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General Information
Symbol
Dmel\chic221
Species
D. melanogaster
Name
FlyBase ID
FBal0034343
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
chickadee221
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Linked to:
SalI-EcoRI restriction fragment
Comment:

The rough boundaries of the P excision mutation were mapped to a restriction fragment. The deletion takes out 5' noncoding and some coding sequence of chic. The position of the restriction fragment on the reference sequence was inferred by a FlyBase curator

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Deletion of 5' non-coding and some of coding region of chic.

Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

actin filament & eye disc | somatic clone

photoreceptor cell & eye disc | somatic clone

Detailed Description
Statement
Reference

Germline stem cell number is significantly reduced in chic221/chic01320 larval testes compared to controls. In contrast to wild type testes, elongated spermatid bundles are located close to the apical tip in newly eclosed flies. Spermatogonia and spermatocytes are rare or not detected.

chic221 mutant germline stem cell (GSC) clones are seen next to the hub in the testes at 3 days post clone induction, but this number decreases over time; in contrast to wild type clones, by 11 days post clone induction no chic221 mutant GSCs are seen. chic221 mutant GSCs are able to differentiate and progress to spermatocytes, but chic221 mutant spermatid clones are observed, suggesting that the clones are unable to complete terminal differentiation.

Mean filopodium length is reduced compared to wild type in cultured primary neurons derived from chic221/chic05205a embryos.

Cultured primary neurons derived from chic221/Df(2L)GpdhA embryos show a significant increase in the number of filopodia compared to control neurons. The mean length of the filopodia is reduced in the mutant neurons compared to controls.

chic221/Df(2L)GpdhA embryos show stalling of motor axons compared to wild type.

chic221 homozygous stage 16 embryos show laterality defects in the proventriculus and anterior midgut. The laterality of the other parts of the embryonic gut, including the hindgut and the posterior part of the midgut is normal in these mutants. The proventriculus and the anterior midgut do not rotate (as in wild-type) in these mutants at stages 15 to 17.

At a stage when the first cells have just invaginated from the salivary gland placode, cell shapes within mutant placodes often appear irregular compared to wild type. At later stages, the salivary glands invaginate but are irregular in shape, and the placodal and surrounding epidermal cells on the surface of the embryos appear disrupted.

Homozygous chic221 mutants exhibit CNS defects in less than 10% of embryos.

Stage 9 chic01320/chic221 oocytes show premature cytoplasmic streaming.

Single cell class IV dendrite arborisation (da) neuron clones that are homozygous for chic221 do not show defects in the establishment or maintenance of dendritic tiling.

chic221 embryos show normal salivary glands.

16% of chic01320/chic221 egg chambers have border follicle cell migration defects.

chic221 homozygotes have thin cuticles, and approximately 30% of cuticle preps have dorsal holes, indicating varying degrees of dorsal closure defects. At stage 14-15 these embryos show incomplete cell stretching and misalignment of the two lateral epidermal cell sheets during dorsal closure. The prominent actin cable seen in leading edge cells at this stage in wild-type embryos is much reduced in chic221 homozygotes.

Mutant embryos show defects in motor axon extension, including the ISNb and ISN branches.

Homozygous embryos have slightly disorganised longitudinal connectives, although some have small gaps in the longitudinal connectives.

Mutant embryos have significant defects in muscle formation.

Homozygous clones in the eye disc cause a reduction in actin polymerisation. Homozygous clones that overlap the morphogenetic furrow disrupt the timing of photoreceptor differentiation. Large clones in the eye disc show a disorganisation and reduction of photoreceptor differentiation. Mutant cells in the region of the morphogenetic furrow do not undergo the normal shape changes and instead retain large apical profiles. Apical constriction of cells at the lateral edges of mutant clones in the eye disc is seen.

Heterozygous flies have no structural brain abnormalities.

Lethal in combination with chicsand-1 or chicsand-2. chic05205a/chic221 embryos show mild defects in the Fas2-positive longitudinal fascicles of the central nervous system.

Microtubules are bundled to the cortex of stage 8 egg chambers. Premature cytoplasmic streaming occurs in stage 8 egg chambers. Microtubule phenotype more closely resembles that of capu mutants than does that of the weaker chic01320 allele.

Semilethal in combination with chicgdh-5. 71% escapers have ectopic wing crossveins, held up wings and are male sterile.

The egg chambers of chic01320/chic221 and chic01320/Df(2L)GpdhA females usually have too few nurse cells that are mostly binucleate. The variation in nurse cell number is great, with some chambers having as many as 30. 10% of egg chambers show a failure of border cell migration.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

chic[+]/chic221 is a suppressor | partially of visible phenotype of twf110

chic[+]/chic221 is a suppressor of abnormal neuroanatomy phenotype of Fmr1Δ113M

chic[+]/chic221 is a suppressor of visible | heat sensitive phenotype of peb1

Other
Phenotype Manifest In
Enhanced by
NOT suppressed by
Enhancer of
Statement
Reference

chic[+]/chic221 is an enhancer of neuropil phenotype of DAAMEx68

chic[+]/chic221 is an enhancer of fascicle phenotype of DAAMEx68

chic[+]/chic221 is an enhancer of connective phenotype of DAAMEx68

chic[+]/chic221 is an enhancer of lateral longitudinal fascicle phenotype of DAAMEx68

chic[+]/chic221 is an enhancer of embryo phenotype of DAAMEx68

chic[+]/chic221 is an enhancer of ellipsoid body phenotype of cibP

NOT Enhancer of
Suppressor of
Statement
Reference

chic221 is a suppressor of ventral adult lateral neuron & axon phenotype of Hsap\APPUAS.Tag:MYC, Scer\GAL4P2.4.Pdf

chic[+]/chic221 is a suppressor of LNv neuron phenotype of Fmr1Δ113M

chic[+]/chic221 is a suppressor of eye | heat sensitive phenotype of peb1

chic[+]/chic221 is a suppressor | partially of macrochaeta phenotype of cpbF19/cpb6.15

chic[+]/chic221 is a suppressor | partially of trichogen cell & actin filament & pupa phenotype of cpbF19/cpb6.15

Other
Additional Comments
Genetic Interactions
Statement
Reference

A chic221 heterozygous mutant background modifies the actin remodelling and subsequent basolateral invasion of epithelial cells seen in flies expressing CskGD9345 in a stripe of cells at the anterior/posterior boundary of the larval wing disc under the control of Scer\GAL4ptc-559.1.

Expression of Apc2Scer\UAS.T:Avic\GFP in germ cells under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 does not suppress the germline stem cell (GSC) loss seen in chic221/chic01320 mutant testes.

Expression of shgScer\UAS.T:Avic\GFP-rs in germ cells under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 does not suppress the germline stem cell (GSC) loss seen in chic221/chic01320 mutant testes.

Unlike wild-type embryos or Df(3R)X3F heterozygotes, heterozygous chic221 embryos in a Df(3R)X3F/+ genetic background display multi-nucleation during cellularization even at 18[o]C.

Cultured primary neurons derived from Sop21/+ chic221/+ and DAAMEx68/+ chic221/+ double heterozygous embryos have a normal number of filopodia.

Cultured primary neurons derived from chic221/+ ena23/+ double heterozygous embryos show a significant reduction in the number of filopodia compared to control neurons.

A chic221 heterozygous background enhances the loss of rotation in the proventriculus and anterior midgut seen in zip3 homozygotes.

chic221/+ partially rescues the bristle phenotype of twf110 homozygous animals.

A chic221 heterozygous background partially suppresses the rough eye phenotype seen in Fmr1sev.PW mutants.

A chic221 heterozygous background enhances the patterning defects found in Scer\GAL4GMR.PF>cindrdsRNA.PC.PD.Scer\UAS mutants. The mean interommatidial precursor cell number and the number of cone and/or 1[o] cell errors is increased in these double mutants.

The Scer\GAL4elav-C155/DAAMC.Scer\UAS.P\T gain-of-function phenotype (i.e the appearance of thicker commissures and nerve roots) is not affected by a chic221/+ background.

A chic221 heterozygous background increases the proportion of DAAMEx68 mutant embryos that exhibit CNS defects.

Expression of capuΔN.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 does not suppress the premature cytoplasmic streaming seen in stage 9 chic01320/chic221 oocytes.

The Btk29Ak00206 salivary gland phenotype is enhanced in chic221, Btk29Ak00206 double mutants as more cells remain on the surface at stage 14 compared with Btk29Ak00206 single mutants. The amount of actin disorganization that precedes the salivary gland phenotype is also increased in these double mutants. Additionally, chic221, Btk29Ak00206 double mutants exhibit a higher level of uncoordinated endoreplication at early stage 12, prior to the invagination defects, than Btk29Ak00206 single mutants.

The increased LNv dorso-ventral and medio-lateral extension phenotype is suppressed in Fmr1Δ113M brains that also carry a chic221/+ mutation.

77% of chic01320/chic221 ; th5/+ egg chambers have border follicle cell migration defects. 48% of chic01320/chic221 ; th21-2s/+ egg chambers have border follicle cell migration defects.

The abnormal midline crossing of axons seen in robo1 heterozygotes is suppressed if the embryos are also heterozygous for chic221.

Clones in the eye disc which are doubly mutant for captE636 and chic221 show predominantly the chic221 mutant phenotype.

cibP/+ ; chic221/+ double heterozygotes show a cib-like mutant phenotype, with a partially split fan-shaped body (it is split along the midline in 10% of flies), a ventrally opened ellipsoid body and a normal mushroom body. This interaction is synergistic. Addition of chic221 to cibP/Y flies exacerbates the cibP phenotype; cibP/Y ; chic221/+ males have a fan-shaped body that is split in the middle, a strongly disturbed ellipsoid body (it is flat and very often split along the midline) and disorganised mushroom body medial lobes that rarely reach their normal position. cibP/Y ; chic221/+ males are also sterile and show a thoracic bristle defect with shorter and forked ends than normal.

The severity of the central nervous system defects of chic05205a/chic221 embryos is enhanced by Abl2/+ and further enhanced by Abl2/Abl4.

Xenogenetic Interactions
Statement
Reference

Heterozygosity for chic211 suppresses the Scer\GAL4P2.4.Pdf>Hsap\APPScer\UAS.T:Hsap\MYC-induced increase in axonal arborization.

The frequency of motor neuron axon stalls seen in chic221 embryos is increased by Khc::Ggal\MLCKKA.ftz.

One copy of chic221 suppresses the frequency of midline crossovers seen in Khc::Ggal\MLCKKA.ftz embryos. However, Khc::Ggal\MLCKKA.ftz chic221 double mutant embryos show major defects in the formation of the central nervous system axon scaffold, with gaps or thinning of the longitudinal connectives, as axon bundles appear to preferentially cross the midline.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (41)