. "5 The Frailty of Adaptive Hypotheses for the Origins of Organismal Complexity--MICHAEL LYNCH." In the Light of Evolution: Volume 1. Adaptation and Complex Design. Washington, DC: The National Academies Press, 2007.
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In the Light of Evolution, Volume I: Adaptation and Complex Design
lacking mesoderm (the cnidarians), and by inference must have simply been lost from various invertebrate phyla (Technau et al., 2005). Numerous examples of morphological simplification exist in animals (e.g., limb loss in lizards and salamanders, coelom loss in nematodes, and mouth and anal loss in hydrothermal-vent worms), and a plausible, albeit controversial, case has even been made that prokaryotic cell architecture is a simplified derivative of that of eukaryotes (Kurland et al., 2006).
Could nonadaptive processes have played a role in the evolution of something as intricate as cell architecture or developmental complexity? There are at least two ways by which such a cascade of events might be precipitated. First, intrinsically deleterious genome-level changes, such as those resulting from intron and mobile-element proliferation, must impose selection pressures for cellular defense mechanisms. It has been argued that by imposing a need to process mRNAs before their exposure to ribosomes, the establishment of spliceosomal introns provided the evolutionary pressure that led to the origin of the nuclear membrane (Lopez-Garcia and Moreira, 2006; Martin and Koonin, 2006), and Koonin (2006) has further suggested that the nonsense-mediated decay (NMD) and ubiquitin signaling pathways evolved as secondary mechanisms for minimizing the accumulation of aberrant transcripts and proteins resulting from splicing errors. This line of thinking could be taken in a number of additional directions. For example, the assembly of spliceosomal subunits occurs within intranuclear Cajal bodies (Stanek and Neugebauer, 2006), and aberrant transcripts flagged by the NMD pathway are degraded in cytoplasmic P bodies (Sheth and Parker, 2006). The nature of cause and effect in these relationships is difficult to resolve, as all hypothetical lines of defense against introns appear to have been present in the stem eukaryote (Lynch et al., 2006), raising the possibility that the colonization of nuclear genes by introns followed the origin of permissive cellular features, rather than the other way around. Nevertheless, the idea that internal constraints played a role in cellular evolution is secure under either scenario.
Second, because cellular and developmental features reflect the transformation of gene-level information into gene expression, the opportunities for phenotypic evolution must ultimately be constrained by the physical resources existing at the genomic level, which as noted above are strongly influenced by nonadaptive aspects of the population-genetic environment. Reductions in Ng are expected to lead to increases in intron number and size, expansions in UTR lengths, losses of operons, the modularization of regulatory regions, and the preservation of duplicate genes by subfunctionalization (among other things; Table 5.2). Thus, as will be discussed more fully below, to the extent that an increase in gene-architectural complexity is a precondition for the emergence of greater complexity at the organismal level (including the hallmarks of multicellularity: multiple cell