First, I’d like to thank the panelists for their thoughtful comments on my book; I can’t tell you how honored I am that so many people took the time to think seriously about my work and respond to it. Also, I’d like to thank Sharyn Clough for organizing this event; without her hard work none of this would have happened. In some ways I suppose that I should be pleased that there were no serious criticisms of either the analysis of the nature of selection or of the analysis of the level of selection debates that Massimo and I presented. I bring this up here because our interpretation of selection and fitness (based on Matthen and Ariew’s work) informs the approach we took to several areas that the panelists did touch on. So let me spend a few minutes of my time explaining, in the broadest outlines, what we were up to.

Three distinct levels of analysis in evolution: 1)Individual 2)Population 3)Ensemble The individual level focuses, roughly, on individual organisms. More specifically, it focuses on actual physical/causal processes that interact with particular entities capable of differential reproductive success. The population level focuses, roughly, on actual populations – groups of entities that experience relevantly sets of physical/causal processes of the above sorts. The ensemble level considers collections of such populations, and as such is essentially a tool for analyzing the statistical distribution of the results of processes at the individual level that effect the population level.

Two Versions of Selection & Fitness “Informal” or “vernacular” fitness: An organism’s “propensity” to leave (successful) offspring in a particular context (either overall in a particular environment, or given a particular kind of interaction) “Predictive” or “formal” fitness: The average rate of increase of organisms in a population with one variant of a trait as opposed to another variant of that trait. Nature Selection in the formal Sense: The expected differences in reproductive success of members of a particular population divided on the basis of the trait of interest. Nature Selection in the informal Sense: The relationship of particular kinds of physical processes and particular variations in traits where that variation is related by those physical processes to differences in reproductive success of some entity

So: Why does this matter? Gene Centricism and Development: Paul Roberts v. Karola Stotz Microbiotic communities, “altruism,” and selection: John Dupré Functions versus causes: Paul Griffiths And of course - Metaphors, models, and conceptual rigor: Seth White I think it matters to at least the following issues -

“Genes are (sort of) like a recipe. You of course can’t get a cake without an oven, flour, sugar, etc. But nonetheless the recipe has a certain primacy, because it contains the information... [G]enes are important, and different from other components of the developmental process. With all due respect to cytoplasmic inheritance and maternal effects, there doesn’t seem to be much here.” – Günter Wagner, in response to our book The argument (?): Only heritable changes matter to evolution, and since genes (as nucleic acid sequences) are the (only or only serious) units of heredity, the only changes in populations that have evolutionary consequences are those that involve changes in genes or gene frequencies etc. Note that this claim is independent of questions about e.g. what gets selected in natural selection, etc.

Developmental Resources: Resources necessary for development versus Sources of heritable variation What matters to biological evolution is heritable variation; if the variation is heritable then it can have evolutionary consequences. So evolution isn’t necessarily about changes in genes, but changes in any heritable developmental resources at all. (Or, with respect to natural selection and adaptations, at the very least any heritable variation that can have fitness consequences…) Clinal variation in yarrowplant populations (Achillea lanulosa), Sierra Nevada, California. At the informal level, our attention should be drawn to physical interactions with particular kinds of traits, and the ways that those traits are reproduced through development At the formal level, our attention should be focused on the changes in trait frequencies, and what changes in developmental resources those changes are associated with…

Non-genetic (or not-fully genetic) heritable developmental resources: “Ordinary” epigenetic stuff: DNA methylation, chromatin condensation, etc. Membrane Inheritance / Templating: Cortical membrane-based inheritance, templating of other cellular structures including cytoskeletal structures. Other intra-cellular stuff: Various material resources (including, in yeast at least, prions), metabolic cycles and states, chemical gradients, etc. Intercellular organization (in multi-cellular organisms): Tissue fields, morphogen gradients, etc. (cellular inheritance through development) Symbiotic inheritance: Bacteria, yeasts, etc. (including perhaps organelles such as chloroplasts, mitochondria, etc.) “Niche” construction and inheritance Environmental construction (figurative or literal) Environmental selection (passive or active) including host selection, etc. Behavioral inheritance / learning: various forms, including at least passive learning (via e.g. transmission of chemical signals re: food preferences), differential attention to environmental factors, and/or active “mimicry.” Few people doubt the importance of (many of) these resources for development (in different cases), but are they important to evolution?

Questions: 1)How common is the heritable variation in each (kind of) system? How much of that variation is usually “visible” (to selection, etc)? How much of that variation is usually suppressed? Under what conditions is that variation “released”? 2)How important is the heritable variation in each (kind of) system? (and important for what?) In particular lineages? During particular (evolutionary) events or time- periods? If important for (key) evolutionary innovations, then the heritable variation is important! So even if, at some particular time, in some particular model organisms, with some particular set of techniques, it looks like genetic variation “is different from other components of the developmental process” and that, with “respect to cytoplasmic inheritance and maternal effects, there doesn’t seem to be much here” that is not yet a good reason to privilege genetic over other developmental resources with potential heritable variation…

Developmental Niche Construction Karola Stotz suggests extending our analysis to include “Developmental Niche Construction” – a perspective which “combines ideas of the active organism altering its environment (niche construction), developmental systems theory and extended (non- or extra-genetic) inheritance, evo-eco-devo and phenotypic plasticity.” With Karola, Massimo and I agree that understanding evolutionary change, and perhaps especially innovations and novelties, will require new ways of thinking about the genesis and maintenance of stability as well as what happens when stability breaks down, and I think we are each working towards some version of the integrated perspective that Karola recommends. But while such a perspective will, I agree, be necessary for evolutionary biology to fulfill its promise of explaining the origin, spread, and maintenance of traits in populations, Massimo and I were (we thought) relatively cautious in the book to permit room for such a perspective while not demanding one.

John Dupré draws out attention to microbes, and I’d like to link some of those comments to the suggestions made by Karola. For example, the “problem” of multi-cellularity is usually understood to be about how cells learn to get along, and the answer is generally assumed to have something to do with the genetic similarity of the cells in question. But this won’t do at all. It seems increasingly plausible that many bacteria “species” can only live in close symbiosis with other “species” of bacteria, and that these biofilms are most plausibly thought of as multicellular organisms in their own right, complete with functional specialization... Now, it is true that there is extensive gene exchange in and among biofilm communities, and some have suggested that it is this that maintains sociality in bacterial communities. But there has been little attention to the possibility that shared non-genetic resources are part of what maintain sociality. Biofilm communities are clearly structured, and “altruism” can be associated with any shared developmental resources, not just genetic resources… Note that in structured hierarchical communities, development can (and does) occur over different time and space scales, and each is important…

Paul Griffiths focuses on Massimo’s and my defense of a ‘modern history’ version of etiological functions, including in our individuation of one kind of (or one notion of a) gene; Paul urges us to accept in addition causal functions in at least some contexts, namely those linked to “causal capacities of the organism that are relevant to understanding its evolutionary fate.” I’m going to resist that suggestion… “Biting the bullet” Taken seriously, the claim is that UCG has the function to code for Serine is indeed hostage to discoveries about whether its place in that casual chain is the result of selection or ‘merely’ of chemistry. The phrase “codes for” however is without functional overtones. So sure, UCG codes for Serin (notwithstanding concerns about the informational ascription of coding talk). But that doesn’t mean that the function of UCG is to so-code. So what about the regress?

1)Ascriptions of selected functions are generated by (hypothetical) causal analysis of the capacities of ancestral organisms to survive and reproduce in ancestral environments (Griffiths 2003) 2)Hence, if we cannot identify which capacities of ancestral organisms to subject to causal analysis without knowing what parts of those organisms were selected for in their environments, then we face a vicious regress. 3)Therefore, a purely causal analysis of the adaptive role played by parts of ancestral organisms must be possible without knowing what those parts were adaptations for. 4)Furthermore, ancestral organisms cannot be easier to causally analyze than living organisms on which we can actually experiment (Stotz and Griffiths 2002) Here I think keeping separate the formal and informal selection helps us see why 1 through 3 don’t imply that there are non-etiological functions in biology…

1)Ascriptions of selected functions are generated by (hypothetical) causal analysis of the capacities of ancestral organisms to survive and reproduce in ancestral environments (Griffiths 2003) Yes – this is done by looking for opportunities for informal selection with respect the causal capacities of ancestral organisms. 2)Hence, if we cannot identify which capacities of ancestral organisms to subject to causal analysis without knowing what parts of those organisms were selected for in their environments, then we face a vicious regress. Here I want to note that informal selection of the sort appealed to in (1) doesn’t require that formal selection (a statistical trend) has taken place. Hence we can identify cases of informal selection without knowing whether that selection has had any effect on the evolution of the traits in question. So we don’t need to know what the traits in question were for (or even that they were for anything) to apply the first part of (1).

3)Therefore, a purely causal analysis of the adaptive role played by parts of ancestral organisms must be possible without knowing what those parts were adaptations for. Not exactly… A purely causal analysis of the way in which the parts in question interact with a variety of events/forces in the world must be possible (informal selection) without knowing what the parts are for (or even if they are for anything) The question of ‘for-ness’ is a question that appeals to the formal sense fitness and selection – ‘for-ness’ ties the informal causal analysis to the formal expected changes in the distribution of traits… 4)Furthermore, ancestral organisms cannot be easier to causally analyze than living organisms on which we can actually experiment (Stotz and Griffiths 2002) Yup. But sometimes the assumptions regarding the likely course of the evolution of a population – the likely links between the causal capacities of the parts in question and the statistical outcomes – are likely to be correct…

Metaphors and science Seth White notes that one of the main themes in the book is troublesome metaphors. I should say that the working subtitle for the book was “Metaphors and models in organismal biology.” With Seth, I am confident that metaphors in science are not always problematic, and I agree that as long as one remains focused on the limitations of the metaphors currently in use, they can in fact be helpful. I think as well that Seth’s interest in metaphors in ecology is well-placed; there is a lot of work to be done unpacking and criticizing both contemporary and past metaphors. Notions like “invasive” species, “restoration” ecology, and the like are, I think, ripe for serious critical work… I could say more about this, but given the time limitations…