FB2024_03 , released June 25, 2024
Allele: Dmel\pebhnt-1
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General Information
Symbol
Dmel\pebhnt-1
Species
D. melanogaster
Name
FlyBase ID
FBal0005509
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
hntXE81, hntXE
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
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

peb1/pebhnt-1 and peb1/pebEH704a transheterozygous egg chambers show a significant decrease in follicle rupture (ex vivo, octopamine-treated egg chambers), as compared to peb1 heterozygous controls.

There is a delay in neuronal determination of photoreceptor cell precursor clusters in homozygous clones in the eye disc compared to the adjacent wild-type clusters. The developing photoreceptor cell preclusters show defects in cell arrangement and occasionally cell number, with defects first seem at the five cell precluster stage. The cluster sometimes does not rotate properly. R3/R3 type symmetrical ommatidia (where the R3 or R4 cell has not taken up the correct position) are found at the borders of homozygous clones in the eye. In these ommatidia, either the R3 or R4 cell, or both, is mutant and the chirality of these ommatidia is sometimes also incorrect. Homozygous clones in the eye result in a scar. The scar contains no photoreceptor cells but pigment cells are still present. The photoreceptor cells have developed, but have fallen out of the retinal epithelium onto the lamina of the optic lobe of the brain and the basal fenestrated membrane of the retina. Mutant cells in larval eye discs show depletion or more diffuse localisation of F-actin, especially in the more posterior part of the mutant clone. Mosaic ommatidia have a lower concentration of F-actin in their photoreceptor cells than normal and it is found more basally than in the wild-type neighbouring cells.

Mutant embryos do not retract their germband during stage 13. In mutants embryos the early aspects of tracheal cell fate specification and morphogenesis are indistinguishable from wild-type. During stages 14 and 15, mutant embryos exhibit several tracheal defects, foremost of which is the constriction and expansion of the dorsal trunk to form sac-like structures. Similar defects are seen in the smaller tracheal branches which collapse and become misshapen. By stage 16 many sacs have pinched off and tubes no longer connect these sacs. the lumen is no longer continuous and secondary branching does not occur. Tracheal defects are most severe in the posterior region of the embryo. The tracheal epithelium in pebhnt-1 mutant embryos has ultrastructurally normal zonula adherentes that are present apicolaterally as in wild-type. Regions of the trachea are either collapsed or expanded compared with wild-type and in places the lumen is severely reduced in size. There are no obvious defects in either the polarity or the general cytological organisation of the surviving tracheal cells in pebhnt-1 mutants either prior to or during loss of normal epithelial architecture. In pebhnt-1 mutant trachae the epicuticle is secreted but there are no taenidial folds in either the collapsed or the expanded regions.

Genetic mosaic embryos show phenotypes that reveal a correlation between the genotype of the amnioserosa and the success or failure of germ band retraction. 100% of mosaics where germband retraction was successful had peb+ tissue in the amnioserosa. 100% of embryos with a fully mutant amnioserosa failed to undergo germ band retraction. The genotype of the anterior or posterior midgut is not correlated with the success or failure of germ band retraction. Analysis of distribution of mutant cells in mosaic amnioserosa suggests that peb function is important in those amnioserosa cells that abut the epidermis.

79% of embryos have abdominal segment 5.0 +/- 0.5 at the posterior tip, indicating a failure of germband retraction.

Homozygous embryos exhibit weak germ band retraction defects. Kr staining reveals abnormalities in the amnioserosa.

Germband retraction and dorsal closure fail to occur in homozygous embryos.

Nondefective in gonad assembly.

Within constraints of the embryo being folded due to the hnt mutation, the muscle pattern is normal and movement is vigorous and well coordinated.

The germ band does not retract in pebhnt-1 embryos. Embryos are U-shaped with the head facing posteriorly.

embryonic lethal no germ band retraction; embryo U-shaped with head facing posteriorly. Germ line clones obtained; no maternal effect in homozygous germ-line clones (Perrimon, Engstrom, and Mahowald, 1989).

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by
Statement
Reference

pebhnt-1 has phenotype, enhanceable by srpneo45

pebhnt-1 has phenotype, enhanceable by ush2

Suppressed by
NOT suppressed by
Statement
Reference

pebhnt-1 has amnioserosa phenotype, non-suppressible by InRhs.PF

Other
Additional Comments
Genetic Interactions
Statement
Reference

The tracheal system in pebhnt-1/Df(3L)H99 mutant embryos, loses its integrity despite the absence of programmed cell death.

Blocking amnioserosal cell death by making the mutant embryos also mutant for Df(3L)H99 does not alter the effect of mutant clones. InRhs.PF partially suppresses the germ band retraction defect of pebhnt-1 embryos. The amnioserosa apoptosis defect is not suppressed.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Comments

The failure of germband retraction can be rescued by pebhs.PY.

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

l(1)EH275a is not allelic to peb; l(1)EH275a1 complements pebhnt-1, pebX001, pebEH704a and peb1.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (18)