Pierrick Bourrat responds

[I invited Pierrick Bourrat to respond to my two posts about his new paper and to comments to those posts. He kindly agreed, and he provided the following guest post, which I have edited only for formatting.]

First of all, I would like to thank Matthew Herron for his interest in my work and his invitation to respond to his posts. Also, I would like to thank Rick Michod and Deborah Shelton for their comments.

I will respond to several issues pointed out both in the posts and the comments.

About the usefulness of the export of fitness view of ETI: I agree that it is a useful way of thinking about it, as long as it is used as a heuristic. This means that I am not inclined to think that building models with the assumption that the fitness of a cell would have been 0 had it been in an environment with not social partners will be able to explain in some deep sense ETIs (and even more so the origin of fitness at some level). In his comment to Matthew’s first post, Rick Michod claims that I somehow confuse realized fitness from a more counterfactual notion of fitness.  Well, to be honest, I do not see how one could simulate (I do not mean ‘explain’) the evolution of a process if the variables in the model do not correspond to realized properties of the system. If I want to model a particular phenomenon, I ought to use variables and parameters that represent the target system and clearly, at least for me, this counterfactual notion of fitness does not represent any properties the cells have because they always have social partners. It is common to use expected rather than realized fitness in models, but this assumption is justified when we can assume that population are large and the environment is overall not fluctuating too much. With the counterfactual notion of fitness, aside from being useful for explaining the ETIs, I fail to see how it could be successfully integrated in models (by successfully, I mean how it could represent meaningfully the target system).

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Expression and form: Arash Kianianmomeni on gene regulation

Kianianmomeni Figure 1

Figure 1 from Kianianmomeni 2015. Gene regulatory mechanisms behind the evolution of multicellularity. Model illustrating the role of gene regulatory mechanisms in the evolution of multicellular Volvox from a Chlamydomonas-like ancestor.

Arash Kianianmomeni’s latest paper in Communicative & Integrative Biology addresses the possible roles of gene regulation and alternative splicing in the evolution of multicellularity and cellular differentiation (Kianianmomeni, A. 2015. Potential impact of gene regulatory mechanisms on the evolution of multicellularity in the volvocine algae. Commun. Integr. Biol., 37–41. doi 10.1080/19420889.2015.1017175). The article is an ‘Addendum’ to a 2014 study by Kianianmomeni and colleagues in BMC Genomics. Communicative & Integrative Biology often invites authors to write these addenda after they have published a (usually high impact) paper elsewhere, providing authors the opportunity to publish material that was not included in the original paper due to space limitations or because it was opinionated or speculative. I may address the BMC Genomics article in a future post, but right now there is more new volvocine research than I have time to write about (it should be an exciting Volvox meeting this summer!).

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Pierrick Bourrat on levels, time, and fitness, part 2: collective fitness

Last week, I posted some thoughts on Pierrick Bourrat’s new paper in Philosophy and Theory in Biology, focusing on his criticism of Rick Michod’s ‘export of fitness’ framework. This week, I’ll take a look at the second of Bourrat’s criticisms, regarding the transition from MLS1 to MLS2, as first defined by Damuth & Heisler, during a transition in individuality.
MLS1 and MLS2 refer to two different versions of MultiLevel Selection. As Bourrat describes it (and this is pretty much in line with other authors), fitness in MLS1 is defined in terms of the number of particles (or lower-level units, or cells) produced, while in MLS2 the fitnesses of the particles and collectives (or cells and multicellular organisms) are measured in different units. Cell-level fitness (for example) is defined in terms of the number of daughter cells, organism-level fitness is based on the number of daughter organisms. (As with last week’s post, I’ll generally stick to cells and organisms, though the principles apply equally to any two adjacent levels.

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Pierrick Bourrat on levels, time, and fitness, part 1: zero fitness?

Pierrick Bourrat’s new paper in Philosophy and Theory in Biology criticizes aspects of the influential ‘export of fitness’ framework developed by Rick Michod and colleagues and extended by Samir Okasha (Bourrat, P. 2015. Levels, time and fitness in evolutionary transitions in individuality. Philos. Theory Biol., 7: e601. doi: 10.3998/ptb.6959004.0007.001). According to this view, an evolutionary transition in individuality, for example from unicellular to multicellular life, involves a transfer of fitness from the lower level units (e.g. cells) to the higher level unit (e.g. nascent multicellular organism). Fitness is defined as the product of viability and fecundity, and the emergence of a division of labor between reproductive (germ) and non-reproductive (somatic) units at the lower level exports fitness to the higher level. Full disclosure: Rick Michod was my Ph.D. co-advisor, and he has had a huge influence on my thinking about this topic.

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Evolutionary Transitions to Multicellular Life published

Iñaki Ruiz-Trillo and Aurora Nedelcu have recently edited a new book on the evolution of multicellularity, Evolutionary Transitions to Multicellular Life.  The 22 chapters are divided into five sections: “Multicellularity in the Tree of Life,” “Model-Systems,” “Theoretical Approaches,” “Genomics Insights,” and “Molecular Mechanisms,” and the forward is written by Nicole King. Volvox  shows up in the chapters by Susan C. Sharpe, Laura Eme, Matthew W. Brown and Andrew Roger (“Timing the origins of multicellular eukaryotes through phylogenomics and relaxed molecular clock analyses”); by myself and Aurora Nedelcu (“Volvocine algae: from simple to complex multicellularity”); by Cristian A. Solari, Vanina J. Galzenati and John O. Kessler (“The evolutionary ecology of multicellularity: the volvocine green algae as a case study”); by John O. Kessler, Aurora M. Nedelcu, Cristian A. Solari and Deborah E. Shelton (“Cells acting as lenses: a possible role for light in the evolution of morphological asymmetry in the volvocine algae”); and by Daniel Lang and Stefan A. Rensing (“The evolution of transcriptional regulation in the Viridiplantae and its correlation with morphological complexity”).

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Ann Gauger teaches us about Volvox, part 2

Last time, I criticized Ann Gauger’s Evolution News and Views article “A Simple Transition to Multicellularity — Not!” for asserting that the requirement for kinesins in Volvox inversion implied a requirement for novel genes in the evolution of multicellularity. In a similar vein, Dr. Gauger presents programmed cell death and sex as problems for this transition:
The somatic cells commit suicide by a process known as apoptosis — programmed cell death — that I wrote about here. This process involves a minimum of several novel genes as well.
Where does this assertion that programmed cell death in Volvox “involves a minimum of several novel genes” come from? Programmed cell death (PCD) occurs in many unicellular eukaryotes, including Chlamydomonas reinhardtii. Furthermore, two types of metacaspases, genes involved in PCD in many algae and plants, are found in both Chlamydomonas and Volvox.
Metacaspases

Partial alignment of representative type I and type II metacaspase predicted sequences from red algae (Porphyra yezoensis; Py), green algae (Chlamydomonas reinhardtii, Cr; Volvox carteri, Vc), vascular plants (Arabidopsis thaliana; At), excavates (Trypanosoma cruzi, Tc; Leishmania braziliensis, Lb), diatoms (Thalassiosira pseudonana, Tp; Phaeodactylum tricornutum, Pt), haptophytes (Emiliania huxleyi; Eh), pelagophytes (Auroecoccus anaphagefferens; Aa), yeasts (Schizosaccharomyces pombe, Sp; Saccharomyces cerevisiae, Sc) showing the conservation of the cysteine-histidine dyad and the insertion characteristic of plant type II metacaspases. From Nedelcu, A.M. 2009. Comparative genomics of phylogenetically diverse unicellular eukaryotes provide new insights into the genetic basis for the evolution of the programmed cell death machinery. J. Mol. Evol., 68: 256–268. doi 10.1007/s00239-009-9201-1.

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Ann Gauger teaches us about Volvox, part 1

Over at Evolution News and Views (ENV), the blog for the Discovery Institute, Ann Gauger has a new article about Volvox (“A Simple Transition to Multicellularity — Not!”). This isn’t the first time ENV has weighed in on the evolution of multicellularity (see here and here, for example), but since their website doesn’t allow comments, this is the first time I’ve had a platform from which to respond.
The article starts out with a mostly accurate description of Volvox biology, although the description as
…among the simplest animals to have more than one cell type

is cringe-worthy: Volvox is no more an animal than is a tomato:

DogTomatoVolvoxTree

An accurate, if low-resolution, phylogeny.

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