Given that maternal Bicoid activates the expression of hunchback, what would be the consequence of adding extra copies of the bicoid gene by transgenic means to a wild-type female with two copies, thus creating a female fly with three or four copies of the bicoid gene? How would the hunchback expression be altered? What about the expression of other gap genes and pair-rule genes?

The bicoid gene is a coordinate maternal–effect gene. If loss of bicoid function in the egg leads to lethality during embryogenesis, how are females homozygous for bicoid produced? What is the phenotype of a male homozygous for bicoid loss-of-function alleles?

The bicoid gene is a coordinate maternal–effect gene. A female that is homozygous for a loss-of-function bicoid allele is mated to a wild-type male. What are the phenotypes of their progeny?

The bicoid gene is a coordinate maternal-effect gene.

A female Drosophila heterozygous for a loss-of-function bicoid allele is mated to a male that is heterozygous for the same allele. What are the phenotypes of their progeny?

The Drosophila homeotic mutation spineless aristapedia (ssᵃ) results in the formation of a miniature tarsal structure (normally part of the leg) on the end of the antenna. What insight is provided by (ssᵃ) concerning the role of genes during determination?

Embryogenesis and oncogenesis (generation of cancer) share a number of features including cell proliferation, apoptosis, cell migration and invasion, formation of new blood vessels, and differential gene activity. Embryonic cells are relatively undifferentiated, and cancer cells appear to be undifferentiated or dedifferentiated. Homeotic gene expression directs early development, and mutant expression leads to loss of the differentiated state or an alternative cell identity. M. T. Lewis [(2000). Breast Can. Res. 2:158–169] suggested that breast cancer may be caused by the altered expression of homeotic genes. When he examined 11 such genes in cancers, 8 were underexpressed while 3 were overexpressed compared with controls. Given what you know about homeotic genes, could they be involved in oncogenesis?

The specification of the anterior–posterior axis in Drosophila embryos is initially controlled by various gene products that are synthesized and stored in the mature egg following oogenesis. Mutations in these genes result in abnormalities of the axis during embryogenesis. These mutations illustrate maternal effect. How do such mutations vary from those produced by organelle heredity? Devise a set of parallel crosses and expected outcomes involving mutant genes that contrast maternal effect and organelle heredity.

The pair-rule gene fushi tarazu is expressed in the seven even-numbered parasegments during Drosophila embryogenesis. In contrast, the segment polarity gene engrailed is expressed in the anterior part of each of the 14 parasegments. Since both genes are active at similar times and places during development, it is possible that the expression of one gene is required for the expression of the other. This can be tested by examining expression of the genes in a mutant background—for example, looking at fushi tarazu expression in an engrailed mutant background, and vice versa. Given the hierarchy of gene action during Drosophila embryogenesis, what might you predict to be the result of these experiments?