What is a (Volvox) species?

Hisayoshi Nozaki and colleagues have just described some Volvox samples from two lakes and a pond in Japan.

Figure 1A from Nozaki et al. 2016. Volvox sp. Sagami asexual spheroid with daughter colonies (d).

Figure 1A from Nozaki et al. 2016. Volvox sp. Sagami asexual spheroid with daughter colonies (d).

The newly collected strains have a lot in common with another recently described species, Volvox ferrisii, but there are some important differences as well:

…it could be clearly distinguished from all previously described monoecious species of Volvox sect. Volvox by its small number of eggs or zygotes (5–25) in sexual spheroids, with short acute spines (up to 3 μm long) on the zygote walls and elongated anterior somatic cells in asexual spheroids.

In spite of these differences, Nozaki and colleagues stop short of calling the newly collected strains a new species. Why?

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It’s not evolution, just adaptation

…”evolve” is not the correct term. The microbes adapted. – Cornelius Hunter

We heard several accusations during the recent Presidential campaign that one or the other candidate, or an interviewer, had taken a quote out of context. Of course, every quote is taken out of context. That’s what a quote is; otherwise it’s just the whole speech, or interview, or whatever. The important question is whether or not it’s taken out of context in a way that changes its meaning.

One thing I don’t do, and never have done, on this blog is intentionally misrepresent other people’s positions.  The quote above, from a recent post by Cornelius Hunter on Evolution News and Views, means just what it says. He really is arguing that microbial adaptation observed in Lenski-style experiments is not evolution.

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Initiation of cell division in Chlamydomonas

Deborah Shelton and colleagues have published a new article arguing that the reigning model of cell division initiation in Chlamydomonas reinhardtii needs to be revised [full disclosure: Dr. Shelton and I were labmates in Rick Michod’s lab at the University of Arizona]. The evolution of multicellularity almost certainly involved changes in cell cycle regulation; for example, there is good evidence that changes to the cell cycle regulator retinoblastoma were involved in the initial transition to multicellular life in the volvocine algae. So understanding cell cycle regulation is vital for understanding the evolution of multicellularity.

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Proxima b is a challenge to materialism, according to David Klinghoffer

David Klinghoffer, a Senior Fellow at the Discovery Institute, thinks the discovery of a relatively close, relatively Earth-like planet presents a challenge not only to evolutionary theory (Klinghoffer thinks every new discovery presents a challenge to evolutionary theory), but to any materialist worldview (“Put Up or Shut Up for Evolution? Nearest ‘Habitable’ Planet Found Orbiting Proxima Centauri“):

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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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Retrogenes in Volvox and Chlamy

The evolution of multicellularity in the volvocine algae appears to have happened primarily through co-option of existing genes for new functions. For example, the initial transition from a unicellular life cycle to a simple multicellular one involved the retinoblastoma gene, as Hanschen and colleagues elegantly demonstrated (see “The evolution of undifferentiated multicellularity: the Gonium genome“). A Volvox gene involved in cellular differentiation, regA, was likely co-opted from an ancestral role in environmental sensing, and a similar origin appears to explain the use of cyclic AMP for the signaling that causes multicellular aggregation in cellular slime molds (see “Volvox 2015: evolution“). 

Some of the changes leading to complex multicellularity, though, clearly did involve new genes. Two gene families involved in building the extracellular matrix that makes up most of a Volvox colony, the pherophorins and metalloproteinases, have undergone multiple duplication events leading to greatly expanded gene families (see “Heads I win; tails you lose: Evolution News & Views on Gonium, part 2“). One mechanism by which genes are duplicated is retroposition, in which a messenger RNA is reverse transcribed into DNA and inserted into the genome:

Fig S1A from Jakalski et al. 2016. Basic mechanism of retroposition. DNA is transcribed into a pre-mRNA by RNA polymerase, introns are spliced out, and a poly(A) tail is added to the 3′ end, resulting in a mature messenger RNA. The mRNA is then reverse-transcribed to DNA and inserted into a new genomic location.

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The evolution of undifferentiated multicellularity: the Gonium genome

Blogging took a backseat to the wedding of two dear friends two weekends ago and to morel hunting last weekend, so I’m only now getting around to a post that should have been written weeks ago (I promised on April 22 that it would be out the following week). Last month, Erik Hanschen and colleagues published the Gonium pectorale genome, filling in some crucial bits of the transition to multicellular life in the volvocine algae. This was a big project, taking several years and involving over 20 authors from over a dozen institutions. The final paper is open access in Nature Communications.

I did post an effort to explain some aspects of the paper to the cdesign proponentsists at Evolution News and Views, who, by their own admission, failed to understand it (“After reading this paper, we’re none the wiser.”). I also complained of the science media’s tendency to refer to all algae as ‘pond scum.’ The lead author of the genome paper kindly followed up with a guest post addressing some of ENV‘s other misunderstandings, such as the purpose of model organisms in biology and the difference between ‘assertion’ and ‘evidence’. But now it’s time to dig into what the genome paper actually says.

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Buy your Ph.D.

100 pages ought to do it, I think. If you’re worried that that won’t pass the weight test, just add on a great big appendix; nobody’s going to read it. Think of the time and money you can save! Think of the poor slobs pipetting their youth away while you’re partying. Don’t think about how your committee is going to react to a data-free dissertation at your defense. What can they say? They have to pass you; it’s 200 pages!

StudyBay

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