Developmental genetics of the mutant combgap in Drosophila melanogaster. I. Effect on the morphology and chaetotaxy of the prothoracic leg.

genetic basis of cellular differentiation in higher organisms can be studied TE:ifferent levels: (a) at the molecular level, limiting the study to changes in the process of cellular metabolism and physiology (e.g., studies of GALL and CALLAN. see CALLAN 1963; DAVIDSON et al. 1965; BEERMANN 1964,1965; PAVAN 1965; SCHULTZ 1965; CLEVER 1966) or to differential protein realization (PAIGEN and GANSCHOW 1965) ; (b) at the developmental level, tracing the gene effects from their first appearance (studies of HADORN and his collaborators, see HADORN 1965. 1966); or (c) at the level of pattern differentiation (STERN 1954a7 1965, 1968) at the final step of gene-controlled cell product. This last category of investigation forms the basis of the present study on genetic control of cellular differentiation in higher organisms. STERN (1956) has proposed that pattern differentiation in higher organisms is a consequence of several gene-controlled steps which, preceding the final pattern formation, evoke a “regional differentness” termed prepattern, and the realized pattern is the result of localized cellular response to that prepattern. According to this concept, the mutant genes should exert their influence on differentiation either by changing the prepattern itself or by changing the ability of cells to respond to the prepattern stimuli. Earlier studies have shown that most of the mutants affecting the bristle patterns are responsible fo r initiating a change in the terminal step or steps of pattern formation (TOKUNAGA and STERN 1965; STERN 1968). However, the behavior of the mutant gene eyD in genetically produced mosaics (STERN and TOKUNAGA 1967) and in transplants (TOKUNAGA 1968) has reinstated the possibility for the existence of a prepattern gene. The effects of prepattern us. competence genes can be resolved by the time of their action in development. The distinction can be made either by analysis of the interaction between different pattern mutants (LEES and WADDINGTON 1942; ANDERS 1955; MUKHERJEE 1965; MUKHERJEE and MITRA 1967) or by mutants in genetic mosaics (STERN 1936, 1956. 1968; STERN and HANNAH 1950; TOKUNAGA 1961, 1962, 1968; MUKHERJEE and STERN 1965). MUKHERJEE