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General Information
Symbol
Dmel\twi1
Species
D. melanogaster
Name
FlyBase ID
FBal0017297
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
twiID96, twiID, twi1096, twi1D96, twist1
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
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
The gl-positive corpora cardiaca precursor cells are missing in stage 12 mutant embryos.
Mutant embryos form tracheal dorsoventral structures reminiscent of dorsal branches that elongate and undergo stalk-cell intercalation.
22% of twi1/+ flies show defects in TDT organization but all twi1/+ flies show a wild-type number of DLM fibers.
Invagination of the keyhole cells still occurs during proventriculus development.
The hindguts of mutant embryos are able to undergo a significant amount of elongation.
Homozygous mutants completely lack somatic musculature. The addition of twi2x.Scer\UAS driven by Scer\GAL4twi.PB to homozygous twi1 leads to animals in which somatic muscles form but with an aberrant pattern. Visceral muscle progenitors are missing as well as the majority of both pericardial and cardial heart cells. Instead multinucleated somatic muscles are found dorsally where the heart normally develops and around the gut.
Hindgut ectoderm fails to elongate properly (germband retraction fails), but forms and expresses wg and D in restricted domains, as for wild type case, even though mesoderm is lacking.
In mutant embryos, formation of the tracheal tree is severely perturbed: there is no dorsal trunk and there is only some development of dorsal and ventral branches.
Malpighian tubules arrest early in their morphogenesis in homozygous embryos. The tubules are spherical at stages 16 and 17 (when they are elongated in wild-type embryos) and have more cells than recently evaginated tubules. The tip cells are present. The hindgut is apparently normal, although it is contorted due to the twistings of the mutant embryo.
Embryos develop a twisted phenotype.
Motor axons grow out of the CNS even though it is drastically malformed. In each hemisegment the nerves form a major dorsally projecting branch and in 39% cases a minor laterally projecting branch. The axons stay close together until the branch opens up at the dorsalmost tip, where there is some short range defasciculation. Active zones can be detected along the nerves.
The endoderm becomes internalized during gastrulation, but does not form an epithelium. Heterozygous twi1 embryos from heterozygous dl1 mothers lack various amounts of mesoderm in a temperature-dependent manner. Gaps in the visceral mesoderm are correlated with gaps in the overlying midgut epithelium.
Embryos lack mesodermal derivatives and die after about 24 hours. CNS develops but at the time of death lacks a smooth sheath of neural lamella, instead the surface is entirely pebbled in texture.
In spite of normal AMG and PMG invagination, neither anterior nor posterior midgut primordia shows any sign of extension towards each other, but remain as large mesenchymal cell masses immersed in yolk at the ends of the embryo. The cells of these primordia fail to arrange into an epithelium.
Somatic muscles absent. Majority of sensory nerves form normally, though incidence of misrouted axons is significantly increased, elongation of axons is slowed and sensory neurons which fail to send out an axon are frequent. These defects are seen most strongly in trh1, twi1 double mutants where neither trachea nor muscles are present.
Homozygous embryos do not form a ventral furrow. Mesectodermal domain is shifted ventrally.
Interacts with RpII140wimp maternal effect.
Dorsalized embryos: all cuticle cells along the dorsoventral axis behave like dorsal cells of the wild type embryo. zen expression pattern refines at stage 5, dpp pattern does not refine at all, twi and sna are expressed during late stages of embryogenesis.
No changes in phenotype of tor13D embryos.
Small ventral furrows (consisting of 8-10 cells) are seen in twi1 mutant embryos. They are often quite deep and long and always run along the ventral midline. By the end of germ band extension the furrow flattens out again and forms a continuous epithelium with the ectoderm. Two deep folds form where the dorsal ectoderm and neuroectoderm meet.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Enhancer of
Statement
Reference
Other
Statement
Reference
dl1, twi1/twi[+] has lethal phenotype
dl1, twi1/twi[+] has lethal | dominant phenotype
dl[+]/dl1, twi1 has lethal phenotype
Phenotype Manifest In
Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
twi1 has ventral furrow phenotype, suppressible | partially by foghs.PM
Enhancer of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference
twi1/+ results in disruption of the somatic muscle pattern when in double heterozygous combination with one of the following (% of stage 16 embryos with missing, misattached or duplicated muscles in at least 2 hemisegments is given in parentheses): akirinEP906 (18.1%), akirinKG01343 (21.6%) or brmI21 (23%).
There is a significant reduction in the number of DLM fibers in brnpr-3/+; twi1/+ double mutants (5.8 fibers vs 6 in wild type) and an even greater reduction in brnpr-3/+; twi1/+, Mef2P544/+ triple mutants (5.2 fibers). However, no such reduction is seen in twi1/+; Mef2P544/+ double mutants. twi1/+, Mef2P544/+ double heterozygotes display higher levels of defects in TDT organization than either single heterozygote. 82% of brnpr-3/+; twi1/+, Mef2P544/+ triple mutants show defects in TDT patterning (a higher level than any of the double mutant combinations), including additional small cells, internal fibers and the rerouting of some fibers to the periphery.
95% of twi1/+; dl1/+ animals raised at 18oC survive to adulthood whereas only 0.6% of those raised at 25oC do. This temperature sensitive lethality is not significantly affected by the presence or absence of scM6/+ or sc+t.XSE.
When twi1/+ is added to daScer\UAS.cGa, Scer\GAL4twi.PB embryos, a dramatic suppression of somatic muscle fate. No increase in other mesodermal tissues is seen.
When twi1/+ is added to daScer\UAS.cGa, Scer\GAL4twi.PB embryos, there is a dramatic suppression of somatic muscle fate. No increase in other mesodermal tissues is seen.
Heat-induced foghs.PM expression rescues ventral furrow formation, though the furrow is narrower than that formed in wild-type embryos subjected to ectopic fog expression.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
C. Nusslein-Volhard.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (10)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (71)