disruption of wing hairs is seen in a cell autonomous fashion. Prehairs emerge near the cell centre, or at the wrong locations along the cell periphery. Very occasionally, twin hairs were seen in wild-type cells bordering the clone.
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Statement
Reference
stan[+]/stanE59 is a non-enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053
stanE59 is a non-enhancer of cell polarity defective phenotype of pkpk.sev
hideSuppressor of
Statement
Reference
stan[+]/stanE59 is a suppressor of visible phenotype of Scer\GAL4hs.2sev, dgoScer\UAS.cFa
hideNOT Suppressor of
Statement
Reference
stan[+]/stanE59 is a non-suppressor of visible phenotype of Scer\GAL4en-e16E, kermitGS2053
stanE59 is a non-suppressor of cell polarity defective phenotype of pkpk.sev
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Reference
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Statement
Reference
pwnunspecified, stanE59 has trichome & adult abdomen | somatic clone | cell non-autonomous phenotype, suppressible | somatic clone by fzScer\UAS.cSa/Scer\GAL4αTub84B.PL
hideEnhancer of
Statement
Reference
stanE59 is an enhancer of ommatidium phenotype of S48-5
stanE59 is an enhancer of ommatidium phenotype of Vangsev.PR
hideNOT Enhancer of
Statement
Reference
stan[+]/stanE59 is a non-enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, nmoScer\UAS.cUa
stan[+]/stanE59 is a non-enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053
stanE59 is a non-enhancer of ommatidium phenotype of pkpk.sev
hideSuppressor of
Statement
Reference
stan[+]/stanE59 is a suppressor of wing hair phenotype of Scer\GAL4hs.2sev, dgoScer\UAS.cFa
stanE59/stan3 is a suppressor of trichome & adult abdomen phenotype of Scer\GAL4ptc-559.1, fzScer\UAS.cSa
stanE59/stanE59 is a suppressor of trichome & adult abdomen | somatic clone | cell non-autonomous phenotype of Scer\GAL4αTub84B.PL, VangScer\UAS.cWa
hideNOT Suppressor of
Statement
Reference
stan[+]/stanE59 is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, nmoScer\UAS.cUa
stan[+]/stanE59 is a non-suppressor of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053
stanE59 is a non-suppressor of ommatidium phenotype of pkpk.sev
hideOther
Statement
Reference
pwnunspecified, stanE59 has trichome & adult abdomen | somatic clone phenotype
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Statement
Reference
stan[E59]/+ significantly suppresses the wing defects induced by the overexpression of dgo[Scer\UAS.cFa] under the control of Scer\GAL4[hs.2sev].
stan[E59] shows increased crossing of dendrites in the dendritic arbor of the ddaC class IV neurons compared to wild type in double heterozygous combination with each of esn[KO6], Rho1[E3.10], trc[1], trc[2], fry[1], fry[02240], Vang[stbm-6] or Vang[A3] (none of the single heterozygotes show this phenotype).
The reversal of cell polarity that is seen in cells posterior to clones in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) where the clones are expressing dsecto.Scer\UAS under the control of Scer\GAL4αTub84B.PL is still seen if the clones are induced in a stan- background (the cells within the clone are stanE59/stanE59 while the cells surrounding the clone are stan3/stanE59). Clones of stanE59 fzunspecified double mutant cells in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) do not change the cell polarity of their wild-type neighbouring cells. Clones of cells in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) that are expressing fzScer\UAS.cUa under the control of Scer\GAL4αTub84B.PL in a stan- background (the cells within the clone are stanE59/stanE59 while the cells surrounding the clone are stan3/stanE59) do not change the cell polarity of the stan3/stanE59 cells surrounding the clone. Clones of cells in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) that are co-expressing stanScer\UAS.cUa and fzScer\UAS.cUa under the control of Scer\GAL4αTub84B.PL in a stan- background (the cells within the clone are stanE59/stanE59 while the cells surrounding the clone are stan3/stanE59) do not change the cell polarity of the stan3/stanE59 cells surrounding the clone. The reversal of cell polarity that is seen in cells anterior to clones in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) where the clones are expressing ftScer\UAS.cMa under the control of Scer\GAL4αTub84B.PL is still seen if the clones are induced in a stan- background (the cells within the clone are stanE59/stanE59 while the cells surrounding the clone are stan3/stanE59). Clones of cells in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) that are expressing fjScer\UAS.cZa under the control of Scer\GAL4αTub84B.PL in a stan- background (the cells within the clone are stanE59/stanE59 while the cells surrounding the clone are stan3/stanE59) result in a reversal of cell polarity in cells anterior to the clone (hairs in front of the clone point forwards), as occurs in clones induced in a wild-type background. The reversal of cell polarity that is seen in cells posterior to clones in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) where the clones are expressing dsecto.Scer\UAS under the control of Scer\GAL4αTub84B.PL is still seen if the clones are induced in a fzunspecified stan- background (cells within the clone are stanE59/stanE59 while the cells surrounding the clone are stan3/stanE59). The reversal of cell polarity that is seen in cells anterior to clones in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) where the clones are expressing ftScer\UAS.cMa under the control of Scer\GAL4αTub84B.PL is still seen if the clones are induced in a fzunspecified stan- background (cells within the clone are stanE59/stanE59 while the cells surrounding the clone are stan3/stanE59). Hair and bristle polarity is randomised throughout the tergite in dsunspecified stan3/stanE59 double mutant flies. The reversal of cell polarity phenotype that is seen in cells posterior to clones in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) where the clones are doubly mutant for ptc16 and Df(2R)enE is still seen if the clones are induced in a stan3/stanE59 background, as occurs in clones induced a wild-type background. The reversal of cell polarity phenotype that is seen in cells posterior to clones in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) where the clones are doubly mutant for ptc16 and Df(2R)enE is not seen if the clones are induced in a dsunspecified stan3/stanE59 double mutant background instead of a wild-type background. Clones of cells in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) where the clones are triply mutant for ptc16, Df(2R)enE and stanE59 and have been induced in a dsunspecified background do not result in a reversal of cell polarity in cells surrounding the clone.
A stanE59/+ background does not affect the Scer\GAL4hs.2sev>shgdCR3h.Scer\UAS.T:Avic\GFP-rs ommatidial phenotype.
In wings largely made up of pwnunspecified stanE59 homozygous somatic clones, the remaining heterozygous cells have normal polarity. pwnunspecified stanE59 homozygous somatic clones in the abdomen have a disheveled planar polarity phenotype. These clones occasionally cause non-autonomous effects on planar polarity just outside and usually anterior to the clone. This limited non-autonomous phenotype is suppressed if the clones are also fzScer\UAS.cSa; Scer\GAL4αTub84B.PL (produced by Scer\GAL80αTub84B.PL MARCM method). The non-autonomous effect on planar polarity of VangScer\UAS.cWa; Scer\GAL4αTub84B.PL somatic clones (produced by the Scer\GAL80 MARCM method) in the adult abdomen is suppressed by pwn/pwn stanE59/stanE59. Cells within the resulting clones have randomised planar polarity. The planar repolarisation seen in the adult abdomen of fzScer\UAS.cSa; Scer\GAL4ptc-559.1 adults is suppressed by stanE59/stan3.
S48-5/stanE59 mutants show 45.59%+-7.32 misrotated ommatidia compared to 9.55%+-1.43 seen in S48-5 mutants alone.
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Expression of either stan[Scer\UAS.cUa] or stan[ΔIntra.Scer\UAS] under the control of Scer\GAL4[GMR.PU] rescues the axon targeting defects of homozygous single cell stan[E59] R8 photoreceptor clones.
Expression of stan[Scer\UAS.TTV] or of stan[Scer\UAS.AEY] under the control of Scer\GAL4[477] rescues the increased crossing that is seen in the dorsal dendritic arbor of the ddaC class IV neurons in stan[E86]/stan[E59] third instar larvae. Expression of stan[ΔJM-A.Scer\UAS.TTV] under the control of Scer\GAL4[477] does not rescue the increased crossing that is seen in the dorsal dendritic arbor of the ddaC class IV neurons in stan[E86]/stan[E59] third instar larvae.
The lethality and axonal defects seen in stanE45/stanE59 can be rescued by stanScer\UAS.cUa driven by Scer\GAL41407. This combination does not affect the planar polarity phenotype.
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Bloomington
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hide Recent research papers ( 4 )
Weber et al., 2012, Genetics 191(1): 145--162
Novel regulators of planar cell polarity: a genetic analysis in Drosophila. [FBrf0218210]
Gontang et al., 2011, Development 138(22): 4899--4909
The cytoskeletal regulator Genghis khan is required for columnar target specificity in the Drosophila visual system. [FBrf0216508]
Hakeda-Suzuki et al., 2011, Nat. Neurosci. 14(3): 314--323
Golden Goal collaborates with Flamingo in conferring synaptic-layer specificity in the visual system. [FBrf0213128]
Matsubara et al., 2011, Genes Dev. 25(18): 1982--1996
The seven-pass transmembrane cadherin Flamingo controls dendritic self-avoidance via its binding to a LIM domain protein, Espinas, in Drosophila sensory neurons. [FBrf0215818]