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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Tec29K00206, l(2)k00206, Tec29206, Btk29A206
Key Links
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

P{lacW} insertion in intron 5 (insertion site relative to accession number AB009841).

P{lacW} insertion 6kb upstream of the first exon.

Insertion components
Product class / Tool use(s)
Encoded product / tool
Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

egg chamber & actin cytoskeleton | germ-line clone

Detailed Description

Although the posterior spiracular chamber forms in mutant embryos, it has an abnormal length and shape. The spiracular lumen is significantly reduced in length, the spiracular chamber area is significantly increased, and the filzkorper are shorter than normal. The cells of the spiracular chamber primordium constrict apically as in wild type and start to invaginate, but a small group of apically constricted cells remains at the epidermal surface at the end of germ-band retraction in the mutant embryos. The convergent extension normally seen in stigmatophore cells during embryogenesis does not occur in the mutant embryos, so they fail to properly shape the stigmatophore.

Btk29Ak00206 mutant embryos show global defects in the final muscle pattern.

Btk29Ak00206 embryos exhibit abnormally long salivary glands, none of which fully invaginate. Cell counting and monitoring of mitoses show that the long glands are not the result of recruitment of extra cells into the salivary gland primordium or from the production of extra cells during development. Btk29Ak00206 embryos show an arrest in the salivary gland invagination process at mid stage 12, as evidenced by a lack of increase in gland length and a lack of decrease in placode area compared to wild-type glands. At stage 15, the distal region of Btk29Ak00206 salivary glands looks normal but the cells in the proximal region are elongated in the AP direction. This suggests that the arrest of salivary gland invagination, coupled with the anterior movement of the epidermis during head involution, causes stretching of the salivary glands. Btk29Ak00206 embryos have defective salivary ducts. Duct cell fate appears to be correctly specified, indicating that the duct cells do not undergo normal morphogenesis. The actin becomes disorganized in Btk29Ak00206 embryos early in stage 12 in the ventral cells of the placodes, with an increase in the level of G-actin. This precedes the delay in invagination. In Btk29Ak00206 embryos the wave of endoreplication in the salivary glands is disrupted, resulting in endoreplication occurring throughout the placodes and invaginating glands. Btk29Ak05610/Btk29Ak00206 transheterozygotes also show a long salivary gland phenotype.

Btk29Ak00206 germline clones show multiple defects in oogenesis that all appear to be connected to defects in the cytoskeleton. The shape and morphology of the egg chamber appears different to wild type, due to improper actin cytoskeleton development. G-actin fails to accumulate to wild-type levels in early stage oocyte nuclei and persists in the nuclei at later stages than in wild-type oocytes. Karyosome formation, which usually overlaps with G-actin accumulation, occurs later than in wild type and karyosomes are not always compact and spherical, indicating defects in chromatin condensation. Fusomes have greater levels of F-actin than wild type and appear abnormal in all mutants. Finally, the microtubule-dependent transport of proteins from the nurse cells to the oocyte appears to be affected in Btk29Ak00206 mutants.

In the ovarioles of Btk29Ak00206 germline clones, 8% contain fused egg chambers at 18oC; this value drops to 5% at 25oC.

Cellularizing embryos derived from Btk29Ak00206 germline clones have large and non-rounded microfilament rings like those of Src64BΔ17 mutant embryos.

Homozygous germline clones result in dumpless and maternal effect head defect phenotypes. Some eggs are fertilised and develop to adulthood.

Homozygous embryos do not hatch, and their cuticles show defects in the mouth parts (several components are missing) and posterior spiracles (they are shorter than wild type).

28.2 +/- 3.0% of Btk29Ak00206/Btk29Ak05610 animals die as embryos.

Homozygous embryos show defects in head involution. The head skeleton is abnormal and lacks several structures, including the dorsal bridge, anterior portions of the vertical plate, epistomal sclerite, labrum, H-piece lateral bar, and posterior portions of the mouth hook. Btk29Ak00206/Btk29Ak05610 and Btk29Ak00206/Df(2L)TE29Aa-14 embryos have an indistinguishable cuticle phenotype from homozygous embryos. Ring canals do not grow to normal size in the ovarioles of females with homozygous germ line clones.

Embryos exhibit an abnormal head skeleton due to disrupted head involution.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Enhancer of
Suppressor of

Btk29A[+]/Btk29Ak00206 is a suppressor of increased cell death | heat sensitive phenotype of Scer\GAL4sd-SG29.1, Src64BUY1332

Btk29A[+]/Btk29Ak00206 is a suppressor of decreased cell growth | heat sensitive phenotype of Scer\GAL4sd-SG29.1, Src64BUY1332

Btk29A[+]/Btk29Ak00206 is a suppressor of visible phenotype of ASPP8, Cskj1D8/Csk[+]

Btk29A[+]/Btk29Ak00206 is a suppressor of visible phenotype of ASPP8

Phenotype Manifest In
Enhanced by
Suppressed by
Enhancer of

Btk29A[+]/Btk29Ak00206 is an enhancer of egg chamber phenotype of Src64BΔ19

Btk29A[+]/Btk29Ak00206 is an enhancer of egg chamber phenotype of Src64BΔ17

Btk29A[+]/Btk29Ak00206 is an enhancer of dorsal appendage phenotype of Ras85Dix12a

NOT Enhancer of

Btk29A[+]/Btk29Ak00206 is a non-enhancer of phenotype of ctL188

Btk29A[+]/Btk29Ak00206 is a non-enhancer of phenotype of ctC145

Btk29Ak00206 is a non-enhancer of phenotype of ctC145

Suppressor of

Btk29A[+]/Btk29Ak00206 is a suppressor of wing phenotype of ASPP8, Cskj1D8/Csk[+]

Btk29A[+]/Btk29Ak00206 is a suppressor of wing disc phenotype of ASPP8, Cskj1D8/Csk[+]

Btk29A[+]/Btk29Ak00206 is a suppressor of eye phenotype of ASPP8

Df(2L)TE29Aa-11/Btk29Ak00206 is a suppressor | partially of phenotype of tor12D

NOT Suppressor of
Additional Comments
Genetic Interactions

Btk29Ak00206/+ largely suppresses the ectopic apoptosis in wing discs and notched wing phenotype seen in ASPP8/ASPP8 Cskj1D8/+ animals.

The eye phenotype of ASPP8 homozygotes is suppressed by Btk29Ak00206/+

Btk29Ak00206; pcsgs/pcsgs females show a suppression of the grandchildless phenotype and the early embryonic patterning phenotype compared to pcsgs/pcsgs females. However, the muscle development phenotype of pcsgs embryos is not suppressed by Btk29Ak00206.

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 actin disorganization and salivary gland phenotypes of Btk29Ak00206 single mutants are rescued in Btk29Ak00206; tsrk05633 double mutants. However, there is no decrease in the endoreplication defect seen in Btk29Ak00206 single mutants in the double mutants. Expression of CycEScer\UAS.cRa, under the control of Scer\GAL4prd.RG1, rescues the long salivary gland phenotype either completely or partially in 69% of Btk29Ak00206 embryos. Btk29Ak00206; Src42AE1 embryos show an enhanced salivary gland invagination phenotype compared to Btk29Ak00206 single mutants. More salivary glands show premature endoreplication in the double mutants. The double mutants also show the disorganised actin phenotype although it is not clear whether this is enhanced compared to Btk29Ak00206 embryos. Btk29Ak00206; Src64BPI double mutant embryos suffer gross abnormalities, such as lack of head segments. Btk29Ak00206/+; Src64BPI/+ double heterozygotes have no salivary gland defects, while around one third of Btk29Ak00206/+; Src64BPI double mutants show invagination defects.

The amount of abnormal egg chambers is enhanced in Btk29Ak00206/+; Src64BΔ17 mutants, compared to Src64BΔ17 single mutants.

Reducing the Btk29A dose in Src64BΔ17 homozygotes enhances the defective ovariole phenotype at room temperature: 57% of ovarioles contain fused egg chambers in Btk29Ak00206/+; Src64BΔ17 mutants. 45% of Btk29Ak00206/+; Src64BΔ19 double mutant ovarioles contain fused egg chambers. Most of the fused egg chambers, and some of the unfused, display features of apoptosis.

Strong dominant enhancer of the Ras85Dix12a eggshell phenotype; 0-20% of dorsal appendages are wild type.

The tor12D maternal effect phenotype is partially suppressed by homozygosity for Btk29Ak00206; embryos show a significant increase in the number of ventral denticle belts. The tor12D phenotype is also partially suppressed by Btk29Ak00206/Df(2L)TE29Aa-11.

Btk29Ak00206 Src42Amyri/Btk29Ak05610 Src42Amyri double homozygotes show complete embryonic lethality and some embryos have a dorsal open phenotype. The leading edge cells are only partially elongated during dorsal closure. The dorsal open phenotype is partially rescued by JraAsp.hs.sev. Dominantly enhances the lethality of Src42AJp45.

Dominantly enhances the ring canal phenotype of egg chambers derived from homozygous Src64BΔ17 females, and also the reduction in hatching rate seen in eggs derived from these females.

Xenogenetic Interactions
Complementation and Rescue Data
Partially rescued by

Posterior spiracle defects (length of the spiracular lumen and area of the spiracular chamber) seen in Btk29Ak00206 embryos are rescued by expression of Btk29AScer\UAS.RC under the control of Scer\GAL4salm-459.2.

Posterior spiracle defects seen in Btk29Ak00206 embryos are not rescued by expression of Btk29AScer\UAS.RC under the control of either Scer\GAL4ems.HRE or Scer\GAL4en.PU.

The embryonic lethality of Btk29Ak00206 homozygotes is partially rescued by expression of Btk29Ahs.PR.

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Stocks (2)
Notes on Origin
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (11)
References (29)