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sepal petal stamen carpel stamen petal sepal

Figure 9-14. The basic ABC model of combinatorial gene expression and the development of flower organs. Three classes of homeotic genes specify the identity of the floral whorl components: sepals, petals, stamens, and carpel organs. Class A genes (dark grey) specify sepals, classes A and B (white) specify petals, classes B and C (light grey) specify stamens, and class C alone specifies carpels. For details see (Ng and Yanofsky 2000).

sepal petal stamen carpel stamen petal sepal

Figure 9-14. The basic ABC model of combinatorial gene expression and the development of flower organs. Three classes of homeotic genes specify the identity of the floral whorl components: sepals, petals, stamens, and carpel organs. Class A genes (dark grey) specify sepals, classes A and B (white) specify petals, classes B and C (light grey) specify stamens, and class C alone specifies carpels. For details see (Ng and Yanofsky 2000).

female flowers use homeotic gene differences to produce single-sex flowers (e.g., Ma and dePamphilis 2000), and similar changes can be brought about experimentally with the Silkyl B-class gene homolog.

A general combinatorial system involving many of the same ABC system Mads and other TF genes is conserved among angiosperms (flowering plants), but the details, specific genes, and functions of specific genes vary (Kramer and Irish 1999; Ma and dePamphilis 2000). As with other examples noted earlier, such as tadpoles or pluteal larvae, phenogenetic drift seems to have been at work during the 130 million or so years of angiosperm evolution: either some flower structures have evolved repeatedly, each time recruiting new genes, or an original angiosperm flower has lost structures in different lineages while phenogenetic drift has modified genes or gene use in what is otherwise a generally conserved ABC system. As in the other systems we have discussed, gene duplication with divergence and overlap in function has also played a role.

Sculpting by Cell Death

Organs are sometimes said to be "sculpted" during development—but the metaphor is somewhat inapt, because sculptors work from the outside. Michelangelo may have "seen" David within a solid block of newly cut Carrara marble, but David did not make himself from within that stone. Perhaps we should view even the simplest embryo as much more a master sculptor than Michelangelo. One trick is that the embryo first makes a rather crude form of a structure and then forms the elegant final version by selectively removing unwanted material. This is done by apoptosis, using various pathways mentioned in earlier chapters.

Even some life cycles of bacteria involve autolytic cell death. Cells can die if they are starved of some nutrient or growth factor. Neural connections in the brain are formed through "exploratory" growth of some cells, leading others to follow them; the guide cells die once connections among the latter are made. Neurons can die if they fail to reach cells in an appropriate target tissue, a process triggered by the failure of receptors on the neuron to be bound by ligands secreted by cells in their destination. As mentioned earlier, vertebrate limbs form as paddlelike structures, but once the cartilage segments that will be the bones in the digits form, the tissue between the future fingers or toes dies away (when this doesn't happen in humans, anomalous webbing can result). In a somewhat different way, deciduous plants shed their own leaves by sealing them off from nutrient supplies when faced with stress such as drought or the cold of winter.

Apoptosis occurs in two basic ways. The death sentence can come from the outside. Cells presenting apoptosis-related receptors on their surface undergo a cascade of self-destruction when a ligand (Tissue Necrosis Factor, Fas, or others) is received. This type of externally triggered mechanism is involved in the targeted destruction of infected cells by the immune system. Bmp signaling can also lead to the degradation of cells during development, as occurs in some reaction-diffusion patterning. Apoptotic genes include the oncogenes p21 and p53 (named for their protein size), which antagonize genes that promote cell growth, preventing cells from overgrowing their normal tissue structure. In one common pathway, signal reception activates a member of the Caspase (cysteine-aspartic acid protease) family whose proteolytic activity digests the materials in the cell by anomalous phosphorylation or dephosphorylation of cellular proteins affecting their function. For example, the phosphorylation regulator Pten modifies second-messenger molecules. Apoptosis can be achieved by disrupting the normal cell cycle, so that the cell can no longer divide and eventually withers.

Apoptosis can also be managed by internally derived pathways. Some of these also involve Caspase genes. In one example, an apoptosome containing various proteins forms when internal cellular damage releases Apaf1 from an Apaf1/ Bcl2 complex bound to the mitochondrial surface membrane. Damaged mitochondria also release cytochrome c, which complexes with Apaf1 and Caspase9, to activate a cascade of Caspase-based proteolysis that cleaves proteins in the cytoplasm. Apoptosis can also destroy chromosomal DNA, another effective way to stop a cell in its tracks. Essentially, the logic of apoptosis is to use external signaling or internal cues to produce compounds that effectively mutate (interrupt) existing pathways in the cell, and as expected there are many ways to achieve the net result of cell death.

Timing and Asymmetric Growth

We referred to spatial and temporal asymmetry in Chapter 8 as another set of ways of making a complex organism by simple mechanisms that affect scale and shape (Calder 1984; Carroll, Grenier et al. 2001; Hall 1999; Raff 1996; Thompson 1917; Wilkins 2002). The timing, level, and persistence of growth factors are responsible for these phenomena. Simple beginnings can be amplified hugely in terms of general growth, leading to considerable differences even among closely related species. We referred earlier to the likelihood that some pattern is laid down very early in the embryo and that this can explain how very similar traits like teeth or color stripe patterns can be generated across a large size range of species so closely related that they clearly must use essentially the same patterning mechanism (e.g., similar stripes in very small and very large cats; teeth in voles and elephants). No new duplicate genes or new mechanisms are required, only differences in their expression.

Timing is a relevant phenomenon—when an activity starts, how long it goes on, and its intensity during that period. Hormone- or induction-receptive periods are established in which a signal can be interpreted properly. This is true even at a higher level of trait complexity, such as language learning ability, songbird song learning, rat olfactory pathways, puberty, developmental patterning, and blossoming/leaf abscission.What determines the sensitive times? This is unknown at present for most examples, but some genes are known that relate to periodic events in development.

Chronobiology is a rapidly growing field in genetics. Various genes, including Clock and Chairy, are known to be involved in expression timing, the latter having 90-minute activity cycles in some systems. Melanopsin is involved in calibrating light-related cycles.

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