The two sets of regulators act in opposite ways. Trithorax group proteins are needed to maintain the transcription of Hox genes in cells where transcription has already been switched on. In contrast, Polycomb group proteins form stable complexes that bind to the chromatin of the Hox complex and maintain the repressed state in cells where Hox genes have not been activated at the critical time (Figure 21–25). How such changes in chromatin can store developmental cell memory is discussed in Chapters 4 and 7.
the D-V Signaling Genes create a Gradient of the transcription regulator Dorsal
As with the patterning along the Drosophila A-P axis just discussed, the patterning along the dorsoventral (D-V) axis begins with maternal gene products that define
Figure 21–24 The patterns of expression compared to the chromosomal locations of the genes of the Hox complex. the diagram shows the sequence of genes in each of the two subdivisions of the chromosomal complex. this corresponds, with minor deviations, to the spatial sequence in which the genes are expressed, shown in the photograph of a Drosophila embryo at the so-called germ band retraction stage, about 10 hours after fertilization. the embryo has been stained by in situ hybridization with differently labeled probes to detect the mrNa products of different Hox genes in different colors. (photograph courtesy of William McGinnis, adapted from D. Kosman et al., Science 305:846, 2004. With permission from aaaS.)
Figure 21–25 The role of genes of the Polycomb group. (a) photograph of a wild-type Drosophila embryo. (B) photograph of a mutant embryo defective for the gene Extra sex combs (Esc) and derived from a mother also lacking this gene. the gene belongs to the Polycomb group. essentially all segments have been transformed to resemble the most posterior abdominal segment. In the mutant, the pattern of expression of the homeotic selector genes, which is roughly normal initially, is unstable in such a way that all these genes soon become switched on all along the body axis. (From G. Struhl, Nature 293:36–41, 1981. With permission from Macmillan publishers Ltd.) this axis in the egg (see Figure 21–17), and it then progresses through zygotic gene products that further subdivide the D-V axis in the embryo.
Initially, a protein that is produced by follicle cells underneath the future ventral region of the embryo leads to the localized activation of a transmembrane receptor, called Toll, on the ventral side of the egg membrane. The various maternal genes required for this process are called D-V egg-polarity genes. (Curiously, Drosophila Toll and vertebrate Toll-like proteins also operate in innate immune responses, as discussed in Chapter 24). The localized activation of Toll controls the distribution of Dorsal, a transcription regulator of the NFκB family discussed in Chapter 15. The Toll-regulated activity of Dorsal, like that of NFκB, depends on the translocation of Dorsal from the cytosol, where it is held in an inactive form, to the nucleus, where it regulates gene expression (see Figure 15–62). In the newly laid egg, both Dorsal mRNA and protein are distributed uniformly in the cytosol. After the nuclei in the syncytial blastoderm have migrated to the surface of the embryo, but before cellularization (see Figure 21–15), Toll receptor activation on the ventral side induces a remarkable redistribution of the Dorsal protein. On the dorsal side, the protein remains in the cytosol, but ventrally it becomes concentrated in the nuclei, with a smooth gradient of nuclear localization between these two extremes (Figure 21–26).