Open Close
General Information
Symbol
Dmel\hb12
Species
D. melanogaster
Name
FlyBase ID
FBal0005403
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
hb14F, hb14F21, hunchback12
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G8693387A

Reported nucleotide change:

G?A

Amino acid change:

W256term | hb-PA; W256term | hb-PB

Reported amino acid change:

W256term

Comment:

TGG to TGA

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Nucleotide substitution: G?A.

Mutation is before the first zinc finger domain.

Amino acid replacement: W256term.

Stop codon before the first finger domain.

Point mutation.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

hb12 homo- or heterozygous mutants do not exhibit a rough eye phenotype.

hb12/+ does not cause any detectable change in the segmentation phenotype of homozygous maternal mutant Acsl1 embryos.

Mutant NB7-3 lineages (in segments A1 to A6) consist of two (20%) or three (80%) neurons at stage 13, but only two neurons at stage 15, The GW neuron appears not to survive to stage 15. In mutant embryos, the dorsal subset of the NB 7-1 derived neurons is missing in 97% of hemineuromeres: 80% showing a loss of two, 10% of one, and 7% of three cells. This missing cells are probably fpCC and/or the dorsal-most CQ neuron. aCC or pCC are missing in 39%, aCC and pCC in 11% and RP2 in 67% of mutant hemisegments.

In hbKM, hb12 animals, a duplication of interneuron 2 is seen at the expense of the first born 1/1G neurons. In these mutants the aCC and RP2 motorneurons fail to project their proper dorsal muscle target, suggesting a transformation of GMC-1 to a later born GMC fate. Mutants show a general reduction in the number of motorneuron projections, particularly to the dorsal muscles. Mutants lack the first born MM-CB glia at the midline.

Mutant larval cuticles lack all three thoracic segments and exhibit a large first abdominal segment. In presumptive cephalic regions, zygotic mutants lack elements of the labial segment, including the H piece and labial sense organs, and other head organs are severely disorganised.

The labial lobe is missing in mutant embryos.

When one copy of hbP1only is supplied zygotically (via the father) to hb12/hb15 embryos the A7/A8 fusion mutant phenotype is rescued. When one copy of hbP1only is supplied maternally both the A7/A8 and anterior labial and T1 segments are rescued; only T2 and T3 remain unrescued. When the maternal contribution of hbP1only is increased (three copies) 30% rescued embryos show only the maternal rescue of labial and T1 segments. Most show additional rescue of thoracic segments of mostly T3 character. 5-10% of embryos show rescue of all thoracic segments.

Homozygous embryos exhibit deletion of the third gnathal segment through the third thoracic segment, a deletion between the seventh and eighth abdominal belts and filzkorper defect. In(3R)hbD2/hb12 embryos exhibit only the posterior defect and filzkorper defect.

All thoracic segments and the most posterior gnathal segment are missing.

Cuticle phenotype.

Nondefective in gonad assembly.

Reduction in salivary gland placode size corresponding to the reduced Scr expression domain.

The posterior gt domain is extended slightly toward the posterior and the anterior domain toward the anterior.

Suppression of tor13D embryos: increase in proportion of embryos that formed cuticle with denticles and decrease in proportion of embryos that formed empty sacs.

Narrowing of posterior gt expression domain is blocked and expression is seen in a new posterior domain during gastrulation and germ band extension.

Labial and thoracic segments missing, defects in abdominal segments 7 and 8.

The posterior abdomen is duplicated anteriorly in homozygous embryos derived from females with homozygous germ line clones. In addition, the naked cuticle of abdominal segment A7 and the denticle band of A8 are deleted.

Expression of the hbC20-hb construct in an hb12 genetic background causes fusion of abdominal segments 7 and 8 and defects in the second thoracic segment.

Thoracic structures (except the labial segment) and the eighth segment are missing. Posterior denticle belt is enlarged. Failure of head involution, floor of the pharynx protrudes.

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

hb12/hb[+] is a suppressor of eye phenotype of Scer\GAL4GMR.PF, fruNP0021

hb15/hb12 is a suppressor | partially of EW3 neuron phenotype of Kr1, KrmCD, svp2/svp1

hb15/hb12 is a suppressor | partially of U4 neuron phenotype of Kr1, KrmCD, svp2/svp1

hb15/hb12 is a suppressor | partially of U5 neuron phenotype of Kr1, KrmCD, svp2/svp1

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

A hb12 heterozygous background strongly suppresses the rough eye phenotype found upon expression of fruNP0021 under the control of Scer\GAL4GMR.PF.

KrmCD; Kr1/Kr1 enhances the reduction in later born neurons of the NB7-1 an NB2-3 lineages see in svp1/svp2 embryos so that U4 and U5 are almost completely eliniated, as are EW2 and EW3. This enhanced phenotype is partially suppressed if the embryos are also hb12/hb15.

The addition of Krunspecified to hb12, hbeve.st2ΔKr animals causes a dramatic rescue of most head structure defects, and a few embryos (about 10%) show anterior phenotypes that are indistinguishable from wild-type. Krunspecified; hb12 larvae have head defects.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by

hb12 is partially rescued by hbeve.st2ΔKr

hb15/hb12 is partially rescued by hbP1only

hb12 is partially rescued by hbKM

hb12 is partially rescued by hbKG

hb12 is partially rescued by hb10E1

hb12 is partially rescued by hbhb.0.7bcd

hb12 is partially rescued by hbbcd.3UTR

Comments

Addition of hbeve.st2ΔKr to hb12 mutants specifically rescues the prothorax and returns A1 to its normal size. Rescue with two copies of the transgene further increases the size of the thorax and rescues the dorsal part of T3. T2, however is never present in these embryos. hbeve.st2ΔKr causes a very weak rescue of the head structure defects.

Addition of hbKM rescues the anterior defects, but not the posterior, hbKG and hb10E1 rescue the anterior and posterior defects. Despite complete rescue of the cuticular defects by hbKG and hb10E1 embryos carrying these transgenes are inviable.

Head segments and thoracic segments (except for T2) can be rescued by hbhb.0.7bcd or hbDvir\hb.0.8bcd.

The hbC20-hb, hb12 mutant phenotype can be rescued by activation of the 2.9kb hb transcript.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Class I allele.

Phenotypic class I hb allele.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (61)