Allele 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
Also Known As	Ax¹⁶¹⁷², Ax¹⁶

Allele class	antimorphic allele - genetic evidence, gain of function allele
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03
FB2013_02
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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., 1996, de Celis et al., 1997, Sotillos et al., 1997)
Mutagen	ethyl methanesulfonate
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference 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).
Cytology	Polytene chromosomes are normal (Foster, 1975).
Phenotypic Data
Phenotypic Class
	fertile (Go and Artavanis-Tsakonas, 1998) lethal \| partially (with N^Ax-1) (Grushko et al., 1998) lethal \| recessive (Go and Artavanis-Tsakonas, 1998) lethal \| recessive \| heat sensitive (Foster, 1973) viable (de Celis et al., 1996, Grushko et al., 1998, de Celis and Bray, 2000) viable (with N^Ax-71d) (Grushko et al., 1998) viable (with N^Ax-E2) (Grushko et al., 1998) viable \| reduced (with N^Ax-1) (Grushko et al., 1998) visible (Sotillos et al., 1997, Kankel et al., 2007, Egoz-Matia et al., 2011) visible \| dominant (Go and Artavanis-Tsakonas, 1998, Di Stefano et al., 2011) visible \| dominant \| heat sensitive (Foster, 1973) visible \| recessive (Roch et al., 1998)
Phenotype Manifest In
	macrochaeta (Go and Artavanis-Tsakonas, 1998, de Celis and Garcia-Bellido, 1994) microchaeta (Go and Artavanis-Tsakonas, 1998, de Celis and Garcia-Bellido, 1994) ocellar bristle \| heat sensitive (Foster, 1973) wing (Baonza and Garcia-Bellido, 2000) wing disc (Go et al., 1998) wing vein (Sotillos et al., 1997, de Celis and Garcia-Bellido, 1994, Roch et al., 1998, Egoz-Matia et al., 2011) wing vein \| heat sensitive (Foster, 1973) wing vein L4 (Kankel et al., 2007, Di Stefano et al., 2011) wing vein L5 (Go and Artavanis-Tsakonas, 1998, Kankel et al., 2007, Di Stefano et al., 2011)
Detailed Description
	Statement Reference 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) 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) Flies show missing macrochaetae and reduced density of microchaetae. The fifth wing vein is shortened. (Go and Artavanis-Tsakonas, 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 the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference N^Ax-1/N^Ax-16 has lethal \| partially phenotype, enhanceable by Dp(3;3)bxd¹¹⁰ (Grushko et al., 1998) N^Ax-1/N^Ax-16 has lethal \| partially phenotype, enhanceable by Dp(3;3)MKRS-D2 (Grushko et al., 1998) N^Ax-16 has visible \| dominant phenotype, enhanceable by lid[+]/lid¹⁰⁴²⁴ (Di Stefano et al., 2011) N^Ax-16 has visible phenotype, enhanceable by CG8090^c06331/CG8090[+] (Kankel et al., 2007) 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)
Suppressed by
Statement Reference 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 \| partially by kuz^1405Rev11 (Sotillos et al., 1997) N^Ax-16 has visible phenotype, suppressible \| partially by sca[+]/sca^d09400 (Kankel et al., 2007) N^Ax-16 has visible phenotype, suppressible by A122^A122 (Go and Artavanis-Tsakonas, 1998)
Other
Statement Reference Dp(3;3)bxd¹¹⁰, N^Ax-16 has viable \| reduced phenotype (Grushko et al., 1998) Dp(3;3)MKRS-D2, N^Ax-16 has viable \| reduced phenotype (Grushko et al., 1998)
Phenotype Manifest In
Enhanced by
Statement Reference N^Ax-16 has wing vein L4 phenotype, enhanceable by CG8090^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 L4 phenotype, enhanceable by klu^d00059/klu[+] (Kankel et al., 2007) N^Ax-16 has wing vein L5 phenotype, enhanceable by CG8090^c06331/CG8090[+] (Kankel et al., 2007) N^Ax-16 has wing vein L5 phenotype, enhanceable by f06222^f06222/f06222[+] (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 phenotype, enhanceable by lid[+]/lid¹⁰⁴²⁴ (Di Stefano et al., 2011)
Suppressed by
Statement Reference N^Ax-16 has macrochaeta phenotype, suppressible by A122^A122 (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 A122^A122 (Go and Artavanis-Tsakonas, 1998) N^Ax-16 has microchaeta phenotype, suppressible by M285^M285 (Go and Artavanis-Tsakonas, 1998) N^Ax-16 has phenotype, suppressible by bs⁰³²⁶⁷ (Roch et al., 1998) 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 \| partially by kuz^1405Rev11 (Sotillos et al., 1997) N^Ax-16 has wing vein phenotype, suppressible by A122^A122 (Go and Artavanis-Tsakonas, 1998) N^Ax-16 has wing vein phenotype, suppressible by M285^M285 (Go and Artavanis-Tsakonas, 1998) N^Ax-16 has wing vein phenotype, suppressible by Su(var)3-3[+]/Su(var)3-3^ΔN (Di Stefano et al., 2011)
NOT suppressed by
Statement Reference N^Ax-16 has wing vein L5 phenotype, non-suppressible by sca[+]/sca^d09400 (Kankel et al., 2007)
Additional Comments
Genetic Interactions
Statement Reference 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 lid[10424]/+. (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 & Rescue Data
Fails to complement	N^Ax-9 (Go and Artavanis-Tsakonas, 1998)
Comments
Stocks ( 0 )

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 & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 4 )
Reported As
Symbol Synonym	Ax¹⁶ (Go and Artavanis-Tsakonas, 1998, Go et al., 1998, Di Stefano et al., 2011) Ax¹⁶¹⁷² (Garoia et al., 2000, Baonza et al., 2000, Baonza and Garcia-Bellido, 2000, de Celis and Bray, 2000, Roch et al., 1998, Grushko et al., 1998, Sotillos et al., 1997, de Celis et al., 1997, Gomez-Skarmeta and Modolell, 1996, de Celis et al., 1996, de Celis et al., 1991, de Celis and Garcia-Bellido, 1994, de Celis et al., 1993, Xu et al., 1990, Foster, 1973, Egoz-Matia et al., 2011) N^Ax-16 N^Ax16 (Kankel et al., 2007)
Name Synonym
Secondary FlyBase IDs

References ( 24 )

Generate a list of	All references relating to this allele ( 24 )

List References by type	Research paper ( 24 )
Recent research papers ( 2 )
	Di Stefano et al., 2011, Genes Dev. 25(1): 17--28 Functional antagonism between histone H3K4 demethylases in vivo. [FBrf0212709] Egoz-Matia et al., 2011, Dev. Biol. 351(1): 99--109 Spatial regulation of cell adhesion in the Drosophila wing is mediated by Delilah, a potent activator of βPS integrin expression. [FBrf0213026] Show all research papers ...

Allele Dmel\NAx-16

Allele Dmel\N^Ax-16