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General Information
Symbol
Dmel\dppH46
Species
D. melanogaster
Name
FlyBase ID
FBal0003059
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dppHin46, dppH46, Hin46
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology

Polytene chromosomes normal.

Nature of the lesion
Statement
Reference

0.3 kb molecular deletion completely confined to the dpp gene (St. Johnston et al., 1990)

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

Newly formed spectrosomes in primordial germ cells of stage 11-12 dppH46 embryos are similar in size and morphology to wild-type of the same age. In older embryos, differences are readily apparent and the spectrosomes in dppH46 primordial germ cells fall into three classes. Primordial germ cells in the first class (39%) resemble wild-type and have a single large spherical spectrosome. The second class (28%) display either small diffusely stained spectrosomes or several small fragmented spectrosomes. In the third and final class (33%), primordial germ cells have no spectrosome and can be deformed and irregular in appearance.

dppH46 mutant embryos occasionally show fusion of the embryonic denticle belts.

dppH46 exhibit a phenotype in the development of the dorsal head. The dorso-median strip of epidermis that normally separates the placodes is absent and replaced by hyperplastic placodes in stage 12 embryos.

dppH46 clones generated in the wing at 22-26 hours after pupariation (AP), using the Minute technique, have no effect on venation when they are limited to one surface of the wing. When there is overlap between dppH46 clones on the dorsal and ventral surfaces, there is no consistent cell-autonomous disruption of the posterior crossvein (PCV) within regions of overlap. However, a slight disruption of the posterior end of the PCV, largely outside the region of the clone, has been observed in one case. When overlapping clones cover the region of the fourth longitudinal vein normally intersected by the PCV, the anterior of the PCV can be disrupted.

The corpus cardiacum is normal in size in mutant embryos, but shows defects in migration.

In stage-15 dppH46 mutant embryos, the lymph gland, cardioblasts and pericardial nephrocytes fail to develop from the cardiogenic mesoderm.

The average number of crystal cells per embryo is significantly reduced in homozygous stage 13-14 embryos compared to wild type.

In dppH46 homozygotes cycle 14 mitotic domains 1 and 5 are fused across the midline, and domain 3 is absent.

Ventral denticle belts cover the whole epidermis in mutant embryos.

Head midline epidermis does not form in mutant embryos, with both midline and dorsolateral regions showing characteristics of lateral neuroectoderm. Optic lobe and Bolwig's organ are absent. The dorsal head ectoderm is "invaded" by protocerebral neuroblasts.

Homozygous clones in the wing have no effect on the posterior cross vein (PCV) unless both dorsal and ventral surfaces are homozygous ("double-sided" clones). Double-sided clones that cover half the PCV show loss of the vein in the mutant clone up to or within 2 to 3 cells of the clone boundary. Vein L4 can also be truncated in clones.

The hindgut of mutant embryos is significantly shorter than that of wild-type embryos. Incorporation of BrdU in the large intestine is abolished in mutant embryos.

Gnathal morphology is severely disrupted in mutant embryos.

The cuticle of homozygous embryos consists only of ventral epidermis. This phenotype is not altered if the embryos are derived from homozygous dl1 females. brkM68; dppH46 sna18 Df(2R)twi quadruple mutant embryos secrete cuticles showing partial transformation of ventral into dorsal epidermis.

Gonadal mesoderm development is largely unaffected in mutants. Germ cells do not migrate from endoderm to mesoderm, presumably due to the gastrulation defects.

Embryos are strongly ventralised and germ band extension is abnormal.

Fat body precursor cells do develop in dppH46 embryos.

Homozygous clones induced in first instar larvae produce abnormalities in the dorsal side of the leg. Pattern elements from the dorsal side are missing. Occasional defects in the ventral side of the leg are also seen.

Haploinsufficient.

Suppresses the majority of pattern defects caused by Pka-C1H2 clones in the wing, notum, halteres and antennae and partially suppresses defects in the ventral regions of the leg.

Dominant lethality greater than 50%. Homozygous and transheterozygous embryos were examined with respect to 25 cuticular markers, results demonstrate a graded requirement for dpp along the dorso-ventral axis.

Strong ventralised phenotype. Rings of ventral denticle belts differentiate around the entire dorsoventral axis, almost no dorsal hairs are seen and the antennal and maxillary sense organs are missing. Defective movements of the germ band: due to loss of the amnioserosa and because the dorsalmost cells have acquired the lateral fate of the dorsal ectoderm. Dorsal cell fates are deleted and ventrolateral mitotic domains are expanded.

Ventralized embryos: rings or patches of ventral denticles along dorsoventral axis. Disruption of germ band extension that leads to the invagination of posterior segments into the interior of the embryo.

Fail to complete germ band extension, die with strong ventralized phenotype and no dorsal derived epidermis.

Homozygotes have a ventralized embryonic phenotype: normally ventral epidermal pattern elements are present ventrally and dorsally.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference

dppH46 has lethal | dominant phenotype, suppressible | partially by Df(2L)Gpdh1-A/+

dppH46 has lethal | dominant phenotype, suppressible | partially by Su(dpp)YE10[+]/Su(dpp)YE10YE10

dppH46 has lethal | dominant phenotype, suppressible | partially by Su(dpp)YE12[+]/Su(dpp)YE12YE12

dppH46 has lethal | dominant phenotype, suppressible | partially by Su(dpp)YE28YE28/Su(dpp)YE28[+]

dppH46 has lethal | dominant phenotype, suppressible | partially by Su(dpp)YE31YE31/Su(dpp)YE31[+]

dppH46 has lethal | dominant phenotype, suppressible | partially by Su(dpp)YE5[+]/Su(dpp)YE5YE5

dppH46 has lethal | dominant phenotype, suppressible | partially by eIF-4a[+]/eIF4AYE9

dppH46 has lethal | dominant phenotype, suppressible | partially by Su(dpp)YE2[+]/Su(dpp)YE2YE2

NOT suppressed by
Statement
Reference

dppH46 has lethal phenotype, non-suppressible by Smurf15C

Suppressor of
Statement
Reference

dppH46/dpp[+] is a suppressor | partially of lethal | rescuable maternal effect phenotype of Smurf15C

Phenotype Manifest In
Suppressed by
Statement
Reference

dppH46 has phenotype, suppressible by Su(dpp)39CDE[+]/Su(dpp)39CDE1

NOT suppressed by
Statement
Reference

dppH46 has cuticle phenotype, non-suppressible by Smurf15C

Suppressor of
Statement
Reference

dppH46 is a suppressor | partially of leg | somatic clone phenotype of Pka-C1H2

dppH46 is a suppressor of wing | somatic clone phenotype of Pka-C1H2

dppH46 is a suppressor of scutum | somatic clone phenotype of Pka-C1H2

dppH46 is a suppressor of haltere | somatic clone phenotype of Pka-C1H2

dppH46 is a suppressor of antenna | somatic clone phenotype of Pka-C1H2

Additional Comments
Genetic Interactions
Statement
Reference

Maternal and zygotic homozygosity for lack15C partially suppresses the dominant lethality of dppH46 (83% survival to adulthood), but has no effect on the lethality or cuticle phenotypes due to homozygosity for dppH46. Embryonic lethality due to maternal and zygotic homozygosity for lack15C is partially suppressed (83% survival to adulthood) by heterozygosity for dppH46. The embryonic midgut phenotype of maternal and zygotic lack15C/lack15C embryos is fully suppressed by heterozygosity for dppH46.

The production of extra eve-positive mesodermal cells caused by expression of Ras85DG13Q.Scer\UAS under the control of Scer\GAL4unspecified is suppressed if the embryos are also carrying dppH46.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Partially rescued by

dppH46/dpps11 is partially rescued by dppSal20

dpps20/dppH46 is partially rescued by dppSal20

dpps7/dppH46 is partially rescued by dppSal20

dppH46/dpps3 is partially rescued by dppSal20

dpps28/dppH46 is partially rescued by dppSal20

dpps26/dppH46 is partially rescued by dppSal20

Not rescued by
Comments

Mutant phenotype rescued by P element mediated transformation of a wild type copy of dpp.

Allele class: Hin

Images (0)
Mutant
Wild-type
Stocks (4)
Notes on Origin
Discoverer
Comments
Comments

Previously thought to delete whole of dpp and affect other genes (ie to be in Hin-Df class), hence Df synonyms.

Based on considerations of degree of dominant lethality, dpp alleles can be placed in an allelic series. Progressing from weakest to most severe the series is: dppe87 < dppe90 < dpphr56 < dpphr4 < dpphr92 < dpphr27 < dpphr93 < dppH94 < dppH95 < dppH96 = dppH91 = dppH46.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (56)