posted 27. July 2003 19:43                   

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Abstract. The neutral theory often is presented as a theory of “noise” or silent changes at an isolated “molecular level,” relevant to marking the steady pace of divergence, but not to the origin of biological structure, function, or complexity. Nevertheless, precisely these issues can be addressed in neutral models, such as those elaborated here with regard to scrambled ciliate genes, gRNA-mediated RNA editing, the transition from selfsplicing to spliceosomal splicing, and the retention of duplicate genes. All of these are instances of a more general scheme of “constructive neutral evolution” that invokes biased variation, epistatic interactions, and excess capacities to account for a complex series of steps giving rise to novel structures or operations. The directional and constructive outcomes of these models are due not to neutral allele fixations per se, but to these other factors. Neutral models of this type may help to clarify the poorly understood role of nonselective factors in evolutionary innovation and directionality.

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posted 20. August 2003 20:31                    

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All of these are instances of a more general scheme of “constructive neutral evolution” that invokes biased variation, epistatic interactions, and excess capacities to account for a complex series of steps giving rise to novel structures or operations.

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posted 21. August 2003 01:35                   

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Indeed, the black box of "chance" is already being dissected in studies of molecular evolution, as suggested by conceptual advances such as the codon capture model or the covarion model and by empirical results (cited above) suggesting the importance of biases in mutation in explaining patterns of evolutionary divergence. (p. 179)

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posted 21. August 2003 03:16                    

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One might note that the "biased variation" referred to is a bias in the kind of mutation (e.g., a bias toward deletions), not a directional bias.

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Although recent commentaries give the impression that the differences between classic neo-Darwinism and "evo-devo" are being resolved, we do not believe that this is the case. One cannot integrate these two contradictory views. Either propensities of variation exert an important shaping influence on evolution, or they do not. By implying the former, the "evo-devo" heterodoxy strikes at the root of the New Synthesis: its case for the supremacy of selection and its case against any possible internal causes of directionality. Far from being resolved, the controversy has not even been clearly recognized yet.

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posted 21. August 2003 04:04                    

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With this distinction in mind [the distinction between "mutational" and "systemic"(jf)], the sources of bias invoked above may be listed. In the gene-scrambling and RNA pan-editing cases, and in the fragmentation of introns, the initial state of the system (unscrambled, unedited, unfragmented) is unique or rare with regard to some extensive set of combinatorial possibilities (scrambled, edited, fragmented) that may be reached by mutation and (possibly neutral) fixation. The resulting systemic bias drives a departure from the improbable initial state to one of many alternative states. In the editing model, a deletion: insertion mutational bias plays a subsidiary role. In the gene duplication model, as well as in the explanation for loss of self-splicing and for the origin of protein dependencies in splicing, it is assumed that mutations that reduce activity or affinity or stability are much more common than those with the opposite effect [a bias that plays a prominent role in discussions of the complexification of regulatory networks by Zuckerkandl (1997)]. The resulting directionality consists in duplicate genes undergoing reductions in activity, and introns losing selfsplicing ability, becoming dependent on available proteins as well as trans-acting intron fragments. In both cases, the biases are systemic and result from a history of selection such that the initial state of the system (genes with highly specific activities, introns with independent splicing ability) is unusual with respect to possible alternative states. In all cases, biases are invoked as causes of directionality, with systemic biases playing a much more prominent role. (my bold)

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posted 21. August 2003 13:13                   

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A distinction between two entirely different sources of bias is useful. The more immediately obvious type is a "mutational" bias, an inequality in the rates of mutational change between specific genetic states that arise from specific aspects of the machinery for replication, repair, and transmission of genetic material. Detailed molecular studies invariably reveal such nonuniformities: some nucleotide sites are more mutable than others, DNA polymerases cause deletions more frequently than insertions, mobile elements show insertion site preferences, some chromosomal rearrangements occur more readily than others, and so on. However, even if all rates of mutation between specific genetic states were equal, a second source of bias would exist, because some categories of possible variants will be populated by more genetic states than others, that is, some phenotypic categories are widely distributed in a locally accessible region of conceptual "genotype space." Such "systemic" biases do not arise from the properties of mutational mechanisms themselves, but from aspects of the organization and interaction of parts in a developmental-genetic system. (Emphasis added)

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That's worth some careful thought. I interpret it to mean that due to processes associated with (among other things?) development - gene to phene mappings - phenotypes are not uniformly distributed in genotype space but rather display a non-uniform distribution. That has implications for some sort of "directionality" in evolution - some pathways are more probable than others. It also makes it tough to calculate probabilities associated with phenotype transitions in that space: one can't assume a flat PDF across all alternatives.

RBH

posted 28. August 2003 19:28                    

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I interpret it to mean that due to processes associated with (among other things?) development - gene to phene mappings - phenotypes are not uniformly distributed in genotype space but rather display a non-uniform distribution.

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That has implications for some sort of "directionality" in evolution - some pathways are more probable than others. It also makes it tough to calculate probabilities associated with phenotype transitions in that space: one can't assume a flat PDF across all alternatives.

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