93C3-93C6;93F6-93F8
93D1;93E4-93E5
93D1--2;[]
93C3-93C6;93F6-93F8
l(3)93Ca << bk1 << l(3)AFA7 << l(3)93Fa << bk2 << how
bap null embryos (Df(3R)e-F1/Df(3R)e-D7 embryos carrying tin+t10.7, referred to as "bapDf") show visceral mesoderm defects; the presumptive visceral mesoderm cells do internalise, but they show incomplete coalescence of the clusters during stage 11. At later stages, very few of the visceral mesoderm cells are attached to the endoderm. Cells which originate from trunk visceral mesoderm primordia fuse into syncytia of somatic muscles.
Df(3R)e-D7/Df(3R)e-F1 embryos carrying a tin rescue transgene have an increased number of somatic gonadal precursor cells.
In embryos homozygous mutant for Df(3R)e-D7 LVM founder cell migration initiates similarly to the wild type, but the tracks become progressively irregular during germ band retraction at stage 12. By the end of germ band retraction none of the cells have reached the anterior of the trunk.
tin+t10.7 Df(3R)e-D7/Df(3R)e-F1 embryos lack muscle fibres at the position of the segmental border muscle (SBM) and have unfused myoblasts in or around the SBM position in 57% of hemisegments. In the remaining 43% of hemisegments, the muscle fibres lying within or close to the segmental borders have abnormal shapes and have insertion sites clearly distinct from those of the SBM. The lateral adult muscle precursors are absent or reduced in number, and the ventral adult muscle precursors are duplicated.
Df(3R)e-D7 tin+t10.7 embryos do not form visceral mesoderm.
Homozygous lethal.
All limits from polytene analysis (FBrf0098832)