FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\bcd6
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General Information
Symbol
Dmel\bcd6
Species
D. melanogaster
Name
FlyBase ID
FBal0001080
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
bcdE1
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Amino acid interval 151 to 207 deleted, followed by a frame shift.

Small deletion.

Large deletion.

Deletion of nucleotides 2482 to 2650 and an insertion of nucleotides TA, corresponding deletion of amino acids 156 to 494 that are replaced by 55 out of frame amino acids.

Small deletion of 180bp within the bcd homeobox domain.

Small deletion within the bcd coding region.

2482-2650 deleted + TA inserted; frameshift --> 55 out-of-frame amino acids replacing amino acids 156-494, including homeodomain

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Comment:

A deletion of 169 bases and insertion of the bases TA. The net result is that bcd amino acids 156-494 are replaced by 55 out-of-frame amino acids.

Inserted_sequence:

TA

Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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

bcd6 homozygotes exhibit embryonic lethality, with 100% of embryos failing to hatch. bcd6 heterozygotes exhibit 4% embryonic lethality, which is similar to controls (8%). One copy of bcd+t8.7 is sufficient to rescue bcd6/bcd6 lethality (100%) to levels similar to that of bcd6/+ embryos (8% compared to 4% unhatched in bcd6 heterozygotes). Of those that did hatch, 3% exhibit larval head defects. One copy of bcdK57R is not sufficient to rescue bcd6/bcd6 lethality (100%), with 69% of embryos exhibiting an unhatched phenotype. Of the hatched embryos, 50% exhibited larval head defects. Two copies of bcdK57R partially rescues bcd6/bcd6 lethality, with 25% of embryos failing to hatch. Of these that do hatch, 36% exhibit larval head defects such as reductions in the dorsal arm, dorsal bridge, and labrum, or moderate to strong defects such as the absence of discernable head skeletal structures and general disorganisation of the head. Approximately 10% of embryos lack head and thoracic structures entirely and contain a posterior duplication. One copy of bcdS35T is not sufficient to rescue bcd6/bcd6 lethality (100%), with 37% of embryos exhibiting an unhatched phenotype. Of these that do hatch, 11% exhibit larval head defects. Two copies of bcdS35T rescues bcd6/bcd6 lethality (3% compared to 4% in bcd6 heterozygotes), with 3% of embryos failing to hatch. Of these that do hatch, none exhibit larval head defects. One copy of bcdS35T, with one copy of bcdK57R in a bcd6 homozygote background partially rescues the bcd6 embryonic lethality phenotype, with 31% of embryos remaining unhatched. Of those that do hatch, 26% exhibited larval head defects.

bcd6 embryos have no head structures. The anterior structures resemble posterior ones.

Embryos derived from homozygous females lack head and thoracic segments, and the acron is partially or fully transformed into telson.

Embryos derived from bcd6/bcd1 females lack all head and thoracic structures and have a duplicated set of posterior spiracles at the anterior end.

Embryos derived from homozygous bcd6 mothers show head and thorax replaced by tail structures. Abdominal segments 2 and 4 are missing.

Embryos derived from homozygous females lack all head and thorax segments and some abdominal segments. They have a second telson at the anterior end. The ability of bcdΔQAC to rescue embryos derived from bcd6 females is not affected by either Taf6XS-922 or Taf4S-466.

Embryos derived from heterozygous females have normal cuticles. Larvae derived from heterozygous females have salivary glands with a significantly reduced number of cells compared to wild-type. There is an increase in cell death in the expanded trunk domain of embryos derived from heterozygous females compared to embryos derived from wild-type females.

Cuticle phenotype, additional spiracles develop at the anterior.

Does not prevent the posterior localization of G-iα65A protein.

bcd, nos double mutants show reduced rate of germ band extension, and reduced cell intercalation.

Anterior structures of homozygous embryos are not formed.

Embryos from homozygous females produce only abdomen and telson, with a second telson and filzkorper patches formed at the anterior end.

bcd6, tsl3 embryos, which lack both anterior and terminal gene functions, show no tll expression at either pole. In bcd6 embryos tll transcription is activated at both poles in two terminal caps, the caps are larger than wild type caps. The presence of the bcd has a negative effect on the anterior cap of tll expression so tll expression is equal in the caps.

Anterior gt expression domain is absent, the posterior domain is correctly initiated.

The development of anterior structures can be induced by the injection of bcdTN3 mRNA into the anterior tip of the embryos. P{bcdTN3} expands and shifts the bcd expression domain slightly more anterior towards the gnathal and thoracic regions.

Embryos derived from hb15 bcd6 females show a mirror image duplication of abdominal segments, centered around A6. Embryos derived from hb15 bcd6 females, and also zygotically mutant for hb8 show a mirror image duplication of abdominal segments, centered around A6, and segments A7 and A8 are fused.

Embryonic pole cells do not coalesce correctly into the gonads.

Deletion of head and most of the thorax, replaced by a telson duplicated in the anterior. Transplantation of posterior cytoplasm from wild type embryos into the anterior portion induced posterior segments of reversed polarity in addition to the anteriorly duplicated telson.

The acron is replaced by a second telson in embryos derived from homozygous females.

Inverted duplication of the posterior hb domain.

The head and thorax are replaced by a duplicated telson in embryos derived from homozygous females. Embryos derived from bcd2/bcd6 females have anterior defects. Embryos derived from bcd6/bcd7 females show some development of at least thoracic and frequently head structures when injected at the anterior tip with cytoplasm taken from the anterior tip of wild-type embryos.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by
Statement
Reference
NOT Enhanced by
Statement
Reference

bcd6 has phenotype, non-enhanceable by sra687

bcdΔQAC, bcd6 has embryo phenotype, non-enhanceable by Taf6XS-922

bcdΔQAC, bcd6 has embryo phenotype, non-enhanceable by Taf4S-466

Suppressed by
NOT suppressed by
Statement
Reference

bcdΔQAC, bcd6 has embryo phenotype, non-suppressible by Taf6XS-922

bcdΔQAC, bcd6 has embryo phenotype, non-suppressible by Taf4S-466

Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

The anterior fatemap shift caused by maternal bcd dosage reduction (in bcd6 heterozygotes) is suppressed partially by eliminating fsd maternally (through a fsdKG02393 background).

The defects seen in the progeny of bin34-7/bin32-7 females mated to bin3KG00599/Df(2R)Drlrv25 males and in the reciprocal cross are enhanced by a maternal copy of bcd6/+.

Anisotropic epithelial constriction still occurs in bcd6 nosL7 tsl3 triple mutant embryos that lack anterior-posterior polarity.

9% of bcd6/Bin1R7-18 double heterozygotes die as unhatched embryos with serious head defects including missing mouth parts. These larvae are missing labral structures most frequently the labrum itself and the epistomal sclerite. In some cases the dorsal bridge, dorsal bridge, dorsal and ventral arms, and post pharyngeal wall are absent or reduced in size.

Anterior-posterior polarization of cells in the extending germband is disrupted in embryos from bcd6 nosL7 tsl3 homozygous mothers.

Embryos produced by bcd6, osk6 and tslPZRev32 mutant mothers lack all anterior posterior patterning. This phenotype is partially rescued by the addition of tslCBB.bcd, leading to embryos that differentiate filzkorper material, at one or both poles.

Embryos derived from bcd6 nosL7 tsl3 triple mutant females have uniform yolk stalk diameters during cellularisation (in contrast to wild type where there are three domains of varying yolk stalk diameter along the anterior-posterior axis of the embryo). The shallow cellularisation front of the anterior domain and the greater depth of the pre-cephalic furrow domain are also lost. Other aspects of cellularisation are normal in these embryos. Nuclear spacing is uniform along the anterior-posterior axis in embryos derived from bcd6 nosL7 tsl3 triple mutant females (in contrast to wild type where there is an anterior domain of lower nuclear density). The larger diameter of the actin caps seen in the anterior of the wild-type embryo in cycle 11 and 12 is not seen in embryos derived from bcd6 nosL7 tsl3 triple mutant females.

The embryonic lethality seen in embryos expressing hbScer\UAS.cWa under the control of Scer\GAL4nos.bcd3'UTR.T:Scer\GCN4 (where Scer\GAL4nos.bcd3'UTR.T:Scer\GCN4 is provided maternally) is increased if they are derived from females carrying one copy of bcd6.

The addition of bcdΔA to tsl1, bcd6 embryos rescues the anterior part of the tsl1 mutant phenotype (rescuing the labrum and dorsal bridge) as well as rescuing the bcd6 mutant phenotype. This results in embryos with a posterior terminal mutant phenotype only.

The addition of tsl1 does not effect the ability of bcdΔQAC to rescue the bcd6 phenotype. The addition of bcdΔA to tsl1, bcd6 embryos rescues the terminal system phenotype seen in these animals.

Embryos derived from homozygous bcd6 mothers carrying four copies of Scer\GAL4nos.bcd3'UTR.T:Scer\GCN4 and fathers carrying hbScer\UAS.cWa homozygously show suppression of anterior tail structures and thoracic structures are rescued to variable extent, up to a complete rescue of T2 and T3.

Mutant phenotype of bcd mutant embryos is enhanced by hbbcd.3UTR, due to ectopic activation of gt. Mutant phenotype of bcd, tsl double mutants is partially rescued by hbbcd.3UTR.

In contrast, cytoplasm taken from the anterior tip of embryos derived from exu1/exu2 females shows barely detectable rescuing activity when injected into the anterior tip of embryos derived from bcd6/bcd7 females. Cytoplasm taken from the anterior tip of embryos derived from swa1/swa2 females also shows reduced rescuing activity compared to wild-type cytoplasm when injected into the anterior tip of embryos derived from bcd6/bcd7 females. exu1 does not alter the phenotype of embryos derived from bcd6/bcd7 females.

bcd6 nosL7 embryos exhibit two telsons in mirror image. Injection of wild type posterior pole plasm induces formation of two mirror image abdomens. bcd6 nosL7 tll1 embryos exhibit two telsons in mirror image. Injection of wild type posterior pole plasm induces formation of two mirror image abdomens. bcd6 nosL7 tsl3 embryos develop a cuticle but no segmental pattern. Injection of wild type posterior pole plasm induces formation of anterior abdominal segments towards the end of the embryo.

Xenogenetic Interactions
Statement
Reference

Mdoa\bcdbcd.1 partially rescues the defects seen in embryos derived from bcd6/bcd1 females, with the degree of rescue depending on the Mdoa\bcdbcd.1 line used. In the strongest rescuing line, complete rescue is seen in a small proportion of embryos, as shown by the presence of all three thoracic segments, a complete head skeleton and other anterior structures such as the mouthhooks and labrum. 7.4% of embryos can develop into fully fertile adults, but most embryos show no rescue.

Complementation and Rescue Data
Rescued by
Partially rescued by

bcd6 is partially rescued by bcdY66A.nanos

bcd6 is partially rescued by bcdY73R.nanos

bcd6 is partially rescued by bcdS35T

bcd6 is partially rescued by bcdK57R

bcd6 is partially rescued by bcdNRE1

bcd6 is partially rescued by bcdNRE2

bcd6 is partially rescued by bcdR54A

bcd6 is partially rescued by bcdΔQC

bcd6 is partially rescued by bcdΔC

bcd6 is partially rescued by bcdΔAC

bcd6 is partially rescued by bcdB6

bcd6 is partially rescued by bcdΔ18

bcd6 is partially rescued by bcdΔ16

bcd6 is partially rescued by bcdΔ11

bcd6 is partially rescued by bcdΔ19

bcd6 is partially rescued by bcdΔ7

Comments

bcdT:MS2\MCP alone or in combination with either MS2\MCP::Avic\GFPHsp83.PF or MS2\MCP::Avic\GFPHsp83.T:Disc\RFP completely rescues the bcd6 mutant phenotype.

bcdΔQAC rescues the bcd mutant phenotype of bcd6 tsl1 double mutant embryos, resulting in a tsl single mutant phenotype.

bcdΔA rescues the bcd mutant phenotype of bcd6 tsl1 double mutant embryos.

Mutant phenotype cannot be rescued by bcdT:Ecol\B42 but four copies of bcdT:Ecol\B6 can rescue the thorax and part of the head. can rescue the thorax and part of the head.

Images (0)
Mutant
Wild-type
Stocks (8)
Notes on Origin
Discoverer
Comments
Comments

hb protein expression in early bcd6 mutant embryos has been studied.

Anterior cytoplasm from embryos derived from bcd6 females can rescue both anterior and posterior defects when transplanted into the anterior or posterior end respectively of embryos derived from tor4 females.

Phenotype can be rescued (to varying extents) by injection of egg cytoplasm from D.melanogaster, D.hydei, D.mercatorum, D.pinicola, D.polychaeta, D.pseudoobscura.pseudoobscura, D.virilis, Musca, Lucilia, Phormia and Megaselia, but not rescued by injection of egg cytoplasm by Calliphora or A.mellifera.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
Reported As
Symbol Synonym
bcdE1
(Athilingam et al., 2024, Baumgartner, 2024, Fernandes et al., 2022, Singh et al., 2022, Huang et al., 2020, Yang et al., 2020, Datta et al., 2018, Durrieu et al., 2018, Hannon et al., 2017, Suresh et al., 2017, Liu and Ma, 2015, Cheung et al., 2014, Spahn et al., 2014, Liu and Ma, 2013, Liu et al., 2013, Liu et al., 2013, Lucas et al., 2013, Cheung et al., 2011, Little et al., 2011, Liu and Ma, 2011, Singh et al., 2011, Löhr et al., 2009, Gregor et al., 2008, He et al., 2008, Lopes et al., 2008, Brent et al., 2007, Gregor et al., 2007, Weil et al., 2006, Wratten et al., 2006, Cho et al., 2005, Lebrecht et al., 2005, Singh et al., 2005, Werz et al., 2005, Riede, 2004, Zallen and Wieschaus, 2004, Nibu et al., 2003, Gamberi et al., 2002, Houchmandzadeh et al., 2002, Kennerdell et al., 2002, Niessing et al., 2002, Shaw et al., 2002, Blankenship and Wieschaus, 2001, Hartmann et al., 2001, Janody et al., 2001, Johnstone and Lasko, 2001, Janody et al., 2000, Janody et al., 2000, Niessing et al., 2000, Schaeffer et al., 2000, Wimmer et al., 2000, Crozatier et al., 1999, Niessing et al., 1999, Schaeffer et al., 1999, Tsai et al., 1998, Van Doren et al., 1998, Wolff et al., 1998, Bonneton et al., 1997, Greenwood and Struhl, 1997, Kuhnlein et al., 1997, La Rosee et al., 1997, Namba et al., 1997, Bellaiche et al., 1996, Dahanukar and Wharton, 1996, Dubnau and Struhl, 1996, Klingler et al., 1996, Reuter et al., 1996, Rivera-Pomar et al., 1996, Small et al., 1996, Hacker et al., 1995, Mohler, 1995, Rivera-Pomar et al., 1995, Schulz and Tautz, 1995, Wimmer et al., 1995, Wolfgang and Forte, 1995, Edgar et al., 1994, Frommer et al., 1994, Hanes et al., 1994, Hartmann et al., 1994, Irvine and Wieschaus, 1994, Jongens et al., 1994, Pelegri and Lehmann, 1994, Reuter and Leptin, 1994, Rothe et al., 1994, Salles et al., 1994, Schulz and Tautz, 1994, Simpson-Brose et al., 1994, Bardsley et al., 1993, Ding et al., 1993, Driever, 1993, Klingler and Gergen, 1993, Schroder and Sander, 1993, Gavis and Lehmann, 1992, Hoch et al., 1992, Pignoni et al., 1992, Eldon and Pirrotta, 1991, Hoch et al., 1991, Kraut and Levine, 1991, Parkhurst and Ish-Horowicz, 1991, Riddihough and Ish-Horowicz, 1991, Driever et al., 1990, Finkelstein and Perrimon, 1990, Grau and Gutzeit, 1990, Hulskamp et al., 1990, Jack and McGinnis, 1990, Lasko and Ashburner, 1990, Sugiyama and Okada, 1990, Sugiyama and Okada, 1990, Driever et al., 1989, Driever et al., 1989, Hooper et al., 1989, Lehmann and Frohnhofer, 1989, Struhl et al., 1989, Berleth et al., 1988, Driever and Nusslein-Volhard, 1988, Lehmann, 1988, Schroder et al., 1988, Tautz, 1988, Frohnhofer and Nusslein-Volhard, 1987, Tearle and Nusslein-Volhard, 1987)
Name Synonyms
Secondary FlyBase IDs
    References (136)