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General Information
Symbol
Dmel\baz4
Species
D. melanogaster
Name
FlyBase ID
FBal0001024
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
bazXi106, bazXi, bazXJ106
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

C17189991T

Amino acid change:

Q374term | baz-PA; Q395term | baz-PB; Q374term | baz-PC; Q395term | baz-PD

Reported amino acid change:

Q374term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

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

Amino acid replacement: Q374term.

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 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

embryonic neuroblast & spindle | germ-line clone

eye photoreceptor cell & eye disc & pupa | somatic clone

eye photoreceptor cell & eye disc & pupa | somatic clone | cell non-autonomous

photoreceptor cell & eye | somatic clone

Detailed Description
Statement
Reference

Homozygous clones in the wing disc survive and do not show polarity defects.

Somatic clones of baz4 homozygous mutant cells in the pupal eye disc show extra inter-ommatidial cells and increased frequency of disruptions in the structure of adherens junctions.

Centrosome asymmetry during cytokinesis in mutant pI (sensory organ precursor) cells in the notum is identical to that seen in wild-type pI cells.

Mutant egg chambers show a loss of the anterolateral enrichment of actin normally seen in the oocyte.

Most of the zygotic mutant embryos for baz4 show normal dorsal closure.

Compared with wild-type embryos, baz4 mutants have significantly shorter duration time for actomyosin assembly-disassembly cycles.

baz4 mutant embryos show amnioserosa morphology defects.

The epithelia become disorganised in baz4 zygotic mutants after stages 11-13.

Dead embryos derived from a cross of heterozygous females to wild-type males have cuticles which are largely intact with one or two small holes often at the head.

Stage 11 embryos lacking both maternal and zygotic baz4 exhibit lost or severely disrupted tubule cell polarity.

At early and mid cellularization, baz4 mutants exhibit apical surface puncta and basal junctions. At late cellularization, apical surface puncta persist abnormally compared to wild-type controls. baz4 mutants continue to have apical surface puncta as gastrulations begins, along with abnormal cell shapes.

baz4 mutant embryos display disorganised nervous systems, but the nervous system is not hyper-neuralised.

baz4/Y zygotic mutants die as embryos, typically with one hole in the embryonic cuticle, due to epithelial polarity defects.

Embryos maternally and zygotically mutant for baz4 fail to redistribute and assemble the shg gene product into spot junctions.

Somatic clones homozygous for baz4 in the ovarian follicle cells cause discontinuities and multilayering of the epithelium. When the majority of border cells are part of a clone, the border cell cluster fails to migrate. However, clusters with a minority of mutant cells migrate normally. The morphology of mutant clusters is frequently abnormal - clusters are often elongated, sometimes with cells trailing behind the migrating cluster.

Border cell migration is incomplete in 14% of stage 10 egg chambers from (bazdsRNA.Sym.Scer\UAS)X2; Scer\GAL4slbo.2.6 flies. This increases to 33% in flies also heterozygous for baz4.

heterozygotes have a decreased number of synaptic boutons at neuromuscular junctions.

neuroblast divisions that produce equal-sized daughter cells are not seen in baz4 mutant embryos. In telophase pI cells in the majority of baz4 somatic clones (6/9) the distance from cleavage furrow to the anterior centrosome is greater than that to the posterior centrosome, but it is not clear whether spindle displacement is affected.

Marker analysis suggests that apical-basal polarity is disrupted in the pupal eye disc photoreceptor cells that are part of baz4 mutant clones. In addition. the shape and polarity of wild-type photoreceptors in mosaic ommatidia is often disrupted, although not as severely as in mutant cells. Photoreceptor differentiation, numbers and pattern are all normal in these clones at early pupal stages. However, baz4 mutant clones do not survive in the developing eye at late pupal stages, and the resulting adults eyes have many malformed ommatidia containing fewer than 7 photoreceptors.

Homozygous embryos have holes in the cuticle.

The blastoderm epithelium is multilayered and the cells show a very irregular shape at gastrulation in mutant embryos derived from homozygous female germline clones. In hemizygous embryos derived from homozygous female germline clones abnormal orientation of metaphase plates with respect to the surface of the embryo is seen. In heterozygous embryos derived from homozygous female germline clones the neuroectodermal epithelium almost completely disintegrates. Many mutant embryos derived from homozygous female germline clones do not produce cuticle. Zygotic baz4 mutant embryos form cuticles with large ventral holes and head defects.

Homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic baz function) show a fully penetrant spindle orientation defect in neuroblasts. The position of the budding ganglion mother cell with respect to the apical-basal axis of the neuroblast is random.

Homozygous embryos derived from germ line clones exhibit severe malformations or an absence of epidermis. They also exhibit abnormal zonula adherens formation and mislocalisation of membrane protein neurotactin.

baz4 mutant embryos have large dorsal and ventral holes.

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

baz4 has abnormal neuroanatomy phenotype, non-suppressible by aPKCExc55

Enhancer of
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

baz4/baz[+] is a non-suppressor of abnormal neuroanatomy phenotype of aPKCExc55

Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference

baz4 has embryonic/larval cuticle phenotype, enhanceable by crb11A22/crb[+]

baz4 has embryonic/larval cuticle phenotype, enhanceable by shg[+]/shgR69

baz4 has embryonic/larval cuticle phenotype, enhanceable by aPKCk06403/aPKC[+]

baz4 has embryonic/larval cuticle phenotype, enhanceable by ed[+]/edkg

baz4 has embryonic/larval cuticle phenotype, enhanceable by fjd1/fj[+]

baz4 has embryonic/larval cuticle phenotype, enhanceable by par-1W3/par-1[+]

baz4 has embryonic/larval cuticle phenotype, enhanceable by muskelinf04338/muskelin[+]

baz4 has embryonic/larval cuticle phenotype, enhanceable by Septin5f04717/Sep5[+]

baz4 has embryonic/larval cuticle phenotype, enhanceable by alt[+]/altKG08013

baz4 has embryonic/larval cuticle phenotype, enhanceable by Rho172O/Rho1[+]

baz4 has embryonic/larval cuticle phenotype, enhanceable by asp1/asp[+]

baz4 has embryonic/larval cuticle phenotype, enhanceable by Arf79F[+]/Arf79FC005

baz4 has embryonic/larval cuticle phenotype, enhanceable by hk[+]/hook1

baz4 has embryonic/larval cuticle phenotype, enhanceable by Asap1[+]/AsapKG03963

baz4 has embryonic/larval cuticle phenotype, enhanceable by CG1951EY00129/CG1951[+]

baz4 has embryonic/larval cuticle phenotype, enhanceable by sds22e00975/sds22[+]

baz4 has embryonic/larval cuticle phenotype, enhanceable by Cul5EY00051/Cul-5[+]

baz4 has embryonic/larval cuticle phenotype, enhanceable by Roc2[+]/Roc2EP2487

baz4 has embryonic/larval cuticle phenotype, enhanceable by CG5823[+]/CG5823f04935

baz4 has embryonic/larval cuticle phenotype, enhanceable by CG10702[+]/CG10702f03893

baz4 has embryonic/larval cuticle phenotype, enhanceable by CG11210[+]/Tmem63KG08546

NOT Enhanced by
Statement
Reference

baz4 has bouton phenotype, non-enhanceable by aPKCExc55

NOT suppressed by
Statement
Reference

baz4 has bouton phenotype, non-suppressible by aPKCExc55

Enhancer of
Statement
Reference

baz4/baz[+] is an enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, dgoUAS.cFa

baz4/baz[+] is an enhancer of ommatidium phenotype of Fmr1sev.PW

NOT Enhancer of
Statement
Reference

baz4/baz[+] is a non-enhancer of wing hair phenotype of Scer\GAL4hs.2sev, dgoUAS.cFa

baz4/baz[+] is a non-enhancer of ommatidium phenotype of Vangstbm-153

baz4/baz[+] is a non-enhancer of bouton phenotype of aPKCExc55

Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

baz4/baz[+] is a non-suppressor of wing hair phenotype of Scer\GAL4hs.2sev, dgoUAS.cFa

baz4/baz[+] is a non-suppressor of ommatidium phenotype of Vangstbm-153

Other
Additional Comments
Genetic Interactions
Statement
Reference

Cells in baz4 homozygous clones in a homozygous Magibst wing disc are viable and show no loss of polarity.

The proportion of hemisegments with abnormal number of neurons in the asymmetrically dividing RP2 neural lineage is significantly increased in wtsx1/+;baz4/+ double heterozygous embryos compared to either of the single heterozygotes or wild type.

baz4/+ enhances the planar cell polarity (PCP) defects in the eye induced by the overexpression of dgoScer\UAS.cFa under the control of Scer\GAL4hs.2sev.

zip1/+ enhances the baz4 embryonic phenotype, generating merged dorsal head holes and ventral holes.

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, shgR69, aPKCk06403, edkg, Df(2L)Exel6039, Df(2L)ED1473, Df(2L)Exel7027, Df(2L)Exel6012, Df(2R)Exel7121, Df(2R)Exel7144, Df(2R)ED3943, Df(2R)ED1742, Df(2R)ED3728, Df(2R)ED1791, Df(2R)ED3610, Df(3L)ED4287, Df(3L)ED5017, Df(3L)ED201, Df(3L)ED225, Df(3R)Exel6204, Df(3R)ED5559, Df(3R)Exel6211, Df(3R)ED5623, Df(3R)ED6220, Df(3R)Exel6196, Df(3R)ED5429 or Df(3R)ED6187.

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 fjd1, par-1W3, muskelinf04338, Sep5f04717, altKG08013, Rho172O, asp1, Arf79FC005, hk1, Asap1KG03963, CG1951EY00129, sds22e00975, Cul-5EY00051, Roc2EP2487, CG5823f04935, CG10702f03893 or CG11210KG08546.

Heterozygosity for baz4 has no effect on the frequency of ommatidia that show planar cell polarity defects in Vangstbm-153 homozygotes.

baz4/+ enhances the nucleus mislocalisation defect seen in stage 9-10 sktl2.3/sktlΔ15 oocytes, such that 63% have a mislocalised nucleus.

The baz4/+ phenotype is enhanced in homozygous, heterozygous or trans-heterozygous Dhc64C6-6 or Dhc64C6-8 mutants, resulting in larger cuticle holes and an overall loss of cuticle.

baz4 sdtXP follicle cell clones expressing bazS151A.S1085A.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL4e22c lose their epithelial organisation and form multilayers of cells.

dlg114 baz4 embryos (which lack both maternal and zygotic dlg1 and baz function) have cuticle phenotypes which are indistinguishable from baz4 embryos lacking maternal and zygotic baz function; the embryos show a severe loss of post-gastrulation adherens junctions and fail to produce cuticle.

Marked clones in the eye disc expressing Ras85DV12.Scer\UAS under the control of Scer\GAL4Act5C.PI and which are also homozygous for baz4 show metastatic behaviour.

Most sdtXN baz4 double mutant embryos do not secrete any cuticle, while some embryos have a small number of cuticle grains that appear solid, rather than vesicular. The amount of cuticle produced in sdtXN baz4 mutant embryos is not significantly increased if they also carry Df(3L)H99.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of bazScer\UAS.P\T.T:Avic\GFP or bazS980E.Scer\UAS.P\T.T:Avic\GFP-m6 under the control of Scer\GAL4Act5C.PI in clones in the follicular epithelium rescues the epithelial organisation defects seen in the follicle cells of baz4 females.

The epithelial organisation defects seen in baz4 zygotic mutant embryos are rescued by zygotic expression of bazScer\UAS.P\T.T:Avic\GFP or bazS980E.Scer\UAS.P\T.T:Avic\GFP-m6 under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16.

The epithelial organisation defects seen in baz4 zygotic mutant embryos are not rescued by zygotic expression of bazS980A.Scer\UAS.P\T.T:Avic\GFP-m6 under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16.

Images (0)
Mutant
Wild-type
Stocks (3)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (62)