l(3)93Ca << bk1 << l(3)AFA7 << l(3)93Dk << bk2 << lbe
Breakpoint(s) molecularly mapped
Df(3R)lb/Df(3R)e-F1 are uncovered for lbl, lbe and bap. In these embryos no dramatic change is seen in the ventral nerve cord morphology. However, there seem to be slightly more lateral projections compared to wild-type. The glial cell population is also affected in its positioning and number. An increased number of medially located glial cells is seen, as is a partial loss or abnormal positioning of lateral exit and subperineural glial cells. An additional ~2.3 glial cells are seen per hemineuromere. Defects are also seen i the segmental nerves. The distance between the ISN and SN bundles is much more variable and larger than seen in wild-type.
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.
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.