FlyBase Allele Report: Dmel\Btk[k00206]

(Öztürk-Çolak et al., 2018, Fernández et al., 2014, Jagut et al., 2013, Chandrasekaran and Beckendorf, 2005, Djagaeva, 2005, Djagaeva et al., 2005, Read et al., 2004, Schnorr et al., 2001, Spradling et al., 1999, Roulier et al., 1998, BDGP Project Members, 1994-1999)

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

Phenotype Manifest In

actin cytoskeleton

(Chandrasekaran and Beckendorf, 2005)

actin filament | embryonic stage 5 | germline clone | maternal effect

(Thomas and Wieschaus, 2004)

actin filament | germline clone

(Djagaeva et al., 2005)

cephalopharyngeal skeleton

(Li et al., 2000, Roulier et al., 1998)

dorsal bridge

(Roulier et al., 1998)

egg chamber

(Djagaeva, 2005)

egg chamber & actin cytoskeleton | germ-line clone

(Djagaeva et al., 2005)

embryonic/first instar larval cuticle

(Li et al., 2000)

embryonic/first instar larval cuticle (with Btk^k05610)

(Roulier et al., 1998)

embryonic/first instar larval cuticle (with Df(2L)TE29Aa-14)

(Roulier et al., 1998)

embryonic/larval muscle system

(Beckett and Baylies, 2006)

embryonic/larval posterior spiracle

(Li et al., 2000)

embryonic head

(Roulier and Beckendorf, 1996)

epipharyngeal sclerite

(Roulier et al., 1998)

filzkorper

(Tsikala et al., 2014)

hypostomal sclerite

(Roulier et al., 1998)

karyosome | germline clone

(Djagaeva et al., 2005)

labrum

(Roulier et al., 1998)

mouth hook | posterior

(Roulier et al., 1998)

nurse cell fusome | germline clone

(Djagaeva et al., 2005)

nurse cell ring canal | germline clone

(Roulier et al., 1998)

presumptive embryonic salivary gland

(Chandrasekaran and Beckendorf, 2005)

presumptive embryonic salivary gland (with Btk^k05610)

(Chandrasekaran and Beckendorf, 2005)

salivary gland common duct primordium

(Chandrasekaran and Beckendorf, 2005)

spiracular chamber

(Tsikala et al., 2014)

stigmatophore

(Tsikala et al., 2014)

vertical bridge | anterior

(Roulier et al., 1998)

Detailed Description

Statement

Reference

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.

(Tsikala et al., 2014)

Btk29A^k00206 mutant embryos show global defects in the final muscle pattern.

(Beckett and Baylies, 2006)

Btk29A^k00206 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. Btk29A^k00206 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 Btk29A^k00206 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. Btk29A^k00206 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 Btk29A^k00206 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 Btk29A^k00206 embryos the wave of endoreplication in the salivary glands is disrupted, resulting in endoreplication occurring throughout the placodes and invaginating glands. Btk29A^k05610/Btk29A^k00206 transheterozygotes also show a long salivary gland phenotype.

(Chandrasekaran and Beckendorf, 2005)

Btk29A^k00206 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 Btk29A^k00206 mutants.

(Djagaeva et al., 2005)

In the ovarioles of Btk29A^k00206 germline clones, 8% contain fused egg chambers at 18^oC; this value drops to 5% at 25^oC.

(Djagaeva, 2005)

Cellularizing embryos derived from Btk29A^k00206 germline clones have large and non-rounded microfilament rings like those of Src64B^Δ17 mutant embryos.

(Thomas and Wieschaus, 2004)

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

(Sinka et al., 2002)

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).

(Li et al., 2000)

28.2 +/- 3.0% of Btk29A^k00206/Btk29A^k05610 animals die as embryos.

(Tateno et al., 2000)

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. Btk29A^k00206/Btk29A^k05610 and Btk29A^k00206/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.

(Roulier et al., 1998)

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

(Roulier and Beckendorf, 1996)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Btk^k05610/Btk^k00206 has lethal | embryonic stage phenotype, enhanceable by Src42A^myri

(Tateno et al., 2000)

Enhancer of

Statement

Reference

Btk^k05610/Btk^k00206 is an enhancer of lethal | recessive phenotype of Src42A^Jp45

(Tateno et al., 2000)

Btk^k05610/Btk^k00206 is an enhancer of lethal | embryonic stage | recessive phenotype of Src42A^myri

(Tateno et al., 2000)

Btk^k00206 is an enhancer of lethal | embryonic stage | maternal effect | recessive phenotype of Src64B^Δ17

(Roulier et al., 1998)

Suppressor of

Statement

Reference

Btk29A[+]/Btk^k00206 is a suppressor of increased cell death | heat sensitive phenotype of Scer\GAL4^sd-SG29.1, Src64B^UY1332

(Fernández et al., 2014)

Btk29A[+]/Btk^k00206 is a suppressor of decreased cell growth rate | heat sensitive phenotype of Scer\GAL4^sd-SG29.1, Src64B^UY1332

(Fernández et al., 2014)

Btk29A[+]/Btk^k00206 is a suppressor of visible phenotype of ASPP⁸, Csk^j1D8/Csk[+]

(Langton et al., 2007)

Btk29A[+]/Btk^k00206 is a suppressor of visible phenotype of ASPP⁸

(Langton et al., 2007)

Btk^k00206 is a suppressor of grandchildless phenotype of pcs^gs

(Beckett and Baylies, 2006)

Btk^k00206 is a suppressor of lethal | pupal stage phenotype of Csk^j1D8/Csk^S030003

(Read et al., 2004)

Btk^k00206 is a suppressor of increased occurrence of cell division phenotype of Csk^j1D8/Csk^S030003

(Read et al., 2004)

Btk^k00206 is a suppressor of abnormal mitotic cell cycle phenotype of Csk^j1D8/Csk^S030003

(Read et al., 2004)

Btk^unspecified/Btk^k00206 is a suppressor of grandchildless phenotype of pcs^gs

(Sinka et al., 2002)

Phenotype Manifest In

Enhanced by

Statement

Reference

Btk^k00206 has presumptive embryonic salivary gland phenotype, enhanceable by Src64B^PI

(Chandrasekaran and Beckendorf, 2005)

Btk^k00206 has actin cytoskeleton phenotype, enhanceable by chic²²¹

(Chandrasekaran and Beckendorf, 2005)

Btk^k00206 has presumptive embryonic salivary gland phenotype, enhanceable by chic²²¹

(Chandrasekaran and Beckendorf, 2005)

Btk^k00206 has presumptive embryonic salivary gland phenotype, enhanceable by Src42A^E1

(Chandrasekaran and Beckendorf, 2005)

Suppressed by

Statement

Reference

Btk^k00206 has actin cytoskeleton phenotype, suppressible by tsr^k05633

(Chandrasekaran and Beckendorf, 2005)

Btk^k00206 has presumptive embryonic salivary gland phenotype, suppressible by tsr^k05633

(Chandrasekaran and Beckendorf, 2005)

Btk^k00206 has presumptive embryonic salivary gland phenotype, suppressible by Scer\GAL4^prd.RG1/CycE^UAS.cRa

(Chandrasekaran and Beckendorf, 2005)

Btk^k05610/Btk^k00206, Src42A^myri has embryonic/first instar larval cuticle | dorsal phenotype, suppressible | partially by Jra^Asp.hs.sev

(Tateno et al., 2000)

Enhancer of

Statement

Reference

Btk29A[+]/Btk^k00206 is an enhancer of egg chamber phenotype of Src64B^Δ19

(Djagaeva, 2005)

Btk29A[+]/Btk^k00206 is an enhancer of egg chamber phenotype of Src64B^Δ17

(Djagaeva, 2005, Djagaeva et al., 2005)

Btk29A[+]/Btk^k00206 is an enhancer of dorsal appendage phenotype of Ras85D^ix12a

(Schnorr et al., 2001)

Btk^k00206 is an enhancer of nurse cell ring canal phenotype of Src64B^Δ17

(Roulier et al., 1998)

NOT Enhancer of

Statement

Reference

Btk29A[+]/Btk^k00206 is a non-enhancer of phenotype of ct^L188

(Jackson and Berg, 1999)

Btk29A[+]/Btk^k00206 is a non-enhancer of phenotype of ct^C145

(Jackson and Berg, 1999)

Btk^k00206 is a non-enhancer of phenotype of ct^C145

(Jackson and Berg, 1999)

Suppressor of

Statement

Reference

Btk29A[+]/Btk^k00206 is a suppressor of wing disc phenotype of Scer\GAL4^sd-SG29.1, Src64B^UY1332

(Fernández et al., 2014)

Btk29A[+]/Btk^k00206 is a suppressor of wing phenotype of ASPP⁸, Csk^j1D8/Csk[+]

(Langton et al., 2007)

Btk29A[+]/Btk^k00206 is a suppressor of wing disc phenotype of ASPP⁸, Csk^j1D8/Csk[+]

(Langton et al., 2007)

Btk29A[+]/Btk^k00206 is a suppressor of eye phenotype of ASPP⁸

(Langton et al., 2007)

Btk^k00206 is a suppressor of embryonic segment | maternal effect phenotype of pcs^gs

(Beckett and Baylies, 2006)

Btk^k00206 is a suppressor of eye | somatic clone phenotype of Csk^j1D8, Stat92E^j6C8

(Read et al., 2004)

Df(2L)TE29Aa-11/Btk^k00206 is a suppressor of phenotype of tor^12D

(Li et al., 2000)

Btk^k00206/Btk^k00206 is a suppressor of ventral denticle belt phenotype of tor^12D

(Li et al., 2000)

NOT Suppressor of

Statement

Reference

Btk^k00206 is a non-suppressor of presumptive embryonic/larval muscle system phenotype of pcs^gs

(Beckett and Baylies, 2006)

Other

Statement

Reference

Btk^k00206, Src64B^PI has embryonic head segment phenotype

(Chandrasekaran and Beckendorf, 2005)

Btk^k05610/Btk^k00206, Src42A^myri has embryonic/first instar larval cuticle | dorsal phenotype

(Tateno et al., 2000)

Btk^k05610/Btk^k00206, Src42A^myri has embryo | dorsal closure stage phenotype

(Tateno et al., 2000)

Additional Comments

Genetic Interactions

Statement

Reference

Btk29A^k00206/+ largely suppresses the ectopic apoptosis in wing discs and notched wing phenotype seen in ASPP⁸/ASPP⁸ Csk^j1D8/+ animals.

The eye phenotype of ASPP⁸ homozygotes is suppressed by Btk29A^k00206/+

(Langton et al., 2007)

Btk29A^k00206; pcs^gs/pcs^gs females show a suppression of the grandchildless phenotype and the early embryonic patterning phenotype compared to pcs^gs/pcs^gs females. However, the muscle development phenotype of pcs^gs embryos is not suppressed by Btk29A^k00206.

(Beckett and Baylies, 2006)

The Btk29A^k00206 salivary gland phenotype is enhanced in chic²²¹, Btk29A^k00206 double mutants as more cells remain on the surface at stage 14 compared with Btk29A^k00206 single mutants. The amount of actin disorganization that precedes the salivary gland phenotype is also increased in these double mutants. Additionally, chic²²¹, Btk29A^k00206 double mutants exhibit a higher level of uncoordinated endoreplication at early stage 12, prior to the invagination defects, than Btk29A^k00206 single mutants. The actin disorganization and salivary gland phenotypes of Btk29A^k00206 single mutants are rescued in Btk29A^k00206; tsr^k05633 double mutants. However, there is no decrease in the endoreplication defect seen in Btk29A^k00206 single mutants in the double mutants. Expression of CycE^Scer\UAS.cRa, under the control of Scer\GAL4^prd.RG1, rescues the long salivary gland phenotype either completely or partially in 69% of Btk29A^k00206 embryos. Btk29A^k00206; Src42A^E1 embryos show an enhanced salivary gland invagination phenotype compared to Btk29A^k00206 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 Btk29A^k00206 embryos. Btk29A^k00206; Src64B^PI double mutant embryos suffer gross abnormalities, such as lack of head segments. Btk29A^k00206/+; Src64B^PI/+ double heterozygotes have no salivary gland defects, while around one third of Btk29A^k00206/+; Src64B^PI double mutants show invagination defects.

(Chandrasekaran and Beckendorf, 2005)

The amount of abnormal egg chambers is enhanced in Btk29A^k00206/+; Src64B^Δ17 mutants, compared to Src64B^Δ17 single mutants.

(Djagaeva et al., 2005)

Reducing the Btk29A dose in Src64B^Δ17 homozygotes enhances the defective ovariole phenotype at room temperature: 57% of ovarioles contain fused egg chambers in Btk29A^k00206/+; Src64B^Δ17 mutants. 45% of Btk29A^k00206/+; Src64B^Δ19 double mutant ovarioles contain fused egg chambers. Most of the fused egg chambers, and some of the unfused, display features of apoptosis.

(Djagaeva, 2005)

Strong dominant enhancer of the Ras85D^ix12a eggshell phenotype; 0-20% of dorsal appendages are wild type.

(Schnorr et al., 2001)

The tor^12D maternal effect phenotype is partially suppressed by homozygosity for Btk29A^k00206; embryos show a significant increase in the number of ventral denticle belts. The tor^12D phenotype is also partially suppressed by Btk29A^k00206/Df(2L)TE29Aa-11.

(Li et al., 2000)

Btk29A^k00206 Src42A^myri/Btk29A^k05610 Src42A^myri 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 Jra^Asp.hs.sev. Dominantly enhances the lethality of Src42A^Jp45.

(Tateno et al., 2000)

Dominantly enhances the ring canal phenotype of egg chambers derived from homozygous Src64B^Δ17 females, and also the reduction in hatching rate seen in eggs derived from these females.

(Roulier et al., 1998)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Btk^k05610

(Roulier et al., 1998)

Btk^k05610

(BDGP Project Members, 1994-1999)

Rescued by

Btk^k00206 is rescued by Scer\GAL4^salm-459.2/Btk^UAS.RC

(Tsikala et al., 2014)

Partially rescued by

Btk^k00206 is partially rescued by Btk^hs.PR

(Roulier et al., 1998)

Not rescued by

Btk^k00206 is not rescued by Scer\GAL4^en.PU/Btk^UAS.RC

(Tsikala et al., 2014)

Btk^k00206 is not rescued by Btk^UAS.RC/Scer\GAL4^ems.HRE

(Tsikala et al., 2014)

Comments

Posterior spiracle defects (length of the spiracular lumen and area of the spiracular chamber) seen in Btk29A^k00206 embryos are rescued by expression of Btk29A^Scer\UAS.RC under the control of Scer\GAL4^salm-459.2.

Posterior spiracle defects seen in Btk29A^k00206 embryos are not rescued by expression of Btk29A^Scer\UAS.RC under the control of either Scer\GAL4^ems.HRE or Scer\GAL4^en.PU.

(Tsikala et al., 2014)

The embryonic lethality of Btk29A^k00206 homozygotes is partially rescued by expression of Btk29A^hs.PR.

(Roulier et al., 1998)

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

10469

y¹ w^67c23; P{lacW}Btk^k00206/CyO

Kyoto

111118

y^d2 w¹¹¹⁸ P{ey-FLP.N}2 P{5xglBS-lacZ.38-1}TPN1; P{lacW}Btk^k00206 P{neoFRT}40A/CyO y⁺

Notes on Origin

Discoverer

Comments

Complements: l(2)k14308^k14308. Complements: l(2)k14816^k14816.

(BDGP Project Members, 1994-1999)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (12)

Reported As

Symbol Synonym

Btk29A²⁰⁶

(Tsikala et al., 2014)

Btk29A^k00206

(Öztürk-Çolak et al., 2018, Tsikala et al., 2014, Jagut et al., 2013, Beckett and Baylies, 2006, Christensen and Cook, 2006.8.30, Christensen and Cook, 2006.12.5, Christensen and Cook, 2006.12.5, Christensen and Cook, 2006.12.5, Read et al., 2004)

Btk^k00206

Tec29²⁰⁶

(Tateno et al., 2000, Roulier et al., 1998)

Tec29^K00206

(Chandrasekaran and Beckendorf, 2005)

Tec29^k00206

(Djagaeva, 2005, Djagaeva et al., 2005)

Tec29A²⁰⁶

(Li et al., 2000)

Tec29A^k00206

(Li et al., 2000)

Tec29A^l(2)k00206

(Jackson and Berg, 1999)

btk29A²⁰⁶

(Tsarouhas et al., 2014)

l(2)k00206

(Schnorr et al., 2001, Baba et al., 1999, Spradling et al., 1999)

tec29^k00206

(Thomas and Wieschaus, 2004)

Name Synonyms

Secondary FlyBase IDs

References (29)

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