There is no collier expression in embryos from bicoid mothers or in buttonhead homozygous mutant embryos. In empty spiracles mutant embryos, col expression expands ventrally to include mesodermal precursor cells. These results indicate that col acts downstream of the head gap genes in the transcription regulatory cascade that patterns the anterior part of the head, with buttonhead being absolutely required for col activation. Whereas the segmental nature of the insect head is well established, relatively little is known about the genetic and molecular mechanisms governing this process. The stripe of col expression is included in that of btd , overlaps that of ems , and is restricted both dorsally and ventrally to neuroectodermal cells.
Embryos lacking ems function also show a ventral derepression of col expression.
Further, at stage 10, ems mutant embryos show an abnormal pattern of col mRNA accumulation, with a mandibular stripe in addition to intercalary stripe of col -expressing cells. This suggests a second role for ems in regulating col . These plates are specified by empty spiracles . EMS has the potential to induce sclerotic plates, but this potential is suppressed by the HOM-C genes, including labial , the most anteriorly expressed homeotic gene. The phenomenon is used to explain posterior dominance, the observation that a homeotic gene product will have an effect only in the body region anterior to the normal domain of the gene.