Search Results

This chapter tackles the evolution of cellular organization. How did intricate subcellular machines, such as ribosomes, flagella and ion pumps come to exist? How do cells transmit their functional organization to their offspring, and how did that evolve? And where did cellular organization come from in the first place? Contrary to the claims of Intelligent Design, there is ample evidence that random variation of genes winnowed by natural selection played a large role. But conventional views on these matters are too restrictive. Cells transmit structural organization by a hierarchy of mechanisms that includes genes, self-organization, the continuity of membranes and other structures, and a role for the cytoskeleton in helping a growing cell to model new structures upon the existing ones. How cells as we know them originated remains to be discovered, a subject for speculation and wonder but not yet for explication.

Two cellular mechanisms are essential for development. The first, gene regulation, makes it possible to switch on different genes in different cells, in response either to conditions external to the cell or to the activity of other genes within the cell. The second, cell heredity, ensures that these states of gene activity, once induced, can be stably transmitted through cell division, without the need for the continued presence of an external inducer. In this chapter, we describe how gene regulation and cell heredity are achieved in metazoans, and point to some similar mechanisms that are already present in prokaryotes. The central problem of gene regulation was posed, in a social context, by the scholastic Master Eckhardt: ‘Quis custodiet ipsos custodes?’ [Who regulates the regulators?] Clearly, the proposition that every gene needs a separate regulator gene leads to an infinite regress. There are various ways of resolving the paradox, which include one regulator controls several other genes, including regulators; one gene, even a regulator, is controlled by several other genes; and some genes may be both regulatory and structural. Plenty of examples are known for each case. It is also necessary that some genes be regulated by signals from outside the cell. The essential mechanism of gene regulation was discovered by Jacob & Monod (1961; Fig. 13.1) in E. coli. A regulatory gene codes for a protein, which, by binding to a specific regulatory sequence of another gene, alters the activity of that gene (negatively in the case originally described by Jacob & Monod, but the effect can also be positive). The regulation can be modified by a specific inducing molecule that alters the effect of the regulatory protein by binding to it allosterically. It is interesting that these two properties of regulatory proteins—that they can recognize specific regulatory sequences, and that their effectiveness can be altered by binding allosterically to inducers—are already present in prokaryotes. The complexity of multicellular eukaryotic development requires that an average gene be controlled by many others. Whereas regulatory elements in bacteria are usually simple switches, eukaryotes tend to have ‘smart’ genes, controlled by a complex of several regulatory proteins (Davidson, 1990; Beardsley, 1991).

In the nineteenth century, ideas about development, heredity and evolution were inextricably mixed up, because it seemed natural to suppose that changes that first occurred in development could become hereditary, and so could contribute to evolution. This was not only Lamarck’s view but Darwin’s, expressed in his theory of pangenesis. Weismann liberated us from this confusion, by arguing that information could pass from germ line to soma, but not from soma to germ line. If he was right, geneticists and evolutionary biologists could treat development as a black box: transmission genetics and evolution could be understood without first having to understand development. Since Weismann, developmental biology has had only a rather marginal impact on evolutionary biology. One day, we have promised ourselves, we will open the box, but for the time being we can get along very nicely without doing so. Recent progress in developmental genetics, some of which has been reviewed in the last three chapters, oblige us to reopen the question. In fact, there are three related questions, not one. The first, which is most relevant to the theme of this book, is the ‘levels of selection’ question: why does not selection between the cells of an organism disrupt integration at the level of the organism? This is the topic of section 15.2. The second is the problem of the inheritance of acquired characters. This old problem has reappeared in a new guise. We now recognize the existence of cell heredity, mediated by different mechanisms from those concerned with transmitting information between generations. In section 15.3, we discuss whether cell heredity plays any role in evolutionary change. Finally, in sections 15.4 and 15.5, we ask whether recent molecular information sheds any light on another old problem—that of the extraordinary conservatism of morphological form, maintained despite dramatic changes of function. This conservatism has led anatomists to identify a small number of basic archetypes, or bauplans. There is little doubt that conservatism is real. Consider, for example, the fact that bones and cartilages, which in humans serve in swallowing, sound production and hearing, are derived from elements of the gill apparatus whereby our fish ancestors exchanged gases with seawater, and, before that, in all probability, from elements of a filter-feeding apparatus.