Amino acid replacement: R531term.
Mutation results in premature termination before the ZF DNA-binding domain.
Nucleotide substitution: C?T.
C11258220T
R531term | ab-PA; R521term | ab-PB; R521term | ab-PD; R521term | ab-PF
The amino acid position of the mutation is reported with respect to ab-PA.
wing vein L5 (with ab1)
Heterozygotes show an increase in wing size compared to controls.
abclu-1 homozygotes and abclu-1/abk02807 transheterozygotes hatch and grow normally until 30 hours AEL. The ddaE neurons of abclu-1/abk02807 and abclu-1 larvae do not display such a comb-like design of dendritic arbors as wild-type ddaE neurons. Instead, mutant neurons produce supernumerary terminals that do not necessarily show oriented growth. About 20% of mutant ddaE cells do not extend lateral primary branches and in extreme cases, a single mutant ddaE extends two primary branches dorsally instead. Time-lapse recording of mutant ddaE shows that secondary branches appear with curved morphology and remain associated with fine higher-order branches that are oriented in dorsal and ventral directions. Ventral class I ventral posterior da (vpda) neurons also show dendritic pattern defects.
ddaD and ddaE abclu-1 mutant neuron clones in heterozygous mature larvae take on an abnormal shape abd produce branch terminals in excess. The ddaD neuron shows a statistically significant increase in the dendritic arbor area size while the area size of ddaE neurons is not significantly different. Class II, III and IV neuron clones do not show dendritic pattern defects.
During embryogenesis the SNb axons pause at the edge of muscle 13 and form abnormal branches, instead of forming their wild type axonal extensions onto the muscle fibers. These aberrant branches wander over the prospective target muscles and occasionally form connections at ectopic sites. Mutants do not establish the three branched terminal arbor on muscles 7, 6, 13 and 12. The transverse nerve is often incomplete and invades the ventral muscle field. A few muscles (3, 5, 11, 20) show variably penetrant defects in their attachment to the epidermis, and variable defects in the location of their attachments. The muscle detachment phenotype of other strong alleles is not evident in abclu-1. ab1/abclu-1 heterozygotes show wing vein L5 failing to reach the margin of the wing.
Segmental nerve b fails to make some or all of its stereotyped connections in most segments. CNS development is normal. Ectopic arborization over the ventral muscles from the transverse nerve is often observed: possibly a secondary effect of the failure of segmental nerve b axons to synapse onto their correct targets.
ab1/abclu-1 is a suppressor | partially of some die during P-stage phenotype of mir-125KO.C, mir-let7KO.C
abclu-1 is rescued by Scer\GAL4pk-IG1-1/abUAS.L.cSa
abk02807/abclu-1 is rescued by Scer\GAL4pk-IG1-1/abUAS.L.cSa
abk02807/abclu-1 is rescued by abUAS.S.cSa/Scer\GAL4pk-IG1-1