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Fig. 2. tou mutants genetically interact with pnr and Chip and exhibit loss of DC bristles. (A) Wild-type flies have four DC bristles (1-4). (B) Loss of function tou alleles [tou¹, tou^E44.1 (not shown), tou²] results in phenotypes similar to pnr mutants, which lack DC bristles (asterisk). (C,D) tou² behave as dominant suppressor (tou²; pnr^D1/+) of the excess of DC bristles (arrowheads) observed with pnr^D1 encoding a constitutive activator of ac-sc (pnr^D1/+). (E,F) tou² behave as dominant enhancer (Chip^E tou²) of the loss of DC bristles associated with Chip^E. (G) In contrast, overexpressed tou in the domain of apterous expression (ap^Gal4/EP622) leads to an excess of DC bristles (arrowheads) associated with extra DC precursors in the imaginal disc (J), as revealed by A101 staining, in comparison with staining of wild-type disc (I). (H) Overexpressed tou suppresses the loss of DC bristles associated with Chip^E (ap^Gal4Chip^E/EP622Chip^E) and produces extra sensory organs (arrowheads). (K) tou and osa are antagonistic during neural development. Lowering the dosage of Osa suppresses the loss of DC bristles characteristic of tou² (tou²; osa⁶¹⁶/+). (L) Reducing Iswi function (Iswi²/+; pnr^D1/+) also suppresses excess DC bristles associated with pnr^D1. (M) Overexpression of the dominant-negative Iswi (ap^Gal4/Iswi^K159R) in the domain of ap expression leads to loss of multiple sensory organs, including the DC bristles (asterisks). (N,O) The loss of DC bristles (asterisks) resulting from overexpressed Iswi^K159R in the domain of pnr expression (pnr^Gal4/Iswi^K159R) is aggravated when tou function is simultaneously reduced (tou²; pnr^Gal4/Iswi^K159R), reinforcing the hypothesis that Tou and Iswi could be subunits of a multiprotein complex regulating neural development.

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