FlyBase Allele Report: Dmel\βTub85D[n]

General Information

Symbol

Dmel\βTub85Dⁿ

Species

D. melanogaster

Name

null

FlyBase ID

FBal0000036

Feature type

allele

Associated gene

Dmel\βTub85D

Associated Insertion(s)

Carried in Construct

Also Known As

β2^null, B2t^null, β2tⁿ

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

amorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Fackenthal et al., 1993)

loss of function allele

(Jattani et al., 2009, Fuller et al., 1988)

Mutagen

ethyl methanesulfonate

(Fackenthal et al., 1993)

Progenitor genotype

Cytology

Description

Nucleotide substitution: C?T.

(Fackenthal et al., 1995, Fackenthal et al., 1993)

Amino acid replacement: R276term.

(Fackenthal et al., 1995, Fackenthal et al., 1993)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

3R:9,409,168..9,409,168 [-]

Nucleotide change:

C9409168T

Reported nucleotide change:

C?T

Amino acid change:

R276term | betaTub85D-PA

Reported amino acid change:

R276term

(Fackenthal et al., 1993)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

abnormal meiotic cell cycle | male (with βTub85D⁷)

(Fuller et al., 1988)

decreased fecundity | dominant | male

(Hoyle et al., 2001)

male sterile

(Hoyle et al., 2001)

male sterile, with βTub85D⁴³²

(Hoyle et al., 2001)

male sterile (with βTub85D⁶)

(Fuller et al., 1988)

male sterile (with βTub85D⁷)

(Fuller et al., 1988)

male sterile (with βTub85D⁸)

(Fuller et al., 1988)

male sterile | recessive

(Fackenthal et al., 1993)

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.

(Jattani et al., 2009)

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.

(Hoyle et al., 2001)

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

(Fackenthal et al., 1993)

Affects microtubule function during spermatogenesis.

(Green et al., 1990)

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

(Fuller et al., 1988)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

βTub85Dⁿ has male sterile | dominant phenotype, enhanceable by wrl¹

(Green et al., 1990)

NOT Suppressor of

Statement

Reference

βTub85Dⁿ is a non-suppressor of male sterile phenotype of βTub60D::βTub85D^star

(Fackenthal et al., 1995)

Other

Statement

Reference

βTub56D^βTub85D.PR, βTub85Dⁿ has male fertile phenotype

(Hoyle et al., 2001)

betaTub56D[+]/βTub56D^βTub85D.PR, βTub85D⁴³², βTub85Dⁿ has male fertile phenotype

(Hoyle et al., 2001)

βTub60D::βTub85D^{βTub85D.3'UTR}/ betaTub60D::betaTub85D [+], βTub85D⁴³², βTub85Dⁿ has male sterile phenotype

(Hoyle et al., 2001)

βTub85D⁴³², βTub85Dⁿ, Df(3R)Scx4/+ has male fertile phenotype

(Hoyle et al., 2001)

βTub60D::βTub85D^{βTub85D.3'UTR}, βTub85D⁴³²/βTub85Dⁿ has male sterile phenotype

(Hoyle et al., 2001)

βTub60D::βTub85D^{βTub85D.3'UTR}, βTub85Dⁿ/betaTub85D[+] has male sterile phenotype

(Hoyle et al., 2001)

βTub56D^βTub85D.PR, βTub85D⁴³²/βTub85Dⁿ has male fertile phenotype

(Hoyle et al., 2001)

βTub56D^βTub85D.PR, βTub85D⁴³², βTub85Dⁿ/betaTub85D[+] has decreased fecundity | male phenotype

(Hoyle et al., 2001)

betaTub56D[+]/βTub56D^βTub85D.PR, βTub85Dⁿ has male fertile phenotype

(Hoyle et al., 2001)

βTub60D::βTub85D^{βTub85D.3'UTR}, βTub85Dⁿ has male sterile phenotype

(Hoyle et al., 2001)

βTub56D^βTub85D.int, βTub85Dⁿ has sterile phenotype

(Raff et al., 2000)

βTub85Dⁿ, hay^nc2.tMa has male semi-sterile phenotype

(Mounkes and Fuller, 1999)

βTub85Dⁿ, +/Df(3L)Ez7, hay^nc2.tMa has male sterile | dominant phenotype

(Mounkes and Fuller, 1999)

βTub85Dⁿ, hay[+]/hay^nc2 has male sterile | dominant phenotype

(Mounkes and Fuller, 1999)

βTub85Dⁿ/betaTub85D[+], hay^nc2 has male sterile | dominant phenotype

(Mounkes and Fuller, 1999)

βTub85Dⁿ/betaTub85D[+], hay^nc2.tMa has male semi-sterile phenotype

(Mounkes and Fuller, 1999)

βTub85Dⁿ/betaTub85D[+], Df(3L)Ez7, hay^nc2.tMa has male sterile phenotype

(Mounkes and Fuller, 1999)

βTub85Dⁿ, Df(3R)kar^5l, Dp(3;2)ry⁺ has male fertile phenotype

(Green et al., 1990)

αTub84B^XH, βTub85Dⁿ has male fertile phenotype

(Hays et al., 1989)

αTub84B^+t4.8, βTub85Dⁿ has male fertile phenotype

(Hays et al., 1989)

αTub84B⁷, βTub85Dⁿ has male sterile | dominant phenotype

(Hays et al., 1989)

αTub84B^7.tHa, βTub85Dⁿ has male sterile | dominant phenotype

(Hays et al., 1989)

αTub84B^7XH, βTub85Dⁿ has male sterile | dominant phenotype

(Hays et al., 1989)

Phenotype Manifest In

Other

Statement

Reference

βTub85Dⁿ, mew^M6 has presumptive embryonic salivary gland phenotype

(Jattani et al., 2009)

βTub85Dⁿ, if^B2 has presumptive embryonic salivary gland phenotype

(Jattani et al., 2009)

βTub60D::βTub85D^{βTub85D.3'UTR}, βTub85Dⁿ has spermatid axoneme phenotype

(Hoyle et al., 2001)

betaTub56D[+]/βTub56D^βTub85D.PR, βTub85D⁴³², βTub85Dⁿ has spermatozoon phenotype

(Hoyle et al., 2001)

βTub60D::βTub85D^{βTub85D.3'UTR}/ betaTub60D::betaTub85D [+], βTub85D⁴³², βTub85Dⁿ has spermatid axoneme phenotype

(Hoyle et al., 2001)

βTub60D::βTub85D^{βTub85D.3'UTR}, βTub85D⁴³²/βTub85Dⁿ has spermatid axoneme phenotype

(Hoyle et al., 2001)

βTub60D::βTub85D^{βTub85D.3'UTR}, βTub85Dⁿ/betaTub85D[+] has spermatid axoneme phenotype

(Hoyle et al., 2001)

βTub56D^βTub85D.PR, βTub85D⁴³²/βTub85Dⁿ has spermatozoon phenotype

(Hoyle et al., 2001)

βTub56D::βTub85D^β1-β2.i, βTub85Dⁿ has spermatid axoneme phenotype

(Nielsen et al., 2001)

βTub56D::βTub85D^β1-β2.iii, βTub85Dⁿ has spermatid axoneme phenotype

(Nielsen et al., 2001)

βTub56D::βTub85D^β1-β2.iv, βTub85Dⁿ has spermatid axoneme phenotype

(Nielsen et al., 2001)

βTub56D^βTub85D.PR, βTub85Dⁿ has spermatid axoneme phenotype

(Nielsen et al., 2001)

βTub56D^β1-β2.ii, βTub85Dⁿ has spermatid axoneme phenotype

(Nielsen et al., 2001)

βTub56D^βTub85D.int, βTub85Dⁿ has spermatid axoneme phenotype

(Raff et al., 2000)

Additional Comments

Genetic Interactions

Statement

Reference

Embryos trans-heterozygous for βTub85Dⁿ and mew^M6 exhibit salivary gland migration defects.

Embryos trans-heterozygous for βTub85Dⁿ and if^B2 exhibit salivary gland migration defects.

(Jattani et al., 2009)

Df(3R)Scx4/+ ; βTub85Dⁿ/+ males carrying one copy of βTub85D⁴³² are fertile. Males carrying one copy of βTub56D^βTub85D.PR in a βTub85Dⁿ/+ background are fertile. Males carrying one copy of βTub56D^βTub85D.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::βTub85D^{βTub85D.3'UTR} in a βTub85Dⁿ/+ background are sterile and have abnormal axonemes. Males carrying one copy of βTub60D::βTub85D^{βTub85D.3'UTR} and one copy of βTub85D⁴³² in a βTub85Dⁿ/+ background are sterile and have abnormal axonemes.

(Hoyle et al., 2001)

The addition of βTub56D::βTub85D^β1-β2.i, βTub56D^β1-β2.ii, βTub56D::βTub85D^β1-β2.iii or βTub56D::βTub85D^β1-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.

(Nielsen et al., 2001)

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 βTub56D^βTub85D.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.

(Raff et al., 2000)

hay^nc2.tMa, in a hemizygous hay^-, βTub85Dⁿ/+ background are male sterile. hay^nc2.tMa in a βTub85Dⁿ/+ background are partially male sterile.

(Mounkes and Fuller, 1999)

βTub85Dⁿ heterozygotes fail to rescue the male sterile phenotype of βTub60D::βTub85D^star; no sperm is present in the seminal vesicles.

(Fackenthal et al., 1995)

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.

(Hays et al., 1989)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Not rescued by

βTub85Dⁿ is not rescued by βTub85D⁴³²

(Nielsen et al., 2001)

Comments

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

2453

kni^ri-1 βTub85Dⁿ e¹/TM3, Sb¹

Kyoto

107340

kni^ri-1 βTub85Dⁿ e¹/TM3, Sb¹

Notes on Origin

Discoverer

K. Matthews.

(Fackenthal et al., 1993)

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 wrl^rv1, wrl^rv2 and wrl^rv3.

(Green et al., 1990)

Class I allele.

(Fackenthal et al., 1995)

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

(Matthews, 1995.8.18)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (9)

Reported As

Symbol Synonym

B2tⁿ

(Fuller, 1993, Fuller et al., 1988)

B2t^null

(Mounkes and Fuller, 1999, Fackenthal et al., 1995, Hoyle et al., 1995, Fackenthal et al., 1993)

KM24

Tβ2ⁿ

β2^null

(Popodi et al., 2008, Popodi et al., 2005, Hoyle et al., 2001, Nielsen et al., 2001, Raff et al., 2000, Hoyle and Raff, 1990)

β2t^N

(Jattani et al., 2009)

β2tⁿ

(Fuller, 1986)

βTub85Dⁿ

Name Synonyms

null

(Fackenthal et al., 1995, Fackenthal et al., 1993)

Secondary FlyBase IDs

References (17)

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