Nucleotide substitution: T?A.
Amino acid replacement: L464term.
T16775210A
T?A
L464term | Nrt-PA; L464term | Nrt-PB; L464term | Nrt-PC
L464term
Abl1/Df(3L)st-j7, NrtM2 has lethal phenotype, suppressible | partially by Scer\GAL431/AblUAS.cFa
Abl1/Df(3L)st-j7, NrtM2 has lethal phenotype, suppressible | partially by Scer\GAL431/Abl::Hsap\ABL1::Hsap\BCRP210.UAS
Abl1/Df(3L)st-j7, NrtM2 has lethal phenotype, suppressible | partially by Scer\GAL431/Abl::Hsap\ABL1::Hsap\BCRP185.UAS
Abl1/Df(3L)st-j7, NrtM2 has lethal phenotype, suppressible | partially by Scer\GAL431/AblK417N.UAS
Abl1/Df(3L)st-j7, NrtM54/NrtM2 has abnormal neuroanatomy phenotype
Abl1/Df(3L)st-j7, NrtM2 has lethal phenotype
Abl::Hsap\ABL1::Hsap\BCRP185.UAS, Abl1/Df(3L)st-j7, NrtM2, Scer\GAL431 has visible phenotype
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Abl1/Df(3L)st-j7, NrtM2, Scer\GAL431 has visible phenotype
Abl1/Df(3L)st-j7, NrtM54/NrtM2 has larval ventral nerve cord commissure phenotype
Abl::Hsap\ABL1::Hsap\BCRP185.UAS, Abl1/Df(3L)st-j7, NrtM2, Scer\GAL431 has eye phenotype
Abl::Hsap\ABL1::Hsap\BCRP185.UAS, Abl1/Df(3L)st-j7, NrtM2, Scer\GAL431 has ommatidium phenotype
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Abl1/Df(3L)st-j7, NrtM2, Scer\GAL431 has eye phenotype
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Abl1/Df(3L)st-j7, NrtM2, Scer\GAL431 has ommatidium phenotype
Abl1/Df(3L)st-j7, NrtM2 has symmetrical commissure phenotype
Abl1/Df(3L)st-j7, NrtM2 has axon phenotype
63% of segments have commissure defects in the central nervous system of Abl1 NrtM54/NrtM2 Df(3L)st-j7 embryos.
The lethality of Abl1/NrtM2 Df(3L)st-j7 is partially rescued by AblScer\UAS.cFa or AblK417N.Scer\UAS, expressed under the control of Scer\GAL431.
faxM7 Abl1/In(3L)std11 and faxM12 Abl1/In(3L)std11 individuals are lethal due to disruptions in the CNS longitudinal and commissural axons. The presence of NrtM2 does not affect the lethality. Dosage sensitive interactions exist between NrtM2, faxM7 and faxM12. Abl+mTnabl is unable to rescue the lethality of fax- Nrt- individuals.
Abl1/Df(3L)st-j7 NrtM2 double mutant causes absence of most intersegmental longitudinal axon bundles and most commissural axon bundles. The lethality of NrtM2 Df(3L)st-j7/Abl1 animals is rescued by four copies of P{Dab.G} to almost full viability.
NrtM2 Df(3L)st-j7/In(3L)std11 double mutant embryos show muscle absences and detachments.
The lethality of Abl1/NrtM2 Df(3L)st-j7 is partially rescued by Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS or Abl::Hsap\ABL1::Hsap\BCRP185.Scer\UAS expressed under the control of Scer\GAL431.
Induced on: Df(3L)st-j7. The NrtM2 mutant allele was originally thought to be a mutation in the Dab gene (see FBrf0058531 and FBrf0084025), but sequencing of the chromosome indicates that it is a lesion in the Nrt gene.
Induced on: Df(3L)st-j7.
Complements: l(3)73Bcunspecified.
Haploinsufficiency dependent upon an Abl mutant background (HDA).