25D7;26A8-26A9
25E2-25E4;26B3-26B9
25E1-25E2;26A8-26A9
25D7;26A8-26A9
25D7-25E1;26A8-26A9
cype << bk1 << l(2)25Ea << l(2)26Ad << bk2 << l(2)26Cf
Breakpoint(s) molecularly mapped
Df(2L)x528/Df(2L)Gpdh1-A is embryonic lethal and impacts founder cells for lateral transverse muscle 3, lateral transverse muscle 4, lateral oblique muscle 1 and ventral transverse muscle 1; loss of lateral transverse muscles.
Df(2L)x528/Df(2L)Gpdh1-A embryos show a loss of neuroblasts NB1-1, NB2-5 and NB2-4. This loss is much more pronounced in odd-numbered than even-numbered abdominal segments. However, the loss is similar to mid mutants, suggesting that the it is deletion of the mid gene and not the H15 gene that is causing the phenotype.
Inferred to overlap with: Df(2L)x528.
Df(2L)Gpdh1-A/Df(2L)x528 larvae show a loss of denticle belts; denticle rows 1 to 5 are frequently lost in odd-numbered segments, whereas even-numbered segments show milder defects. Df(2L)H15-x4/Df(2L)Gpdh1-A larvae show a weak loss of denticles phenotype.
Lethal in combination with Df(2L)cl7. Lethal in combination with Df(2L)Gpdh1-78. Lethal in combination with Df(2L)Gpdh1-75. Lethal in combination with Df(2L)cl1. Lethal in combination with Df(2L)cl2.
Heterozygosity for Df(2L)Gpdh1-A results in 8.0% X chromosome nondisjunction and 2.2% fourth chromosome nondisjunction in In(1)FM7/X ; svspa-pol females.
Shows no maternal enhancement of dpphr4.
Dominantly causes tergite defects in less than 50% of run3 heterozygotes.
Midgut development of mutant embryos is wild type.
Homozygous embryos are very abnormal compared to wild-type. The hindgut is short and broad, and the Malpighian tubules do not elongate.
Heterozygosity for this deletion has no effect on the mutant ovarian phenotype of ovoD2.
Enhance mottling in wm4.
H2.0 maps (by in situ hybridisation) to the right of the Df(2L)GpdhA deficiency.
Limits of break 1 from polytene analysis (FBrf0048198) Left limit of break 2 from inclusion of lid (FBrf0067338) Right limit of break 2 from polytene analysis (FBrf0041503)