The product of the maternal effect gene, bicoid (bcd), is a transcript
ion factor that acts in a concentration-dependent fashion to direct th
e establishment of anterior fates in the Drosophila melanogaster embry
o, Embryos laid by mothers with fewer or greater than the normal two c
opies of bcd show initial alterations in the expression of the gap, se
gmentation and segment polarity genes, as well as changes in early mor
phological markers, In the absence of a fate map repair system, one wo
uld predict that these initial changes would result in drastic changes
in the shape and size of larval and adult structures, However, these
embryos develop into relatively normal larvae and adults, This indicat
es that there is plasticity in Drosophila embryonic development along
the anterior-posterior axi. Embryos laid by mothers with six copies of
bcd have reduced viability, indicating a threshold for repairing ante
rior-posterior mispatterning. We show that cell death plays a major ro
le in correcting expanded regions of the fate map, There is a concomit
ant decrease of cell death in compressed regions of the fate map, We a
lso show that compression of the fate map does not appear to be repair
ed by the induction of new cell divisions, In addition, some tissues a
re more sensitive to fate map compression than others.