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
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.
TA
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 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.
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.
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.
bcd6/bcd[+] is an enhancer of lethal | embryonic stage | maternal effect phenotype of Df(2R)Drlrv25/bin3KG00599
bcd6/bcd[+] is an enhancer of lethal | embryonic stage | maternal effect phenotype of bin34-7/bin32-7
bcd6 is an enhancer of lethal | embryonic stage | recessive phenotype of Scer\GAL4GCN4.nanos.bcd3'UTR, hbUAS.cWa
bcd6, nanosL7, tsl3 has abnormal cell polarity | maternal effect | gastrula stage phenotype
Polr2Bwimp, bcd6 has lethal | maternal effect phenotype
Bin1R7-18, bcd6 has embryonic head | maternal effect phenotype, enhanceable by HDAC104556
bcd6 has embryo | maternal effect phenotype, suppressible by tslCBB.bcd/osk6/tslPZRev32
bcd6/bcd1 has embryonic/larval posterior spiracle | ectopic phenotype, suppressible | partially by Mdoa\bcdbcd.1
bcd6/bcd1 has embryonic thorax phenotype, suppressible | partially by Mdoa\bcdbcd.1
bcd6/bcd1 has embryonic head phenotype, suppressible | partially by Mdoa\bcdbcd.1
bcd6 has embryonic prothoracic segment phenotype, suppressible by Scer\GAL4GCN4.nanos.bcd3'UTR/hbUAS.cWa
bcd6 has embryonic mesothoracic segment phenotype, suppressible by Scer\GAL4GCN4.nanos.bcd3'UTR/hbUAS.cWa
bcd6 has embryonic metathoracic segment phenotype, suppressible by Scer\GAL4GCN4.nanos.bcd3'UTR/hbUAS.cWa
bcdΔQAC, bcd6 has embryo phenotype, non-suppressible by Taf6XS-922
tslCBB.bcd, bcd6, tslPZRev32 is a suppressor of embryo | maternal effect phenotype of osk6
bcd6, tsl1 has embryonic/first instar larval cuticle phenotype
Bin1R7-18, bcd6 has embryonic head | maternal effect phenotype
Bin1R7-18, bcd6 has dorsal arm of apodeme of rostrum-haustellum joint | maternal effect phenotype
Bin1R7-18, bcd6 has epipharyngeal sclerite | maternal effect phenotype
Bin1R7-18, bcd6 has embryonic/larval mouth | maternal effect phenotype
Bin1R7-18, bcd6 has dorsal bridge | maternal effect phenotype
Bin1R7-18, bcd6 has median tooth | maternal effect phenotype
bcd6, osk6, tslPZRev32 has embryo | maternal effect phenotype
bcd6, nanosL7, tsl3 has embryo | embryonic stage 4 phenotype
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/+.
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.
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.
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.
bcd6 is rescued by bcd6xTag:MS2
bcd6 is rescued by bcdnanos.PC
bcd6 is rescued by bcdY68A.nanos
bcd6 is rescued by bcdY72A.nanos
bcd6 is rescued by bcd1-489AR.nanos
bcd6 is rescued by bcd1-489.nanos
bcd6 is rescued by bcd5ala.nanos
bcd6 is not rescued by bcd1-202AR.nanos
bcd6 is not rescued by bcd77-202.nanos
bcd6 is not rescued by bcd89-202.nanos
bcd6 is not rescued by bcd2-74.G4DBD
bcd6 is not rescued by bcd2-94.G4DBD
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.
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.
Strong bcd allele.
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.