[5A2-5A2];[5A6-5A6];
A set of isogenic deficiency stocks created by FLP-induced recombination between FRT-carrying transgenic insertions; molecularly defined deletion endpoints correspond to initial location of the progenitor insertions. Initial set of 519 isogenic deletions provides 56% genome coverage.
The current Exelixis collection at the Bloomington Stock Center differs from the original described in FBrf0175003 : a significant number were shown not to carry a deletion and have been removed from the collection; a number of stocks have been lost; a number of additional deletions are included that were generated after publication.
5A2;5A6
The outer optic anlagen and brain are reduced in size in Df(1)Exel6235 mutant second instar larvae. Mutant larval brains show defects in proliferation as measured by the number of phospho-histone 3 (PH3) positive cells compared to controls; the outer optic anlagen shows a 5.07-fold decrease in PH3-positive cells, the inner optic anlagen shows a 2.51-fold decrease in PH3-positive cells and the medial brain shows a 2.82-fold decrease in PH3-positive cells
Mutants show lethality at all postembryonic stages. Mutants show developmental defects, with the time taken to reach the molt to second instar from hatching being increased relative to controls.
Mutant pharate adults have significantly smaller optic lobes than control animals. The optic lobes are also disorganised; the incoming photoreceptor axons have marked projection errors in both the lamina and deeper layers of the optic lobe, and in the most severe cases the projections terminate deep in the brain.
The third larval instar outer optic anlage (OOA) is dramatically reduced in size in mutant animals compared to controls, and is not visible at all in some mutant brains. The inner optic anlage appears grossly normal in these animals.
The OOA appears normal in shape and size in mutant stage 16 embryos, however defects are seen in early second instar larvae, where the OOA is hypoplastic and disorganised, with the arms of the OOA failing to form the U-shaped structure seen in controls.
Limits computationally determined from location of progenitor P insertion on genome sequence between P{EP}CG3249EP1400 and P{EP}Tre1EP496