FB2021_06, released December 14, 2021

Allele: Dmel\twi1

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General Information
Symbol
Dmel\twi1
Species
D. melanogaster
Name
FlyBase ID
FBal0017297
Feature type
allele
Associated gene
Dmel\twi
Associated Insertion(s)
Carried in Construct
Also Known As
twiID96, twiID, twi1096, twi1D96, twist1
Key Links
Allele class

loss of function allele

amorphic allele - genetic evidence

hypomorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

amorphic allele - genetic evidence

(Reuter et al., 1993, Arora and Nusslein-Volhard, 1992, Michelson et al., 1990)

hypomorphic allele - genetic evidence

(Reuter et al., 1993)

loss of function allele

(Morize et al., 1998, Prokop et al., 1996)
Mutagen
ethyl methanesulfonate
(Tearle and Nusslein-Volhard, 1987, Simpson, 1983)
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
       
      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 )
       
      Disease-implicated variant(s)
       
      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.

      (Park et al., 2011)

      Mutant embryos form tracheal dorsoventral structures reminiscent of dorsal branches that elongate and undergo stalk-cell intercalation.

      (Caussinus et al., 2008)

      22% of twi1/+ flies show defects in TDT organization but all twi1/+ flies show a wild-type number of DLM fibers.

      (Lovato et al., 2005)

      Invagination of the keyhole cells still occurs during proventriculus development.

      (Josten et al., 2004)

      The hindguts of mutant embryos are able to undergo a significant amount of elongation.

      (Johansen et al., 2003)

      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.

      (Castanon et al., 2001)

      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.

      (San Martin and Bate, 2001)

      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.

      (Franch-Marro and Casanova, 2000)

      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.

      (Jack and Myette, 1999)

      Embryos develop a twisted phenotype.

      (Misquitta and Paterson, 1999)

      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.

      (Prokop et al., 1996)

      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.

      (Tepass and Hartenstein, 1994)

      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.

      (Edwards et al., 1993)

      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.

      (Reuter et al., 1993)

      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.

      (Younossi-Hartenstein and Hartenstein, 1993)

      Homozygous embryos do not form a ventral furrow. Mesectodermal domain is shifted ventrally.

      (Arora and Nusslein-Volhard, 1992)

      Interacts with RpII140wimp maternal effect.

      (Parkhurst and Ish-Horowicz, 1991)

      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.

      (Ray et al., 1991)

      No changes in phenotype of tor13D embryos.

      (Strecker et al., 1991)

      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.

      (Leptin and Grunewald, 1990)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      NOT Enhancer of
      Statement
      Reference

      twi1 is a non-enhancer of lethal | maternal effect | embryonic stage phenotype of Gugunspecified

      (Zhang et al., 2002)
      Other
      Statement
      Reference

      dl1, twi1/twi[+] has lethal phenotype

      (Wrischnik et al., 2003)

      dl1, twi1/twi[+] has lethal | dominant phenotype

      (Wrischnik et al., 2003)

      dl[+]/dl1, twi1 has lethal phenotype

      (Wrischnik et al., 2003)

      dl[+]/dl1, twi1 has lethal | dominant phenotype

      (Wrischnik et al., 2003)
      Phenotype Manifest In
      Enhanced by
      Suppressed by
      Statement
      Reference

      twi1 has ventral furrow phenotype, suppressible | partially by foghs.PM

      (Morize et al., 1998)
      Enhancer of
      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%).

      (Nowak et al., 2012)

      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.

      (Lovato et al., 2005)

      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.

      (Wrischnik et al., 2003)

      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.

      (Castanon et al., 2001)

      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.

      (Castanon et al., 2001)

      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.

      (Morize et al., 1998)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      twi1 is rescued by Scer\GAL4twi.PB/twiUAS.cBa

      (Castanon et al., 2001)
      Partially rescued by

      twi1 is partially rescued by twi2x.UAS/Scer\GAL4twi.PB

      (Castanon et al., 2001)
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (2)
      Notes on Origin
      Discoverer

      C. Nusslein-Volhard.

      (Simpson, 1983)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (10)
      Reported As
      Symbol Synonym
      twi1096
      (Martin-Bermudo and Brown, 2000, Edgar et al., 1994)
      twi1
      (Irizarry et al., 2020, Trébuchet et al., 2019, Kahsai and Cook, 2018, Tevy et al., 2014, Nowak et al., 2012, Kuzin et al., 2011, Park et al., 2011, Salzer et al., 2010, Christensen et al., 2009.2.28, Caussinus et al., 2008, Christensen et al., 2008.12.28, Lovato et al., 2005)
      twi1D96
      (Tepass and Hartenstein, 1994, Raz and Shilo, 1992)
      twi1D
      (Mellerick and Nirenberg, 1995)
      twiID96
      (Nowak et al., 2012, Bai et al., 2007, Biemar et al., 2005, Ganguly et al., 2005, Josten et al., 2004, Tapanes-Castillo and Baylies, 2004, Castanon et al., 2001, San Martin and Bate, 2001, Franch-Marro and Casanova, 2000, Taylor, 2000, Pham et al., 1999, Morize et al., 1998, Oda et al., 1998, Becker et al., 1997, Prokop et al., 1996, Bronner et al., 1995, Raghu and Hasan, 1995, Taylor et al., 1995, Wimmer et al., 1995, Costa et al., 1994, Graba et al., 1994, Lilly et al., 1994, Nguyen et al., 1994, Edwards et al., 1993, Gonzalez-Crespo and Levine, 1993, Shishido et al., 1993, Winick et al., 1993, Parkhurst and Ish-Horowicz, 1991, Ray et al., 1991, Strecker et al., 1991, Bodmer et al., 1990, Leptin and Grunewald, 1990, Michelson et al., 1990, Simpson, 1983)
      twiID
      (Ismat et al., 2010, Gao et al., 1996, Lord et al., 1995, Costa et al., 1993, Reuter et al., 1993, Younossi-Hartenstein and Hartenstein, 1993, Arora and Nusslein-Volhard, 1992, Leptin, 1991, Tearle and Nusslein-Volhard, 1987)
      twist1096
      (Misquitta and Paterson, 1999)
      twist1
      (Manning et al., 2013, Sandmann et al., 2007)
      twistID96
      (Großhans and Wieschaus, 2000)
      Name Synonyms
      twistID96
      (Ruiz-Gomez et al., 2002)
      Secondary FlyBase IDs
        References (72)