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Roles of achaete and scute in bristle development on the notum.
a. Phenotype of scM6, a scnull with a nonsense-codon mutation ('X'') before the HLH domain . Unlike previous nulls this allele is not associated with deletions or inversions that confound gene-phenotype analyses (e.g., b, c). Bars indicate frequencies of MC presence. Sites are listed in enhancer order (dashed lines; cf. Fig. 3.4 for details and Fig. 2.6 for MC key; mc = microchaetes). Surprisingly, sc is not needed for bristles that were thought to depend on it (b), including scutellars (PSC, ASC) whence scute got its name .
b, c. 'Classical' (but incorrect) roles of ac and sc as deduced from nulls that involve major DNA alterations. In each case, deletion of a gene (ac or sc) was achieved by crossing over between inverted chromosomes with breakpoints at different AS-C sites . With such complex 'knock outs' it is impossible to distinguish the effects of gene inactivation from the effects of disabling enhancers. Thus, the complementary sets of bristles affected by these constructs (b vs. c) give a false impression of the relative roles of sc and ac (cf. a). b. Phenotype of a scnull, In(1)sc8Lsc4R, where L and R denote left or right halves of inversions contributing to the recombinant. The deletion removes sc and the PNP enhancer, and the inversion moves proximal enhancers ASA, etc., away from achaete to the other (heterochromatic) end of the chromosome. Thus, the only enhancers still able to influence ac are mc, PSA, PDC, and ADC. Other PSA and ADC enhancers must exist in the deleted or detached domains (probably in the sc promoter region ) because these bristles are often missing. c. Phenotype of an acnull, In(1)y3PLsc8R, which removes ac and enhancers for PSA, PDC, and ADC. Microchaetes may be only partly affected because their enhancers extend past the deletion . Although proximal enhancers PNP, etc., are disconnected from ac by the inversion, they remain linked to sc and therefore can apparently still function normally.
All data are from . N.B.: The yellow (y) gene has its own set of cis-enhancers [1442, 1443], and mutations therein produce a menagerie of pigment patterns [1435, 3055] (as variegated as dog or cat breeds) -- suggesting that some of the same spatiotemporal trans-factors that control the AS-C may also regulate yellow .