Fig. 6. The repression function of Eve is required for normal axonal morphology. All embryos carry both the RN2-Gal4 and UAS-lacZ transgenes (marking RP2, aCC and pCC) in an RP2 mutant background, and were stained with anti-ß-gal. (A) RP2A/RP2B (no Eve protein expressed in the marked cells). Scale bar: 20 µm. (B-J) Embryos contain in addition to the genotype in A, one copy of an eve transgene expressing the following modified Eve proteins: (B) Eve HD only (domain `H' in map at top; note that there is some rescue of lateral axonal outgrowth); (C) Eve N-terminus plus HD (domains `N' and `H' in map; note the slight rescue, similar to B); (D) the entire Eve protein without the Groucho interaction domain (`LFKPY' in map; note the considerable but incomplete rescue); (E) the Eve protein without the Atrophin interaction domain (`R' in map; note the considerable but incomplete rescue); (F) full-length Eve (note the essentially complete rescue, including cell body positioning); (G) Eve HD fused with repressor domain from En (Eve domain `H' plus En amino acids 1-298; note the essentially complete rescue); (H) Tc-Eve (from Tribolium; note the essentially complete rescue); (I) Sa-Eve (from grasshopper; note the near-complete rescue); and (J) Evx1 (from mouse; note the near-complete rescue).

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