Ulvophyte multicellularity: the sea lettuce genome

Ulva

Sea lettuce (Ulva sp.), Jericho Beach, Vancouver, BC, February 28, 2011.

David Kirk called the Chlorophyte green algae “master colony-formers” because multicellularity has evolved so many times within this class:

Although members of most chlorophycean genera and species are unicellular flagellates, multicellular forms are present in 9 of the 11 chlorophycean orders (Melkonian 1990). Multicellularity is believed to have arisen independently in each of these orders, and in some orders more than once.

In contrast, multicellularity has probably only evolved once or twice in the probable sister group of the Chlorophyceae, the Ulvophyceae. So when numbers like 25 get thrown around for the number of times multicellularity has evolved, something like half of those times were in the green algae.

We know a lot less about how multicellularity evolved in the Ulvophyceae than we do in the volvocine algae within the Chlorophyceae. A big step forward in understanding ulvophyte multicellularity happened last week, though, with the publication of the Ulva mutabilis genome.

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Life cycles in major transitions, and some clueless critique

Jordi van Gestel and Corina Tarnita have published a ‘Perspective’ in PNAS, “On the origin of biological construction, with a focus on multicellularity“:

…we propose an integrative bottom-up approach for studying the dynamics underlying hierarchical evolutionary transitions, which builds on and synthesizes existing knowledge. This approach highlights the crucial role of the ecology and development of the solitary ancestor in the emergence and subsequent evolution of groups, and it stresses the paramount importance of the life cycle: only by evaluating groups in the context of their life cycle can we unravel the evolutionary trajectory of hierarchical transitions.

van Gestel 2017 Fig. 2

Figure 2 from van Gestel and Tarnita, 2017. Relationship between life stages in hypothesized life cycles of solitary ancestors and group formation in derived group life cycles. (Upper) Simplified depiction of hypothesized ancestral solitary life cycles of the green alga Volvox carteri, the cellular slime mold Dictyostelium discoideum, and the wasp Polistes metricus. Life cycles here consist of a life stage expressed under good conditions (black) and a life stage expressed under adverse conditions (green). For the latter life stage, we show an environmental signal that might trigger it and some phenotypic consequences. (Lower) Simplified depiction of group life cycles of: V. carteri, D. discoideum, and P. metricus. Developmental program underlying life stages in solitary ancestor is co-opted for group formation (shown in green): differentiation of somatic cells (V. carteri), fruiting body formation (D. discoideum), and appearance of foundress phenotype (P. metricus).

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Multicellularity rundown

Too many papers, not enough time: each of these deserves a deep dive, but my list just keeps getting longer, so I’m going to have to settle for a quick survey instead. To give you an idea of what I’m up against, these papers were all published (or posted to bioRxiv) in July and August, 2016. By the time I could possibly write full-length posts about them all, there would probably be ten more!

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Heads I win; tails you lose: Evolution News & Views on Gonium, part 1

Figure 6 from Hanschen et al. 2016. Multicellularity hinges on the evolution of cell cycle regulation in a multicellular context with subsequent evolution of cellular differentiation (here, cell size-based) and increased body size.

Figure 6 from Hanschen et al. 2016. Multicellularity hinges on the evolution of cell cycle regulation in a multicellular context with subsequent evolution of cellular differentiation (here, cell size-based) and increased body size.

Remember how I said they’re prolific? Before I’ve even had a chance to write up my thoughts on the Gonium genome paperEvolution News & Views has already published theirs. The story has also been picked up by the Washington PostNew HistorianGenNews, and ScienceDaily (that last one looks like just a reprint of the press release from University of the Witwatersrand). By the way, the genome paper is open access, so you don’t need a subscription to see it for yourself.

We already know that cdesign proponentsists are not fans of research into the evolution of multicellularity, and that they have trouble understanding it. In an unsigned article on the Gonium genome at ENV, they admit that

After reading this paper, we’re none the wiser.

That’s too bad. I’m here to help.

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The flip side of the Galileo Gambit: Denyse O’Leary on multicellularity

Figure 7 from Anderson et al. 2016. Evolution of GKPID’s new function by unveiling a latent protein-binding site. (A) The binding surface for Pins in GKPIDs is derived from the GMP-binding surface of gk enzymes. Homology models of Anc-gkdup (left) and Anc-GK1PID (right) are shown as white surface, with all side chains that contact either GMP or Pins as yellow sticks. Pink sticks show GMP; green ribbon shows Pins backbone, with the side chains of all Pins residues that contact the GK protein shown as sticks. The phosphate group on GMP and on Pins residue 436 are shown as orange and red sticks. Black dotted lines, protein-ligand hydrogen bonds. In the AncGK1PID structure , substitutions at sites in the binding interface are shaded red, including key substitution s36P. The binding modes of extant gk enzymes and GKPIDs are similar and support the same conclusions (see Figure 7—figure supplement 1). (B) The structure of the hinge and GMP/Pins-binding lobes is conserved between the Pins-bound GKPID (blue, rat Dlg, 3UAT), the apo-gk enzyme (brown, S. cerevisiae guanylate kinase 1EX6), and the apo-gk-s36P mutant (gray, 4F4J), all in the open conformation.

Figure 7 from Anderson et al. 2016. Evolution of GKPID’s new function by unveiling a latent protein-binding site. (A) The binding surface for Pins in GKPIDs is derived from the GMP-binding surface of gk enzymes. Homology models of Anc-gkdup (left) and Anc-GK1PID (right) are shown as white surface, with all side chains that contact either GMP or Pins as yellow sticks. In the AncGK1PID structure , substitutions at sites in the binding interface are shaded red, including key substitution s36P. (B) The structure of the hinge and GMP/Pins-binding lobes is conserved between the Pins-bound GKPID (blue, rat Dlg, 3UAT), the apo-gk enzyme (brown, S. cerevisiae guanylate kinase 1EX6), and the apo-gk-s36P mutant (gray, 4F4J), all in the open conformation.

Cdesign proponentsists really don’t seem to like research on the evolution of multicellularity. Pretty much any time real scientists learn something new about the origins of multicellularity, writers on intelligent design blogs Evolution News & Views and Uncommon Descent feel compelled to tell us why it’s wrong (for example, here, here, here, here, here, here, here, here, here, here, here, here, and here).

So I shouldn’t be surprised that Denyse O’Leary has weighed in on the latest work out of Ken Prehoda’s lab, in which Prehoda and colleagues identified a mutation crucial for forming and maintaining tissues in animals. Worse, from O’Leary’s point of view, the article describes the evolution of a new protein function, which is anathema to intelligent design thinkers. To say this post is badly argued is overly generous; it’s absolutely devoid of any substantive argument.

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