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General Information
Symbol
Dmel\crb11A22
Species
D. melanogaster
Name
FlyBase ID
FBal0001817
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
crb2, crb11A, crumbs11A22
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Polytene chromosomes normal.
Nature of the lesion
Statement
Reference
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 ( 1 )
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
zonula adherens & photoreceptor | somatic clone
Detailed Description
Statement
Reference
crb11A22 mutant eyes show irregular shaped, and often broader, rhabdomeres that are in contact, displaying a 'fused rhabdomere' defect; a more severe eye phenotype is observed upon the Scer\GAL4GMR.PU-driven expression of either crbextraTM.UAS.GFP or crbintra.UAS.Tag:MYC,EGFP. One week of continuous light exposure (light stress) induces more severe photoreceptor cell defects in crb11A22 mutants, including occasional cell death, as compared to wild-type controls; these defects are more severe upon the Scer\GAL4GMR.PU-driven expression of crbextraTM.UAS.GFP, crbC749W.UAS, crbT1283M.UAS, crbN1486S.UAS or crbC1540Y.UAS.
Homozygous clones in the wing disc survive and do not show polarity defects.
A majority of embryos expressing crbY10A in a crbGX24w-/crb11A22 background exhibit lethality due to dorsal closure defects, ranging in severity from open cuticle, dorsal holes, closed cuticles but failure to hatch, or kinked larvae.
crb11A22 mutant two hour-old embryos show chromosome defects such as chromosome-free centrosomes, chromosomal bridges and abnormal microtubule pattern during mitosis.
Homozygous crb11A22 mutant rhabdomeres of photoreceptor cells are bulky, occasionally fused with each other, develop a shorter stalk membrane and fail to expand throughout the depth of the retina. crb11A22 mutant photoreceptor cells undergo light-dependent degeneration.
Terminal tracheal cells mutant for crb11A22 alone appear wild-type for branch number and lumen morphology.
Mutant embryos show defects in cell shape. Tracheal and dorsal cells appear rounded and with bulged and protruded apical domains. Adherens junctions, when present, occupy a more apical position than normal.
crb11A22 mutant ocelli display disorganization of the cornea and photoreceptor cells, rhabdomeres that have variable shapes and are scattered throughout the retina, severe disorganization of adherens junctions between the corneagenous cells and the photoreceptor cells and between adjacent photoreceptor cells, and a loss of cell polarity in photoreceptor cells. Ocellar photoreceptor cell stalk membranes are also indistinguishable in these mutants. Photoreceptor cells of crb11A22 mutant ocelli show signs of degeneration after light exposure, with evidence of apoptotic cells.
Homozygous clones in the adult eye show abnormal rhabdomere morphology and some photoreceptor cells are missing.
Stage 17 crb2 mutant embryos show defects in the transition from luminal liquid-clearance to air-filled airways. Tube size defects and defective airway protein clearance are also seen. No air-filling defects are observed in crb2 heterozygotes.
Adult animals with whole mutant heads for crb11A22 do not display any notable defects in either overall head capsule structure or gross eye morphology. However, sectioning mutant adult eyes reveal photoreceptor abnormalities as demonstrated by the disorganization of their apical domain and abnormal short stalk membrane. crb11A22 mutant heads are significantly bigger than wild-type heads. The crb11A22 phenotype is characterised by a size increase that is proportional across the head, in that the ration between major landmarks of the head remains the same in crb11A22 and wild-type heads. Comparison of the width of the head capsule, as measured by the distance between the two compound eyes, indicates that the crb11A22 mutant heads are approximately 1.3 times bigger than those of wild-type. This is also the case for eye size. Quantification of the eye surface area indicates that the crb11A22 mutant eyes are 1.3 times bigger than those of wild-type. Consistent with a global increase in head and eye size, the number of photoreceptor clusters present in the differentiating eye disc is greater in crb11A22 mutant discs than the wild-type discs. When this analysis is extended to counting the ommatidia specified in the pupal eye, it is found that crb11A22 retinas have, on average, approximately 170 more ommatidia than wild-type retinas. Expression of crbextraTM.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4ey.PH fully rescues the crb11A22 head overgrowth phenotype. Expression of crbextra.Scer\UAS under the control of Scer\GAL4ey.PH fails to rescue the crb11A22 head overgrowth phenotype. Expression of crbTM.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4ey.PH fails to rescue the crb11A22 head overgrowth phenotype. Surface area quantification of crb11A22 mutant clones in genetically mosaic eye discs reveals that the total area of crb11A22 mutant tissue is significantly larger than that of wild-type homozygous tissue. The number of facets per unit of surface area in crb11A22 and wild-type eyes is identical, suggesting that cell size is not affected by crb11A22. Consistent with this conclusion, no difference in apical cell perimeter between crb11A22 mutant and wild-type cells in third instar eye discs. The number of apoptotic events do not differ in crb11A22 mutant and wild-type clones. Analysis of patterning and final ommatidial cell number in pupal retinas reveal no difference between crb11A22 mutant and wild-type retinas. The anterior-most region of crb11A22 mutant eye discs display a higher number of mitotic cells than in the wild-type. Quantification of the number of mitotic events indicates that this increase is statistically significant. Clathrin-coated-like pits appear at high frequency at the stalk membrane of crb11A22 mutant adult photoreceptors, which are rarely detected in wild-type photoreceptors.
Homozygous clones in the wing disc do not have a growth advantage or disadvantage; the ratio of mutant clone area: area of the wild-type twin spot is approximately 1.
In contrast to wild type, crb11A22 eyes: do not have a regular trapezoid arrangement of rhabdomeres; rhabdomeres are bulkier and often contact each other; rhabdomeres do not reach the basal lamina but remain in the distal region of the retina; the stalk membrane is reduced in length by ~50%.
Photoreceptor cells of mutant flies kept in the dark for 13 days do not have a wild-type morphology. The mutants also show severe light-dependent retinal degeneration which can be prevented by raising the flies on a medium lacking vitamin A.
Homozygous clones that cover large areas of the wing can be recovered, indicating that loss of crb function does not compromise cell viability. Homozygous clones in the wing that abut the dorsoventral boundary produce a broadening of the wing margin in a cell-autonomous manner. Homozygous clones in the wing lose wing veins in a cell-autonomous manner.
crb2 mutant photoreceptor cells display shortened stalk membranes that are reduced to approximately 50% of their normal length.
The adherens junctions in stage 9 and 10 crb2 zygotic mutants fragment and become randomly positioned around the cell cortex and along the basolateral membrane as epidermal cells dissociate. The gut epithelium of crb2 mutants maintains basic epithelial structure at stage 10.
crb2/+ embryos show normal cardiac cell alignment.
Homozygous embryos show a disruption in ectodermal cell polarity from stage 8. Stage 13 homozygous embryos have a relatively normal central nervous system.
Adherens junctions are fragmented in stage 9 crb2 zygotic mutant embryos.
Most cuticle is absent in mutant embryos and the remaining cuticle forms many small granules. The zonula adherens never assembles from spot adherens junctions.
Clones in the eye show lack of rhabdomere elongation. The rhabdomeres remain at the top of the retina and appear thicker than wild-type rhabdomeres. Adherens junctions stretch further basolaterally than in wild type. Those at the distal portion of the retina are variable in size and those that are proximal are discontinuous and thin. The adherens junctions attaching the photoreceptors to the floor of the retina remain relatively intact.
When flies with eyes containing homozygous clones are kept in constant light conditions for 7 days, the retina shows massive degeneration. This phenotype is not seen under low light conditions, instead their rhabdomeres are thicker and shorter compared to wild-type and are often found in close contact with other rhabdomeres of the same ommatidium. The rhabdomeres fail to reach the basal lamina and extend from the distal pole near the lens to only about one third of the normal length. In addition, the stalk membrane is reduced in length, however the tightly stacked internal structure of the rhabdomere is unaffected. When grown in vitamin A-deficient conditions in continuous light, mutant photoreceptors cells show smaller. thinner rhabdomeres, other morphogenetic defects similar to mutant animals raised on standard medium in the dark. However only minor signs to photoreceptor degeneration is seen.
In mutant clones in the eye the ommatidia show minor irregularities in arrangement and interommatidial bristle number and position. Rhabdomere shape, zonula adherens integrity and stalk membrane formation are all affected. Rhabdomeres extend only 40-60% of their normal length and are confined to the distal part of the retina. Secondary and tertiary pigment cells die, though not until well after eclosion. Rhabdomeres are larger than normal and may touch each other. At 50% of pupal development zonula adherens are fragmented though by 70% pd they have mostly recovered. Defects in photoreceptor cells are more pronounced proximally than distally. Photoreceptor cell stalk membrane is 50% shorter than wild type. Even in crb2/+ photoreceptors there is a 10% reduction in stalk membrane length.
Homozygous follicle cell clones induced before formation of the follicular epithelium (FE) may lead to epithelial discontinuities or multilayering defects in posterior follicle cells. Small homozygous follicle clones, induced after the FE has formed, show no morphological defects.
arm4; crb2 double mutants exhibit a severe crb-like cuticle phenotype.
Epithelial cells of ectodermal origin lose their apicobasal polarity resulting in the loss of epithelial integrity and cell death. Both epidermal and amnioserosa cells of stage 10 lack zonula adherens junctions (ZA) and the number of spot adherens junctions (SAJ) is lower. The structure of all ectodermally derived epithelia is affected to varying extents.
First defects in zonula adherens formation are seen at the onset of germband extension on the dorsal side of the embryo in the developing amnioserosa. The distribution of adherens junction material at the apicolateral boundary is more irregular.
Ectopic acridine orange and nile blue staining in epidermis.
Strong crb phenotype. Embryos almost completely lack cuticle due to cell death in epidermal primordium. P{lacZ}6-81 enhancer detection line specifically expresses Ecol\lacZ in the tracheal system, and reveals that morphogenetic abnormalities in the developing tracheal system result in a only a few aggregates of tracheal cells. Morphogenetic abnormalities and cell death were detected in the presumptive foregut and hindgut by fkh protein staining. Salivary glands also undergo cell death.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
NOT suppressed by
Enhancer of
Statement
Reference
crb11A22 is an enhancer of visible phenotype of RetMEN2B.GMR
crb11A22/crb[+] is an enhancer of visible phenotype of CycEJP
crb11A22/crb[+] is an enhancer of lethal phenotype of kst1/kst2
crb11A22/crb[+] is an enhancer of lethal phenotype of kstB1-14.1/kst1
crb11A22/crb[+] is an enhancer of lethal phenotype of kstB1-14.1/kst2
NOT Enhancer of
Statement
Reference
crb11A22 is a non-enhancer of visible phenotype of RetMEN2A.GMR
Suppressor of
NOT Suppressor of
Statement
Reference
crb11A22 is a non-suppressor of visible phenotype of RetMEN2A.GMR
Other
Phenotype Manifest In
Enhanced by
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference
crb11A22/crb[+] is an enhancer of embryonic/larval cuticle phenotype of baz4
crb11A22 is an enhancer of eye phenotype of RetMEN2B.GMR
crb11A22/crb[+] is an enhancer of eye phenotype of CycEJP
crb11A22/crb[+] is an enhancer of rhabdomere | somatic clone phenotype of kst1/kst2
NOT Enhancer of
Statement
Reference
crb11A22 is a non-enhancer of eye phenotype of RetMEN2A.GMR
Suppressor of
Statement
Reference
crb11A22/crb[+] is a suppressor | partially of wing phenotype of Scer\GAL4bbg-C96, ebiHMS01390
crb11A22/crb[+] is a suppressor of rhabdomere of eye photoreceptor cell phenotype of eys[+]/eys1, prom1
crb11A22/crb[+] is a suppressor of eye phenotype of N264-39
crb11A22/crb[+] is a suppressor of eye phenotype of DlRevF10
crb11A22/crb[+] is a suppressor of eye phenotype of aph-1D35
crb11A22/crb[+] is a suppressor of eye phenotype of Serunspecified
NOT Suppressor of
Statement
Reference
crb11A22 is a non-suppressor of wing disc | somatic clone phenotype of wtsx1
crb11A22 is a non-suppressor of eye phenotype of RetMEN2A.GMR
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference
crb11A22/+ partially rescues the wing notch and reduced wing size seen in flies expressing ebiHMS01390 under the control of Scer\GAL4bbg-C96.
Expression of flwScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4332.3 does not lead to any obvious phenotype in embryos expressing crbY10F in a crbGX24w-/crb11A22 background. Expression of flwScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4332.3 largely suppresses the embryonic lethality and dorsal closure defects in embryos expressing crbY10A in a crbGX24w-/crb11A22 background, although some embryos exhibit irregular zippering at the posterior canthus and bunching of the epidermis. flw6/flw6 or flw6 hemizygosity enhances the embryonic lethality and dorsal closure defects seen in embryos expressing crbY10A in a crbGX24w-/crb11A22 background. Arp3EP3640/+, or expression of Rho1N19.Scer\UAS, RokCAT-KG.Scer\UAS or MoeK.T559D.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4332.3 partially suppresses the embryonic lethality and dorsal closure defects seen in embryos expressing crbY10A in a crbGX24w-/crb11A22 background. Arpc1Q25st/+, Rok2/Rok2 or Rok2 hemizygosity, or expression of Rac1N17.Scer\UAS or MoeScer\UAS.T:Hsap\MYC under the control of Scer\GAL4332.3, fails to suppress the embryonic lethality and dorsal closure defects seen in embryos expressing crbY10A in a crbGX24w-/crb11A22 background. Expression of PakAID.Scer\UAS.T:Zzzz\FLAG or shgScer\UAS.cSa under the control of Scer\GAL4332.3 partially suppresses the embryonic lethality and dorsal closure defects seen in embryos expressing crbY10A in a crbGX24w-/crb11A22 background, resulting in some adult survival. Expression of flwScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4332.3 does not lead to any obvious phenotype in embryos expressing crb+tfos in a crbGX24w-/crb11A22 background. SCARΔ37/+ or Arp3EP3640/+ does not lead to any dorsal closure defects in embryos expressing crb+tfos in a crbGX24w-/crb11A22 background. Expression of PakScer\UAS.T:Myr-Src64B under the control of Scer\GAL4332.3 in embryos expressing crb+tfos in a crbGX24w-/crb11A22 background leads to complete embryonic lethality with most embryos exhibiting dorsal closure defects ranging in severity from open cuticle and dorsal holes, to closed cuticles but failure to hatch.
Trans-heterozygous crb11A22/+ chp2 flies exhibit rhabdomeres with significantly smaller width than wild-type. The length of the rhabdomeres is not affected. The prom1 ommatidia phenotype is largely suppressed by crb11A22. Most of the rhabdomeres are individualised and a single, continuous inter-rhabdomeral space is formed. The eys1 ommatidial phenotype is partially suppressed by crb11A22. The number of rhabdomere clusters and individual rhabdomeres is increased, but no inter-rhabdomeral space is formed. The prom1/+, eys1/+ fusion phenotype is suppressed along the entire length of the rhabdomeres by heterozygous crb11A22.
Terminal tracheal cells that are homozygous mutant for both crb11A22 and Syx7brd1615 are almost completely rescued for cysts, although, defects in branch number are enhanced as compared to Syx7brd1615 alone.
Transheterozygous wusG0162 crb2 stage 17 embryos show defects in in the transition from luminal liquid-clearance to air-filled airways.
Expression of mamEPgJ3-285 under the control of Scer\GAL4ey.PH in crb11A22 mutant clones suppresses the over-proliferation seen in crb11A22 mutant clones. Heterozygous crb11A22 suppresses the aph-1D35/+ small eye phenotype. Heterozygous crb11A22 suppresses the Serunspecified/+ small eye phenotype. The suppression is achieved without altering the size of the facet lenses. Heterozygous crb11A22 suppresses the DlRevF10/+ small eye phenotype. The suppression is achieved without altering the size of the facet lenses. Heterozygous crb11A22 suppresses the N264-39/+ small eye phenotype. The suppression is achieved without altering the size of the facet lenses.
The cuticle phenotype of dead embryos derived from baz4/+ embryos derived from a cross of baz4/+ females to wild-type males is enhanced if the females also carry one copy of crb11A22.
The growth advantage of wtsx1 clones in the wing disc over their wild-type twin spots is not affected if the clones are also homozygous for crb2.
68.7% of salivary glands fail to invaginate, 25.6% partially invaginate and 5.7% completely invaginate in crb2 Df(3L)H99 double mutant embryos.
The loss of wing margin and wing vein thickening seen in Df(1)N-8/+ animals is suppressed by crb2/+.
yrt75, crb2 double mutant photoreceptor cells show shortened stalk membranes. There is no significant difference between stalk length in double mutants compared to crb2 single mutants. yrt75 suppresses the cuticle phenotype of crb2 maternal or zygotic mutant embryos. Defects in junctional integrity and cellular organization of the epidermis are strongly rescued in double mutants compared to crb2 mutant embryos.
96% of sli2/+, crb2/+ embryos show normal cardiac cell alignment.
gktG85/gktG85 ; crb2/+ embryos show a severe disruption in epithelial polarity at stage 11.
l(2)gl4 shows marked rescue of the crb2 phenotype, as the majority of the cuticle is restored in the double mutant embryos. Embryos lacking both crb and scrib maternal and zygotic function (derived from scrib673 crb2 homozygous germline clones) have a phenotype similar to that of embryos derived from scrib673 homozygous germline clones (lacking scrib maternal and zygotic function). Formation of the zonula adherens is largely rescued in crb2 ; l(2)gl4 or crb2 scrib673 double mutant embryos. crb2 ; Df(3L)H99 double mutant embryos have crb-mutant like cuticle defects, but the number of cuticle vesicles produced is greatly increased compared to crb2 single mutants. These cuticle vesicles have a normal junctional complex containing a zonula adherens and a septate junction.
The addition of BacA\p35GMR.PH to crb2 animals suppresses the light sensitive degeneration phenotype seen in mutant clones in the eye, though the phenotypes associated with low light conditions remain.
crb2/crb+, kst1/kst2 mutants have normal zonula adherens but photoreceptor stalk membranes are much shorter than in wild type, kst homozygous or crb heterozygous photoreceptor cells.
Xenogenetic Interactions
Statement
Reference
crb11A22 significantly rescues the eye neurodegeneration phenotype caused by expression of Hsap\APPAβ42.Scer\UAS.cUa under the control of Scer\GAL4GMR.PU. The increased cell death phenotype which is seen in the eye imaginal discs of animals expressing Hsap\APPAβ42.Scer\UAS.cUa under the control of Scer\GAL4GMR.PU is also significantly suppressed.
Complementation and Rescue Data
Comments
Expression of crbScer\UAS.cWa under the control of Scer\GAL4332.3 fails to significantly rescue the lethality and dorsal closure defects in embryos expressing crbY10A in a crbGX24w-/crb11A22 background.
Expression of crbScer\UAS.cWa under the control of Scer\GAL4nullo.PG rescues the defects in cell shape which is seen in the dorsal cells of crb11A22 embryos. Expression of crbintraTM.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4nullo.PG partially rescues the defects in cell shape which is seen in the dorsal cells of crb11A22 embryos. Expression of crbextraTM.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4nullo.PG fails to rescue the defects in cell shape which is seen in the dorsal cells of crb11A22 embryos.
Expression of crbextraTM.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4ey.PH fully rescues the crb11A22 head overgrowth phenotype. Expression of crbextra.Scer\UAS under the control of Scer\GAL4ey.PH fails to rescue the crb11A22 head overgrowth phenotype. Expression of crbTM.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4ey.PH fails to rescue the crb11A22 head overgrowth phenotype.
Scer\GAL4elav.PU-mediated expression of crbScer\UAS.cWa, crbextra.Scer\UAS or crbintra.Scer\UAS.T:Zzzz\FLAG nearly completely restores the overall morphology of crb11A22 photoreceptor cells. Scer\GAL4elav.PU-mediated expression of crbScer\UAS.cWa or crbintra.Scer\UAS.T:Zzzz\FLAG but not crbextra.Scer\UAS partially restores the length of the stalk membrane in crb11A22 photoreceptor cells.
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Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments
Strong crb allele.
The phenotype of amorphic crb mutants is essentially the same as the phenotype of amorphic sdt mutants. Embryos doubly mutant for sdt and crb mutants show the same phenotype as embryos singly mutant for either gene. Double mutants for Egfr and sdt or crb show an enhancement of the sdt or crb mutant phenotype. Phenotype can be alleviated by a duplication for sdt+, Dp(1;2)sn+72d.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (77)