Abstract

GENETIC analysis has been used successfully for identifying the elements responsible for biological processes1,2, and understanding the logic of their interactions. This approach has, however, been little used in the study of morphogenesis in multicellular organisms, chiefly because of a dearth of viable mutants and the difficulties of interpreting the altered primary gene function from the mutant phenotype. The existence of pleiotropy in particular makes this analysis difficult3,4. An alternative approach would be to study the effect of mutations on individual cell behaviour5. This approach depends on the well founded assumption that normal morphogenesis results from the ordered integration of discrete cell autonomous functions. This can be done in Drosophila in genetic mosaics, where the heterozygous, phenotypically wild-type individual is a carrier of clones of homozygous mutant cells. This approach has the advantage that morphogenetic mutants, even if they are lethal to the individual, can be detected, studied and interpreted directly at the cellular level.

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