Open Close
General Information
Symbol
Dmel\pydB12
Species
D. melanogaster
Name
FlyBase ID
FBal0285508
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Mutagen
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
deletion
Comment:
Deletion of all but the distant upstream exons of pyd resulting from FLP-catalyzed recombination using the FRT-containing transposons P{RS5}CG83795-HA-1806 and PBac{WH}pydf05901.
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
FLP-mediated site-specific recombination between P{RS5}CG83795-HA-1806 and PBac{WH}pydf05901 generates a 37kb genomic deletion that eliminates the coding sequence of all known and predicted pyd isoforms and also deletes an adjacent locus, CG8379.
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
Homozygous pydB12 and transheterozygous pydB12/Df(3R)p-XT103 flies are adult viable, with slightly reduced zygotic viability (23-24% of progeny, as opposed to 33% expected). These zygotic mutant adults exhibit bristle defects and rough eyes. Viability of the progeny of pydB12 homozygous mothers is strongly compromised, with mutant animals achieving adulthood at 1-23% of the expected number. Maternal and zygotic pydB12 mutant embryos display 60% embryonic lethality. These embryos exhibit a set of cuticle defects consistent with a failure in head involution and minor defects in dorsal closure. Maternal and zygotic pydB12 mutant embryos can assemble and maintain adherens junctions and assemble a leading edge actomyosin cable. Substantial embryonic lethality (43-58%) is found in flies from pydex147 mothers crossed with pydB12 fathers. The ventral epidermis is intact in pydB12/pydex147 maternal/zygotic mutant embryos and the CNS is not obviously hypertrophied. While approximately 17% of pydB12/pydex147 maternal/zygotic mutant embryos appear wild-type, most mutant embryos (64%) exhibit defects in head involution that result in defective head skeletons, whereas the most severe (19%) display complete failure of head involution, leading to a hole in the cuticle. In addition, some show minor defects in dorsal closure. Dorsal openings in embryos both maternally and zygotically mutant for pydB12 are often oval-shaped, as opposed to 'eye-shaped' as in wild-type. In some cases, failure of the head involution process results in zippering at the anterior canthus being prevented. In extreme cases, zippering at the posterior end seems largely or completely blocked, whereas in others it is simply slowed substantially. Although in most cases dorsal closure is eventually completed, cell shapes often remain quite irregular even when the two sheets meet, with small regions where the sheets do not seal still evident. In a subset of embryos, dorsal closure fails and amnioserosal apoptosis leaves a large hole on the dorsal surface. Dorsal closure in maternal and zygotic pydB12 mutant embryos is significantly slower (>50%) than in wild-type embryos. Maternal and zygotic pydB12 mutant embryos appear indistinguishable from wild-type through germband retraction. In a subset of mutants, all the cell shape changes associated with dorsal closure proceed in an essentially wild-type manner. However a substantial majority of mutant embryos exhibit defects in cell shape changes in the epidermis. By stage 13, some leading edge cells exhibit very narrow leading edges, suggestive of excess constriction of the leading edge actin cable, whereas in others the leading edge is broader, consistent with disruption of the leading edge actin cable. As closure proceeded, these cell shape defects became more widespread. The leading edge of the epidermis was often wavy, and leading edge cells varied from hyperconstricted to broadened at the leading edge. In addition, groups of cells in the lateral epidermis sometimes fail to change shape at all. These mutants are still able to assemble an actin cable at their leading edge at the onset of dorsal closure, despite defects in cell shape. Myosin is also assembled into the leading edge cable in maternal and zygotic pydB12 mutant embryo. The cable is maintained in many cells as closure proceeds and remains localised to the leading edge even in mutants in which the dorsal opening is highly abnormal in shape. At the end of dorsal closure, pydB12 maternal/zygotic mutant embryos retain very deep segmental grooves, extending deep into the embryo both dorsally and ventrally. This defect can be seen as early as the onset of dorsal closure (at this stage wild-type groves have begun to become shallower) and still extend all the way to the leading edge. These grooves remain abnormally deep through to the end of closure, both in embryos in which closure goes to completion and in those in which it fails completely. The ventral epidermis is intact in pydB12 maternal/zygotic mutant embryos and the CNS is not obviously hypertrophied. While approximately 8% of pydB12 maternal/zygotic mutant embryos apear wild-type, most mutant embryos (69%) exhibit defects in head involution that result in defective head skeltons, whereas the most severe (23%) display complete failure of head involution, leading to a hole in the cuticle. In addition, some show minor defects in dorsal closure. Maternal and zygotic mutant progeny of mothers heteroallelic for pydB12 and Df(3R)p-XT103 die as embryos, in contrast to embryos zygotically mutant for pyd (pydB12 or Df(3R)p-XT103) but maternally wild-type, which are embryonic viable. Substantial embryonic lethality (43-58%) is found in flies from pydex147 or pydex180 mothers crossed with pydB12 fathers. Zygotic pydB12 mutants exhibit defects in tracheal development, such as dorsal branch fusion failures and ectopic fusions between neighbouring dorsal branches. Some dorsal branches in pydB12 mutant embruos have more than one terminal cell. Approximately 60% of zygotic pydB12 mutants have severe fusion defects. Elimination of maternal pydB12 further increases the frequency and severity of dorsal branch defects, with 100% of pydB12 maternal+zygotic mutant embryos exhibiting severe dorsal branch defects. Embryos that are maternally and zygotically mutant for pydB12 exhibit highly convoluted trachea.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference
pyd[+]/pydB12 is an enhancer of cell shape defective phenotype of ena23
Phenotype Manifest In
Enhanced by
Statement
Reference
pydB12 has embryo | dorsal closure stage phenotype, enhanceable by ena23/ena[+]
pydB12 has embryonic leading edge cell phenotype, enhanceable by ena23/ena[+]
pydB12 has ventral head epidermis phenotype, enhanceable by ena23/ena[+]
pydB12 has embryonic head phenotype, enhanceable by ena23/ena[+]
Enhancer of
Statement
Reference
pyd[+]/pydB12 is an enhancer of embryo | dorsal closure stage phenotype of ena23
pyd[+]/pydB12 is an enhancer of embryonic leading edge cell phenotype of ena23
pyd[+]/pydB12 is an enhancer of ventral head epidermis phenotype of ena23
pyd[+]/pydB12 is an enhancer of embryonic head phenotype of ena23
Additional Comments
Genetic Interactions
Statement
Reference
Reducing pyd levels, through a pydB12 heterozygous background, strongly enhances the morphogenesis defects found in zygotic ena23 mutants, substantially increasing the frequency of failure of head involution. Reducing ena levels, through an ena23 heterozygous background, substantially enhances the severity of the pydB12 zygotic/maternal phenotype; more than one-third of the mutants exhibit large holes in the cuticle, suggesting disruption of epithelial integrity.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (1)