Table 2.

Genomic aberrations of previously characterized mutations and recessive lethal alleles carried by TM3, TM6, and TM6B

GeneAlleleBalancer(s)Observed aberrationPrevious reports
ebonye1TM3, TM6, TM6BTE (family: 412) at 3R:21,231,832–21,231,838, 6 nt into the 2nd exon
UltrabithoraxUbxbx-34eTM3, TM6TE (family: DMIS176) insertion in the first intron of Ubx at approximately 3R:16,731,980Gypsy insertion (Bender et al. 1983)
knirpskniri-1TM3252-bp deletion at 3L:20,707,101-20,707,352.(Lunde 2003)
pinkppTM31-bp deletion at 3R:6,661,619 resulting in a frameshift1-bp deletion at 3R:6,661,624 (Syrzycka et al. 2007)
lethal (3) 89Aal(3)89Aa1TM3UnknownMapped to 89A2-89A5
ventral veins lackingvvlsepTM3Unknown
StubbleSb1TM3TE (family: 412) insertion in 4th exon of Sb at 3R:16,141,939-16,141,942.TE insertion (Hammonds and Fristrom 2006)
SerrateSer1TM3TE (family: TIRANT) insertion at 3R:27,172,910-27,172,913 in the 3’ UTR of SerTE insertion (Fleming et al. 1990)
HennaHnPTM6Multiple deletions within the first intron and a G->A mutation at splice acceptor site (AG becomes AA) in the third intron of the gene.
spinelessssaP88TM6Gene is split by the In(3LR)P88 (61A1-2;89C2-4) rearrangement.Break in the transcription unit (Duncan et al. 1998)
AntennapediaAntpHuTM6BUnknown. Phenotype may be a result of the In(3R)Hu triple rearrangement (Figure 1).
TubbyTb1TM6BAn in-frame 15-nt deletion in the 2nd exon from 3R:26,656,728-26,656,742; a 69-nt in-frame deletion of 23 amino acids from 3R:26,657,089-26,657,157; and a T->G mutation (Ser->Ala) at 3R:26,657,334.