Perhaps not surprisingly, the Bcd gradient itself shows significant variation. A particular threshold level of Bcd occurs across a range of 30% of the embryonic length in different embryos. Hb, however, is turned on so precisely that in two-thirds of the embryos the Hb boundaries are defined over a region corresponding to less than the size of one nucleus.
Cooperative activation of Hb could sharpen a Bcd-directed Hb gradient to a tightly defined area in a particular embryo. But this does not solve the problem of activating Hb at precisely the same relative position in every embryo. To accomplish this feat, there must be information in addition to the Bcd gradient that can vary with factors such as temperature, exact gene dosage, and the age of the eggs.
That extra information does not appear to come from a variety of other gap genes tested by Wieschaus, or from nanos, a candidate posterior gradient molecule. Mutation of the gene staufen does, however, have a marked effect. Staufen helps carry mRNAs for gradient proteins (such as Bcd) to both the anterior and posterior of the fly embryo. The interplay of several such proteins, either known or unknown, may refine the Hb expression pattern. In any simple model involving Bcd, says Wieschaus, the additional gradient molecule “has to be something that varies in the same way as Bcd.” In this way, effects on the two gradients by factors such as temperature would oppose each other and be cancelled out in the Hb readout. ▪