Mutations in the transcription unit.
Lesion mapped to: 54-56 kb.
gonad & parasegment 10
gonad & parasegment 11
gonad & parasegment 12
abd-AMX1 mutant embryos show a significant increase in the proportion of mitotic neuroblast daughter cells, but not of mitotic neuroblasts, only in the A5 ventral nerve cord segment, as compared to controls.
abd-AMX1 embryos show reduced heart lumen size, reduced ostia cell size and ostia cells are rounder, losing their characteristic elongated shape.
Abdominal hemisegments of abd-AMX1 mutant embryos do not show an increase in glial progeny, but generate ectopic neurons in the dorsal lateral cortex owing to homeotic transformation of NB6-4a to NB6-4t (in 100% of hemisegments).
abd-AMX1 mutants are still able to form seven pairs of alary muscles along the cardiac tube, as in wild-type.
NB6-4a-to-NB6-4t neuroblast homeotic transformations occur in abd-AMX1 mutants.
Stage 15 abd-AMX1 embryos have only ~18 genital disc precursor cells, instead of the wild-type number of 22.
Male-specific somatic gonadal precursors are present in male abd-AMX1 mutant stage 13 embryos, while somatic gonadal precursors do not develop in parasegment 10-12.
In mutant embryos, the width of the heart is now the same as that of the aorta when compared with the wild-type. Also the expression pattern of markers suggest that heart cardioblasts have not been specified in the posterior of the dorsal vessel and these posterior cardioblasts have been transformed instead into aorta cardioblasts.
Homozygous embryos show no heart formation and lack dorsal closure.
Failure of somatic gonadal precursor (SGP) specification in mutants.
Germ cells are able to move through the posterior midgut and initially find lateral mesoderm. The germ cells fail to maintain their specific association with the mesoderm and disperse in the posterior of the embryo. Gonadal mesoderm fails to develop.
abd-Aiab3-Uab4/abd-AMX1 larvae have approximately 12 postembryonic neuroblasts in each of the abdominal neuromeres A3 to A7 (compared to 6 in wild-type). Each of these extra neuromeres produces a hundred or more progeny.
Ectopic fat body precursors arise in parasegments 10-12: transformation of somatic gonadal precursor (SGP) cells into primary fat body clusters.
First instar larvae exhibit lateral dots (a paired structure found in A1 segment of wild type) in abdominal segment A2 to A5 and rarely in A6.
Hemizygous embryonic phenotype displays complete transformation of abdominal parasegments 7, 8 and 9 into parasegment 6 and partial transformation of abdominal parasegments 10 to 13 into parasegment 6 (FBrf0043314).
abd-AMX1 has abnormal neuroanatomy | homeotic phenotype, suppressible by CycEAR95
abd-AMX1 has abdominal neuroblast NB6-4 phenotype, enhanceable by CycEAR95
abd-AMX1 has thoracic neuroblast NB6-4 | ectopic phenotype, suppressible by CycEAR95
abd-AMX1 Df(3R)Ubx109 double mutant embryos show a large reduction in alary muscle number, with only occasional muscles observed. Of the few muscles that develop, all were randomly positioned and are not true alary muscle pairs.
Morata.
J. Casanova.
The A and B glial cells do not show a pattern defect.