FlyBase Allele Report: Dmel\N[Ax-16]

General Information

Symbol

Dmel\N^Ax-16

Species

D. melanogaster

Name

FlyBase ID

FBal0012852

Feature type

allele

Associated gene

Dmel\N

Associated Insertion(s)

Carried in Construct

Also Known As

Ax¹⁶¹⁷², N^Ax16, Ax¹⁶, N^Ax-16172

Key Links

Allele class

gain of function allele

antimorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

antimorphic allele - genetic evidence

(de Celis and Garcia-Bellido, 1994, de Celis et al., 1991)

gain of function allele

(de Celis et al., 1997, Sotillos et al., 1997, de Celis et al., 1996)

Mutagen

ethyl methanesulfonate

Progenitor genotype

Cytology

Polytene chromosomes are normal (Foster, 1975).

Description

Amino acid replacement in the EGF-homologous regions of the extracellular domain of the N protein.

(de Celis et al., 1991)

Amino acid replacement: G1174A. Mutant partially sequenced; correlated with single amino acid replacements within six adjacent EGF-homologous elements of the N protein; has Gly at residue 2057 characteristic of Oregon R rather than Ser of Canton S (Kelley, Kidd, Deutsch and Young, 1987). Mutation involves a change from glycine to alanine in residue 1174 in EGF-like repeat 29; GGA --> AGA (Kelley, Kidd, Deutsch and Young, 1987).

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

fertile

(Go and Artavanis-Tsakonas, 1998)

increased cell number | larval stage | somatic clone

(Baonza and Garcia-Bellido, 2000)

lethal | recessive

(Go and Artavanis-Tsakonas, 1998)

lethal | recessive | heat sensitive

(Foster, 1973)

partially lethal (with N^Ax-1)

(Grushko et al., 1998)

viable

(de Celis and Bray, 2000, Grushko et al., 1998, de Celis et al., 1996)

viable (with N^Ax-71d)

(Grushko et al., 1998)

viable (with N^Ax-E2)

(Grushko et al., 1998)

visible

(Egoz-Matia et al., 2011, Kankel et al., 2007, Sotillos et al., 1997)

visible | adult stage

(Sachan et al., 2013)

visible | dominant

(Di Stefano et al., 2011, Go and Artavanis-Tsakonas, 1998)

visible | dominant | heat sensitive

(Foster, 1973)

visible | recessive

(Roch et al., 1998)

Phenotype Manifest In

Detailed Description

Statement

Reference

N^Ax-16 heterozygous adults display a significant decrease in the number of thoracic sensory bristles, as compared to controls.

(Shukla et al., 2017)

N^Ax-16 heterozygous adult females display wing vein defects: shortening of the longitudinal L5 vein.

(Sachan et al., 2013)

Heterozygotes have show truncation of the L4 and L5 wing veins.

(Di Stefano et al., 2011)

Mutant flies show loss of wing vein.

(Egoz-Matia et al., 2011)

Hemizygous males show shortening of the L4 and L5 wing veins.

(Kankel et al., 2007)

The average size of clones induced in N^Ax-M3/N^Ax-16 mutant wing discs are larger all over the wing than in wild-type controls. Clones of over 2000 cells can be seen in the mutant discs (compared to a maximum of 600 in controls). This suggests that proliferation rate in N^Ax-M3/N^Ax-16 mutant wings is higher than in controls.

(Baonza and Garcia-Bellido, 2000)

Flies show missing macrochaetae and reduced density of microchaetae. The fifth wing vein is shortened.

(Go and Artavanis-Tsakonas, 1998)

N^Ax-1/N^Ax-16 larvae have enlarged wing discs compared to wild-type. This phenotype is associated with elevated mitotic activity in the disc, particularly in the peripheral region of the wing pouch.

(Go et al., 1998)

Viable in combination with N^Ax-71d or N^Ax-E2. N^Ax-1/N^Ax-16 females have reduced viability. This viability is further reduced if the flies also carry Dp(3;3)MKRS-D2 or Dp(3;3)bxd¹¹⁰. Lethal in combination with N^Ax-9; unescaped female pupae show a strong antineurogenic phenotype.

(Grushko et al., 1998)

Wing veins are missing.

(Roch et al., 1998)

Flies show shortening of the wing veins.

(Sotillos et al., 1997)

Length of microchaetae, macrochaetae and longitudinal wing veins is reduced with respect to that of wild type. Enhances the N haplo-insufficient phenotype of loss of the wing margin.

(de Celis and Garcia-Bellido, 1994)

Lack of chaetae. N^Ax-1 and N^Ax-16 correct Hw phenotypes in both ectopic and normal positions.

(de Celis et al., 1991)

Viable, enhancer type.

(Xu et al., 1990)

Heterozygous females raised at 29^oC have significantly fewer ocellar bristles and more gaps in the longitudinal wing veins than heterozygous females raised at 22^oC. The temperature sensitive period for both phenotypes occurs during the third larval instar stage. N^Ax-16/N^264-40 females show temperature sensitive lethality. The temperature sensitive period for lethality is during the second larval instar stage.

(Foster, 1973)

Homozygotes resemble N^Ax-1. N^Ax-16 is less fertile than alleles N^Ax-E2, N^Ax-71d and N^Ax-9 (Portin, 1975) and temperature-sensitive for the bristle and wing effects of Ax (Foster, 1975). In heterozygotes with Notch, Ax is expressed and the Notch wing effect is enhanced (Foster, 1975; Portin, 1975). At 29^oC, heterozygotes with N are lethal. In N^Ax-16/N^264-40 heterozygotes, the TSP for lethality is in the second instar and for Ax-morphological effects, it is in the third instar (Foster, 1973; Foster, 1975). In heterozygotes with recessive visibles at Notch, all are complementary at 18^oC and 25^oC; at 29^oC, there are mild indications of noncomplementarity with nd and N^nd-2 (Portin, 1977). Heteroalleles N^Ax-16/N^Ax-E2 and N^Ax-16/N^Ax-71d are viable (Foster, 1975; Portin, 1975); N^Ax-16/N^Ax-E1 is inviable (negative heterosis) and heterozygotes with N^Ax-9 and N^Ax-1 are lethal (negative complementation) (Foster, 1975; Portin, 1975), but Dp(1;2)51b restores viability (Portin, 1977). Heterozygotes with the lethal alleles N^Ax-59b and N^Ax-59d are lethal and mostly inviable upon the addition of Dp(1;2)51b (Portin, 1975; Portin, 1977). On the genetic map of Notch, probably between N^264-40 and N^Co based on the failure to obtain recombinants between N^Ax-16 and N^Ax-9 (Foster, 1975).

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

N^Ax-16 has visible | dominant phenotype, enhanceable by lid[+]/Kdm5¹⁰⁴²⁴

(Di Stefano et al., 2011)

N^Ax-16 has visible phenotype, enhanceable by f06222^f06222/f06222[+]

(Kankel et al., 2007)

N^Ax-16 has visible phenotype, enhanceable by klu^d00059/klu[+]

(Kankel et al., 2007)

N^Ax-16 has visible phenotype, enhanceable by GPHR^c06331/CG8090[+]

(Kankel et al., 2007)

N^Ax-1/N^Ax-16 has partially lethal phenotype, enhanceable by Dp(3;3)MKRS-D2

(Grushko et al., 1998)

N^Ax-1/N^Ax-16 has partially lethal phenotype, enhanceable by Dp(3;3)bxd¹¹⁰

(Grushko et al., 1998)

Suppressed by

Statement

Reference

N^Ax-16 has visible | adult stage phenotype, suppressible by Kap-α3^D93

(Sachan et al., 2013)

N^Ax-16 has visible | adult stage phenotype, suppressible by Kap-α3^D165

(Sachan et al., 2013)

N^Ax-16 has visible | adult stage phenotype, suppressible by Kap-α3^S033513

(Sachan et al., 2013)

N^Ax-16 has visible | dominant phenotype, suppressible by Su(var)3-3[+]/Su(var)3-3^ΔN

(Di Stefano et al., 2011)

N^Ax-16 has visible phenotype, suppressible by sca[+]/sca^d09400

(Kankel et al., 2007)

N^Ax-16 has visible phenotype, suppressible by A122^A122

(Go and Artavanis-Tsakonas, 1998)

N^Ax-16 has visible phenotype, suppressible by kuz^1405Rev11

(Sotillos et al., 1997)

Suppressor of

Statement

Reference

N^Ax-16/N[+] is a suppressor | partially of visible | heat sensitive phenotype of Dcr-2^UAS.cDa, Eogt^GD5084, Scer\GAL4^en.PU

(Müller et al., 2013)

Other

Statement

Reference

Dp(3;3)MKRS-D2, N^Ax-16 has partially lethal phenotype

(Grushko et al., 1998)

Dp(3;3)bxd¹¹⁰, N^Ax-16 has partially lethal phenotype

(Grushko et al., 1998)

Phenotype Manifest In

Enhanced by

Statement

Reference

N^Ax-16 has wing vein phenotype, enhanceable by lid[+]/Kdm5¹⁰⁴²⁴

(Di Stefano et al., 2011)

N^Ax-16 has wing vein L4 phenotype, enhanceable by klu^d00059/klu[+]

(Kankel et al., 2007)

N^Ax-16 has wing vein L5 phenotype, enhanceable by klu^d00059/klu[+]

(Kankel et al., 2007)

N^Ax-16 has wing vein L4 phenotype, enhanceable by GPHR^c06331/CG8090[+]

(Kankel et al., 2007)

N^Ax-16 has wing vein L5 phenotype, enhanceable by GPHR^c06331/CG8090[+]

(Kankel et al., 2007)

N^Ax-16 has wing vein L4 phenotype, enhanceable by f06222^f06222/f06222[+]

(Kankel et al., 2007)

N^Ax-16 has wing vein L5 phenotype, enhanceable by f06222^f06222/f06222[+]

(Kankel et al., 2007)

Suppressed by

Statement

Reference

N^Ax-16 has mechanosensory chaeta | adult stage phenotype, suppressible by Rbfox1^RNAi.UAS/Scer\GAL4^sca-109-68

(Shukla et al., 2017)

N^Ax-16 has wing vein L5 phenotype, suppressible by Kap-α3^D93

(Sachan et al., 2013)

N^Ax-16 has wing vein L5 phenotype, suppressible by Kap-α3^D165

(Sachan et al., 2013)

N^Ax-16 has wing vein L5 phenotype, suppressible by Kap-α3^S033513

(Sachan et al., 2013)

N^Ax-16 has wing vein phenotype, suppressible by Su(var)3-3[+]/Su(var)3-3^ΔN

(Di Stefano et al., 2011)

N^Ax-16 has wing vein L4 phenotype, suppressible by sca[+]/sca^d09400

(Kankel et al., 2007)

N^Ax-16 has wing vein phenotype, suppressible by M285^M285

(Go and Artavanis-Tsakonas, 1998)

N^Ax-16 has macrochaeta phenotype, suppressible by M285^M285

(Go and Artavanis-Tsakonas, 1998)

N^Ax-16 has microchaeta phenotype, suppressible by M285^M285

(Go and Artavanis-Tsakonas, 1998)

N^Ax-16 has wing vein phenotype, suppressible by A122^A122

(Go and Artavanis-Tsakonas, 1998)

N^Ax-16 has macrochaeta phenotype, suppressible by A122^A122

(Go and Artavanis-Tsakonas, 1998)

N^Ax-16 has microchaeta phenotype, suppressible by A122^A122

(Go and Artavanis-Tsakonas, 1998)

N^Ax-16 has phenotype, suppressible by bs⁰³²⁶⁷

(Roch et al., 1998)

N^Ax-16 has wing vein phenotype, suppressible by kuz^1405Rev11

(Sotillos et al., 1997)

NOT suppressed by

Statement

Reference

N^Ax-16 has wing vein L5 phenotype, non-suppressible by sca[+]/sca^d09400

(Kankel et al., 2007)

Suppressor of

Statement

Reference

N^Ax-16/N[+] is a suppressor | partially of wing blade posterior compartment | heat sensitive phenotype of Dcr-2^UAS.cDa, Eogt^GD5084, Scer\GAL4^en.PU

(Müller et al., 2013)

Additional Comments

Genetic Interactions

Statement

Reference

The decreased number of thoracic sensory bristles present in N^Ax-16 heterozygous adults is suppressed by the expression of Rbfox1^{dsRNA.Scer\UAS} under the control of Scer\GAL4^sca-109-68.

(Shukla et al., 2017)

The wing blistering phenotype seen in the posterior compartment of wings in flies expressing Eogt^GD5084 under the control of Scer\GAL4^en.PU in the presence of Dcr-2^Scer\UAS.cDa is dominantly partially suppressed if the flies are also heterozygous for N^Ax-16.

(Müller et al., 2013)

The shortened longitudinal L5 phenotype characteristic for N^Ax-16 heterozygous females is suppressed by combination with a single copy of any of the following alleles: Kap-α3^D93, Kap-α3^D165 or Kap-α3^S033513.

(Sachan et al., 2013)

The wing vein truncation phenotype which is seen in N^Ax-16/+ flies is suppressed by Su(var)3-3^ΔN/+.

The wing vein truncation phenotype which is seen in N^Ax-16/+ flies is enhanced by lid¹⁰⁴²⁴/+.

(Di Stefano et al., 2011)

sca^d09400 suppresses the wing vein L4 but not the wing vein L5 phenotypes of N^Ax-16 hemizygous males.

klu^d00059, CG8090^c06331 or f06222^f06222 enhance the L4 and L5 wing vein shortening phenotypes of N^Ax-16 hemizygous males.

(Kankel et al., 2007)

Homozygous viability is decreased if the flies also carry Dp(3;3)MKRS-D2 or Dp(3;3)bxd¹¹⁰. The antineurogenic phenotype of N^Ax-16/N^Ax-9 female escapers is enhanced in the presence of Dp(3;3)MKRS-D2 or Dp(3;3)bxd¹¹⁰.

(Grushko et al., 1998)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

N^Ax-9

(Go and Artavanis-Tsakonas, 1998)

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

52014

y¹ w^* N^Ax-16

Notes on Origin

Discoverer

Lewis & Bacher.

Comments

N^Ax-16 shows negative complementation with N^Ax-M1.

(de Celis and Garcia-Bellido, 1994)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

Ax¹⁶¹⁷²

(Egoz-Matia et al., 2011, Baonza and Garcia-Bellido, 2000, Baonza et al., 2000, de Celis and Bray, 2000, Garoia et al., 2000, Grushko et al., 1998, Roch et al., 1998, de Celis et al., 1997, Sotillos et al., 1997, de Celis et al., 1996, Gomez-Skarmeta and Modolell, 1996, de Celis and Garcia-Bellido, 1994, de Celis et al., 1993, de Celis et al., 1991, Xu et al., 1990, Foster, 1973)

Ax¹⁶

(Di Stefano et al., 2011, Go and Artavanis-Tsakonas, 1998, Go et al., 1998)

N^Ax-16172

(Sachan et al., 2015, Sachan et al., 2013)

N^Ax-16

N^Ax16

(Shukla et al., 2017, Müller et al., 2013, Kankel et al., 2007)

Name Synonyms

Secondary FlyBase IDs

References (28)

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