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General Information
Symbol
Dmel\βTub85Dn
Species
D. melanogaster
Name
null
FlyBase ID
FBal0000036
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
β2null, B2tnull, β2tn
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

C9409168T

Reported nucleotide change:

C?T

Amino acid change:

R276term | betaTub85D-PA

Reported amino acid change:

R276term

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

Nucleotide substitution: C?T.

Amino acid replacement: R276term.

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
Detailed Description
Statement
Reference

In those homozygous βTub85Dn mutant embryos with the most severe salivary gland migration defect, the distal tip of the salivary gland contacts the circular visceral mesoderm, but does not turn posteriorly during stage 12. The distal tip begins to migrate posteriorly during stage 13, but gland migration stalls at this point and the salivary glands remain associated with the circular visceral mesoderm. By stage 14, only the distal half of the mutant salivary glands are turned posteriorly. By stage 16, βTub85Dn mutant salivary glands are positioned more anteriorly than in wild-type. However, their distal tips are no longer attached to the visceral mesoderm. At this stage, βTub85Dn mutant salivary glands contact the evaginating gastric caecae as in the wild-type.

Migration of the longitudinal visceral muscle founder cells between the salivary gland and the circular visceral mesoderm is delayed in homozygous βTub85Dn mutant embryos at stage 13. Despite this delay, the longitudinal visceral muscle still forms normally in homozygous βTub85Dn mutant embryos.

Homozygous βTub85Dn mutant embryos display defects in fusion competent myoblast migration at stage 14.

Stage 13 βTub85Dn/βTub85D6 embryos display salivary gland migration defects.

Stage 13 βTub85Dn/Df(3R)by10 embryos display salivary gland migration defects.

Homozygous males are sterile. Each gonial cell produces 16 spermatocytes via four rounds of mitosis, but then spermatogenesis fails. The mature spermatocytes do not assemble meiotic spindles, and spermatids do not assemble axonemes or any other postmitotic microtubules. Heterozygous males are fertile, but have reduced fecundity and a reduced amount of motile sperm compared to wild type. Males carrying one or two copies of βTub85D432 in a βTub85Dn/βTub85Dn background are sterile and axonemes are not produced. Males carrying one copy of βTub85D432 in a βTub85Dn/+ background are sterile.

Failed spermatogenesis. Meiosis fails causing cysts with 16 large round 4N spermatids. Sperm tail elongation fails, and failed spermatids have crystalline appearance.

Affects microtubule function during spermatogenesis.

Chromosome segregation during meiosis is sometimes abnormal in βTub85D7/βTub85Dn males.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference

βTub85Dn has male sterile | dominant phenotype, enhanceable by wrl1

NOT Suppressor of
Statement
Reference
Other
Statement
Reference
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

Embryos trans-heterozygous for βTub85Dn and mewM6 exhibit salivary gland migration defects.

Embryos trans-heterozygous for βTub85Dn and ifB2 exhibit salivary gland migration defects.

Df(3R)Scx4/+ ; βTub85Dn/+ males carrying one copy of βTub85D432 are fertile. Males carrying one copy of βTub56DβTub85D.PR in a βTub85Dn/+ background are fertile. Males carrying one copy of βTub56DβTub85D.PR and one copy of βTub85D432 in a βTub85Dn/+ background are fertile, but have reduced fecundity and a reduced amount of motile sperm compared to wild type. Males carrying one copy of βTub60D::βTub85DβTub85D.3'UTR in a βTub85Dn/+ background are sterile and have abnormal axonemes. Males carrying one copy of βTub60D::βTub85DβTub85D.3'UTR and one copy of βTub85D432 in a βTub85Dn/+ background are sterile and have abnormal axonemes.

The addition of βTub56D::βTub85Dβ1-β2.i, βTub56Dβ1-β2.ii, βTub56D::βTub85Dβ1-β2.iii or βTub56D::βTub85Dβ1-β2.iv to βTub85Dn homozygotes leads to almost wild-type axoneme morphology in the testis - in distal sections however many axonemes lose any discernable organisation.

In flies heterozygous for βTub85Dn with a single copy of P{βTub85D-βTub56D.int}, the axoneme morphology in the testis is wild-type. However, 2 copies of P{βTub85D-βTub56D.int} in the heterozygous background (a 2:1 βTub56D:βTub85D ratio) produces sterile males. Meiosis and cytoplasmic microtubules are normal in these males, but spermatids have a mixture of normal axonemes, axonemes lacking the central pair, and axonemes with 10 doublets. In all cases, the basal bodies have the normal 9+2 morphology, and this arrangement maintained for at least 40μm; 10-doublet axonemes are present only in more distal regions of the sperm tail. The tenth doublet is inserted into axonemes de novo laterally and appears abruptly, without obvious precursor structures. Rarely, the loss of the 10th doublet is seen. Occasionally mature 10-doublet axonemes retain the central pair. Occasional axonemes containing more than 10 doublets are seen, but always in an open configuration. Doublet microtubules are also seen in the cytoplasm in these flies. When βTub56DβTub85D.int is added to males homozygous for βTub85Dn, abnormal spermatid axonemes are seen in the testis of these sterile males. At an early stage of axoneme development, instead of the normal 9+2 doublet architecture a 9+0 arrangement is seen. Axoneme morphogenesis is otherwise equivalent to wild-type at this stage. Most A-tubules have acquired the inner dynein arm, accessory microtubules have initiated as protofilament projections from each B-tubule. Some spoke linkers are present. The integrity of 9+0 axonemes is maintained for only a fraction of the normal 1.9mm sperm tail length (average 20μm) Distally axonemes lose coherent organisation or terminate.

haync2.tMa, in a hemizygous hay-, βTub85Dn/+ background are male sterile. haync2.tMa in a βTub85Dn/+ background are partially male sterile.

βTub85Dn heterozygotes fail to rescue the male sterile phenotype of βTub60D::βTub85Dstar; no sperm is present in the seminal vesicles.

αTub84B7/βTub85Dn male heterozygotes are sterile, even in the presence of a wild type copy of αTub84B. This interaction requires the presence of a defective protein as males heterozygous for a deletion of αTub84B7 and βTub85Dn are fertile.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Not rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Ethyl methanesulfonate reversion of the failure to complement between wrl1 and βTub85Dn generated two classes of revertants. One class have a recessive male sterile phenotype, some are extragenic suppressors of the failure to complement. The second class have a dominant male sterile phenotype and include wrlrv1, wrlrv2 and wrlrv3.

Class I allele.

Recovered over Df(3R)by62, although Df(3R)by62 deletes αTub85E, and not βTub85D.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (9)
References (15)