Small deficiency removing the first exon.
Intragenic deletion removing most of the inv transcription unit. The portion of the gene encoding the homeodomain is left intact.
Intragenic deletion removing approximately 27kb of the inv transcription unit, including the transcription start site, the first two exons and most of the second intron.
Gaps are seen in the posterior of the hindgut boundary cell rows in mutant embryos.
The development of the border cells of the hindgut (which normally form an anterior and posterior ring at the ends of the hindgut and bilateral strands that connect the two rings) is not affected in mutant embryos.
Homozygous embryos do not show duplications of the RP2 neuron.
Survives without abnormality over Df(2R)en-SFX31, except for slight defects on the anterior crossvein.
Adult flies are normal in appearance.
Df(2R)enΔ530/en9, inv30 has visible phenotype
fra1, inv30 has abnormal neuroanatomy phenotype
fra1, inv30 has lethal | adult stage phenotype
Df(2R)enΔ530/en9, inv30 has wing vein phenotype
fra1, inv30 has lateral tract phenotype
fra1, inv30 has larval ventral nerve cord phenotype
fra1, inv30 has larval anterior commissure phenotype
fra1, inv30 has larval posterior commissure phenotype
en9.6, inv30 has embryonic epidermis phenotype
91% of Df(2R)enΔ530/en9 inv30 wings exhibit split veins in the posterior compartment.
Approximately 34% of fra1/inv30 double mutants exhibit defects in axonal pathfinding. Stage 15 embryos display dramatic defects in ventral nerve cord architecture, with the posterior commissures missing or fused with the anterior commissures, and longitudinal tracts thinner. Approximately 87% of the segments are affected in these embryos.
Approximately 15% of fra1/inv30 double mutants are adult lethal.