Dmel\P{lacW}Btk29A^k00206 Insertion

General Information
Symbol	Dmel\P{lacW}Btk29A^k00206	Species	D. melanogaster
Name		FlyBase ID	FBti0010229
Feature type	transposable_element_insertion_site
Description
Inserted element	P{lacW}	Expression data
Affected gene(s)	Btk29A, Ecol\lacZ	Viability / fertility
Causes allele(s)	Btk29A^k00206, Ecol\lacZ^{Btk29A-k00206}	Stock availability	2 publicly available
LINE ID	l(2)k00206
Genomic Location
Chromosomal location	2L ( 29A1 )	Sequence location	2L:8,277,179..8,277,186 [-]
Map ( GBrowse )
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
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FB2012_01
FB2011_10
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Detailed Mapping Data
Chromosome (arm)
Sequence Location	2L:8,277,179..8,277,186 [-] 2L:8,277,187..8,277,187 [+] (BDGP Project Members, 1994-1999)
Orientation
Cytological location (computed by FlyBase)	29A1 ( inferred by FlyBase from sequence location )
Cytological location (reported)	29A1-29A2 (in situ hybridization reported) (BDGP Project Members, 1994-1999)
Comments concerning location
Sequence Data
Flanking sequence	AQ034168 (FlyBase, 1992-,
Inserted Element
Construct	P{lacW}
Location-dependent role	lacZ enhancer trap (Bier et al., 1989)
Size	10.691Kb
Associated alleles	Ecol\lacZ^P\T.W w^+mC
Molecular map
Affected Gene(s)
Insertion may affect gene	Btk29A (BDGP Project Members, 1994-1999, Djagaeva et al., 2005, Chandrasekaran and Beckendorf, 2005, Spradling et al., 1999, Schnorr et al., 2001, Djagaeva, 2005, Read et al., 2004, Roulier et al., 1998) Ecol\lacZ (BDGP Project Members, 1994-1999)
Alleles and Phenotypes
Causes alleles	Btk29A^k00206 (BDGP Project Members, 1994-1999, Djagaeva et al., 2005, Chandrasekaran and Beckendorf, 2005, Spradling et al., 1999, Schnorr et al., 2001, Djagaeva, 2005, Read et al., 2004, Roulier et al., 1998) Ecol\lacZ^{Btk29A-k00206} (BDGP Project Members, 1994-1999)

Lethality References lethal \| embryonic stage \| partially (Tateno et al., 2000) lethal \| embryonic stage \| recessive (Li et al., 2000, Roulier et al., 1998) lethal \| recessive (Spradling et al., 1999, Roulier and Beckendorf, 1996)
Sterility References
Phenotype Manifest In
	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, 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) hypostomal sclerite (Roulier et al., 1998) karyosome \| germline clone (Djagaeva et al., 2005) labrum (Roulier et al., 1998) mouth hooks \| 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) salivary gland common duct primordium (Chandrasekaran and Beckendorf, 2005) vertical bridge \| anterior (Roulier et al., 1998)
Detailed Description
Statement Reference Btk29A[k00206]/+ largely suppresses the ectopic apoptosis in wing discs and notched wing phenotype seen in ASPP[8]/ASPP[8] Csk[j1D8]/+ animals. The eye phenotype of ASPP[8] homozygotes is suppressed by Btk29A[k00206]/+ (Langton et al., 2007) Btk29A^k00206 mutant embryos show global defects in the final muscle pattern. (Beckett and Baylies, 2006) 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) 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) 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) 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) 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) 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) 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) 28.2 +/- 3.0% of Btk29A^k00206/Btk29A^k05610 animals die as embryos. (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) 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) The embryonic lethality of Btk29A^k00206 homozygotes is partially rescued by expression of Btk29A^hs.PR. (Roulier et al., 1998) Embryos exhibit an abnormal head skeleton due to disrupted head involution. (Roulier and Beckendorf, 1996)
Expression Data
Reporter Expression

Additional Information
Statement Reference

Marker for
Reflects expression of
External Images
FlyView (LinkOut)
Data on Genetic Line
Line ID	l(2)k00206 (Gene Disruption Project members, 2001-)
Origin as a multiple insertion line
Progenitor(s) within the Genome

Related Aberration or Balancer
Aberration
Balancer
Stocks ( 2 )
Bloomington	10469 y¹ w^67c23; P{lacW}Btk29A^k00206/CyO
Kyoto	111118 y^d2 w¹¹¹⁸ P{ey-FLP.N}2 P{GMR-lacZ.C(38.1)}TPN1; P{lacW}Btk29A^k00206 P{neoFRT}40A/CyO y⁺
Linkouts
Comments
	Location 2L:8277187-8277188 confirmed by FlyBase alignment of dbGSS accession AQ034168 to D. melanogaster arm Release_4 and heterochromatin Release_3.2b. (FlyBase, 2005) NOTE: derived from line carrying multiple insertions. (BDGP Project Members, 1994-1999) 8 bp insertion associated host repeat
Synonyms & Secondary IDs
Reported As
Symbol Synonym	P{lacW]k00206 (FlyBase, 1992-) P{lacW}Btk29A^k00206 (FlyBase, 2005, FlyBase, 1992-) P{lacW}k00206 (FlyBase, 1992-)
Secondary FlyBase IDs

References ( 20 )
Research paper	Langton et al., 2007, Dev. Cell 13(6): 773--782 Drosophila ASPP regulates C-terminal Src kinase activity. [FBrf0202129] Beckett and Baylies, 2006, Dev. Biol. 299(1): 176--192 Parcas, a regulator of non-receptor tyrosine kinase signaling, acts during anterior-posterior patterning and somatic muscle development in Drosophila melanogaster. [FBrf0195055] Chandrasekaran and Beckendorf, 2005, Development 132(15): 3515--3524 Tec29 controls actin remodeling and endoreplication during invagination of the Drosophila embryonic salivary glands. [FBrf0187454] Djagaeva et al., 2005, Dev. Biol. 284(1): 143--156 Src64 is involved in fusome development and karyosome formation during Drosophila oogenesis. [FBrf0187382] Bellen et al., 2004, Genetics 167(2): 761--781 The BDGP gene disruption project: single transposon insertions associated with 40% of Drosophila genes. [FBrf0179132] Read et al., 2004, Molec. Cell. Biol. 24(15): 6676--6689 Drosophila C-terminal Src kinase negatively regulates organ growth and cell proliferation through inhibition of the Src, Jun N-terminal kinase, and STAT pathways. [FBrf0179404] Thomas and Wieschaus, 2004, Development 131(4): 863--871 src64 and tec29 are required for microfilament contraction during Drosophila cellularization. [FBrf0167540] Sinka et al., 2002, Development 129(14): 3469--3478 poirot, a new regulatory gene of Drosophila oskar acts at the level of the short Oskar protein isoform. [FBrf0151262] Schnorr et al., 2001, Genetics 159(2): 609--622 Ras1 interacts with multiple new signaling and cytoskeletal loci in Drosophila eggshell patterning and morphogenesis. [FBrf0139680] Li et al., 2000, Genetics 156(2): 763--774 Identification of autosomal regions involved in Drosophila raf function. [FBrf0129944] Tateno et al., 2000, Science 287(5451): 324--327 Regulation of JNK by Src During Drosophila Development. [FBrf0123214] Spradling et al., 1999, Genetics 153(1): 135--177 The Berkeley Drosophila genome project gene disruption project. Single P-element insertions mutating 25% of vital Drosophila genes. [FBrf0111489] Roulier et al., 1998, Molec. Cell 1(6): 819--829 The Tec29 tyrosine kinase is required during Drosophila embryogenesis and interacts with Src64 in ring canal development. [FBrf0102811] Bier et al., 1989, Genes Dev. 3: 1273--1287 Searching for pattern and mutation in the Drosophila genome with a P-lacZ vector. [FBrf0049800]
Supplementary material	Djagaeva, 2005, Dev. Biol. 284(1): [title not yet available] [FBrf0191723]
Abstract	Roulier and Beckendorf, 1996, A. Dros. Res. Conf. 37: 205 Cytoplasmic tyrosine kinase encoded by Src29A is essential for head development. [FBrf0085845]
FlyBase analysis	FlyBase, 2005, Assessment of transgenic construct insertion sites. Assessment of transgenic construct insertion sites. [FBrf0184339] FlyBase, 1992-, FlyBase curation FlyBase curation. [FBrf0105495]
Computer file	Gene Disruption Project members, 2001-, [title not yet available] [title not yet available] [FBrf0132177] BDGP Project Members, 1994-1999, Berkeley Drosophila Genome Project. Berkeley Drosophila Genome Project. [FBrf0067338]

Dmel\P{lacW}Btk29Ak00206 Insertion

Dmel\P{lacW}Btk29A^k00206 Insertion