This article is from
Journal of Creation 26(1):10–12, April 2012

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Does biological advantage imply biological origin?

123rf.com/Vladimir Nenov Microsope


The origins of sexual dimorphism and multicellularity are two of the greatest mysteries to evolution. For either of them to evolve requires massive restructuring of the biological system from the molecular to the organismal levels. Moreover, there are massive selection and energetic barriers that must be crossed to get from unicellular to multicellular life and to evolve sexual dimorphism. Two recent news articles have claimed that certain biological advantages in sexual dimorphism1 and multicellularity2 provide a reason why they evolved in the first place.

Intra-cell communication and sexual dimorphism

The first study discusses the question: why are there two sexes?3 In terms of evolution, it’s not the best number of mating types because it only allows us to mate with half of the population. However, researchers have proposed that inheriting mitochondrial DNA (mtDNA) from just one parent instead of both may serve to offset this disadvantage. Most sexually reproducing creatures only receive nuclear DNA from their father but get the other half of their nuclear DNA plus their entire cellular structure, including mtDNA, from their mother. The researchers proposed that because this setup only passed one set of mtDNA to offspring, it allowed for more efficient ‘synchronization’ between the nucleus and mitochondria, and between mitochondria, than would be possible if mitochondria were inherited from both parents. According to their modelling, they were correct—uniparental inheritance of mitochondria (UIM) produced fitter offspring than biparental inheritance of mitochondria (BIM) under most realistic selection constraints.

But the researchers also explore this question: “Could uniparental inheritance of mitochondria have arisen to facilitate better co-adaptation of mitochondrial and nuclear genes, and so explain the evolution of two sexes?”,3 to which they ultimately give a positive answer. However, this misplaces the important question for the evolution of any new trait—how it arose in the first place. Essentially, they perform a cost-benefit analysis between UIM and BIM, determine that UIM is the better system, and then conclude that UIM must have evolved from BIM. But this skips over the succession of events that supposedly led to the evolution of UIM from BIM because the researchers assume that since UIM and sexual dimorphism exist, they must have evolved. This is clearly begging the question of evolution, but it’s worse. Evolution is taken as so incontrovertible that questions of how (the succession of evolutionary events) are deemed superfluous, and all that matters is why UIM evolved. However, all they have established is that UIM provides the functional grounds for sexual dimorphism in eukaryotes, and the origin of that function is the very question which the fact of its functionality does not directly address.

Kinship and the evolution of multicellularity

Another recent study showed how high-relatedness between cells is a necessary prerequisite for multicellularity.4 The researchers ran two experiments on the amoeba Dictyostelium discoideum, one where they tested the effects of low-relatedness on Dictyostelium’s ability to form multicellular fruiting bodies, and the other tested the effects of mutation accumulation in a single clonal line. The researchers found that when different lines were mixed, it didn’t take long for ‘cheater’ mutants to take advantage of the fruiting bodies and propagate ahead of the non-cheaters, to the point where there were so many ‘cheaters’ that many lines were unable to form fruiting bodies at all by the end of the experiment. In contrast, fruiting ability was never lost in the mutation accumulation experiment where high-relatedness was maintained, as per conditions in the wild. As a result, the researchers concluded that high-relatedness was necessary and sufficient to maintain the viability of the multicellular stage in Dictyostelium’s life cycle. The researchers then applied their findings to multicellular life in general:

“Thus, we conclude that the single-cell bottleneck is a powerful stabilizer of cellular cooperation in multicellular organisms.”5

This is a fair application of their research. It highlights a necessary prerequisite for functional multicellularity, and it doesn’t extend all the conclusions about high-relatedness in Dictyostelium to all multicellular life. But compare this to the questions the news article says this research answers:

“How could the extreme degree of cooperation multicellular existence requires ever evolve? Why aren’t all creatures unicellular individualists determined to pass on their own genes?”2

This presupposes that functional multicellularity evolved, and proposes that the mere existence of high-relatedness among cells is the reason why it evolved. However, creationists can also presuppose the necessity of high-relatedness among cells for functional multicellularity to be possible without an appeal to evolution.6 We have here confusion between the functional grounds of a trait and the historical cause of a trait. If multicellularity evolved, then it must have evolved from a population of clones, but this tells us very little about the succession of events that led from a unicellular ancestor to the first metazoan or plant. Therefore, it is not a helpful explanation of the evolution of multicellularity.

How useful is Dictyostelium for studying the evolution of multicellularity?

Photo courtesy of Wikipedia Figure 1. Multicellular fruiting bodies of Dictyostelium discoideum.
Figure 1. Multicellular fruiting bodies of Dictyostelium discoideum.

But is Dictyostelium a model organism for studying how the evolution of multicellularity might proceed? The researchers point out that ‘cheaters’ are not a problem for Dictyostelium colonies even if they were the size of a blue whale.7 However, even the news article admits that a blue-whale-sized Dictyostelium colony is not the same thing as a blue whale.2 But it fails to describe why. It is one thing to grow a colony to the size of a blue whale, but it is a different thing to maintain the colony at that size in a multicelled state over a period of decades. The researchers admit that little cell division occurs in the multicelled phase of Dictyostelium.7 In a multicellular stage that has little cell division, there is obviously no need for strategies such as serial differentiation8 to maintain the multicelled state. Thus it is not surprising that the multicelled stage in Dictyostelium does not last very long—a day or less.

Moreover, 80% of the individual Dictyostelium cells survive the multicelled phase, and then go on to reproduce as unicellular organisms. Even volvocine algae,9 which do not possess the separation of totipotency and cellular immortality (e.g. reduced mitotic capacity or multipotency) that is the hallmark true differentiated multicellularity,10 sacrifice thousands of somatic cells in their multicellular phase to produce perhaps a dozen or so germ cells. This proportion drastically increases again out of necessity when the organism possesses a functional cellular differentiation program designed to structure and maintain the multicelled state.8 While there is an analogy to unicellular ‘bottlenecking’ in the dispersal of the spores at the end of Dictyostelium’s multicelled phase, Dictyostelium has nothing like the proportion of cellular sacrifice that occurs in multicelled life. Volvocine algae are likely the closest that life capable of free-living unicellularity can ever come to true differentiated multicellularity, and Dictyostelium doesn’t even approach this level of multicellular coordination, let alone what is found in plants, animals, and fungi. Therefore, Dictyostelium can only tell us so much about multicellular life, and it can provide little information on the historical sequence necessary to evolve true differentiated multicellularity.

Does an advantage provide an origins narrative?

Both of these studies have been said to answer some important questions about evolution. Both have been said to provide a reason why this or that trait evolved because these traits have been demonstrated to convey a certain selective advantage above the presumed ancestral condition, or the acquisition of a new trait has proved impossible without a certain feature.

The reasoning basically goes like this: “Why did x structure evolve? Because it conveyed y advantage.” There is a major fallacy here: note that this doesn’t deal with how it evolved because key causal links between the ancestral and the descendant traits have been ignored. The question of how involves discussions of evolutionary mechanisms, such as specific mutations, specific regulatory and developmental changes, their effects, and the selection mechanisms that have contributed to the preservation of these changes. Explaining the advantages of a rewired system does not explain the rewiring sequence that took place to change the old configuration into something completely new, and it does not directly explain how the wiring got there in the first place. In fact, the soundest inference from such parameters as proper wiring and fitted function is to an intentional creation, not unintentional nature.

Rarely is this sort of detailed, step-by-step narrative ever provided for even the smallest evolutionary events, let alone the massive morphological restructuring involved in turning (for example) a free-living unicellular organism into one with differentiated multicellularity, or even turning a sarcopterygian ancestor into a tetrapod descendant. On the few occasions that such plausible narratives are constructed, they are only for “incidental (and accidental) biological function”, not “essential biological structure”.11

For any fruitful debate to proceed regarding the plausibility of evolution, the right questions need to be asked and answered. Asking why one structure has an advantage over another is the wrong question with which to seek origins answers. A serious researcher would instead inquire into the feasibility of each step along a hypothetical evolutionary path, like from unicellularity to multicellularity.12 However, the science media typically obfuscates these matters, and even researchers fail to appreciate the depths of explanation that evolutionary theory needs to provide a truly compelling narrative for the history of biology capable of outweighing the design explanation with which it competes.

Posted on homepage: 14 June 2013


  1. Hurrell, P., High-energy lifestyles led to evolution of the sexes, Physorg.com, 19 December 2011, www.physorg.com/news/2011-12-high-energy-lifestyles-evolution-sexes.html. Return to text.
  2. Experiments explain why almost all multicellular organisms begin life as a single cell, Physorg.com, 15 December 2011, www.physorg.com/news/2011-12-multicellular-life-cell.html. Return to text.
  3. Hadjivasiliou, Z. et al., Selection for mitonuclear co-adaptation could favour the evolution of two sexes, Proc. Royal Soc. B, Published online 7 December 2011 | doi: 10.1098/rspb.2011.1871. Return to text.
  4. Kuzdzal-Fick, J.J. et al., High relatedness is necessary and sufficient to maintain multicellularity in Dictyostelium, Science 334:1548–1551, 16 December 2011. Return to text.
  5. Kuzdzal-Fick, ref. 4, p. 1548. Return to text.
  6. Doyle, S., Evolution of multicellularity: what is required? J. Creation 23(1):5–7, 2009; creation.com/multicellularity. Return to text.
  7. Kuzdzal-Fick, ref. 4, p. 1550. Return to text.
  8. Doyle, S., Serial cell differentiation: intricate system of design, J. Creation 22(2):6–8, 2008; creation.com/serial-cell-differentiation-intricate-system-of-design. Return to text.
  9. For a discussion of volvocine algae and the evolution of differentiated multicellularity, see Doyle, ref. 6, and Michod, R.E., Nedelcu, A.M. and Roze, D., Cooperation and conflict in the evolution of individuality IV. Conflict mediation and evolvability in Volvox carteri, BioSystems 69:95–114, 2003; esp. pp. 105–106. Return to text.
  10. Doyle, ref 6, p. 7. Return to text.
  11. Doyle, S., Antifreeze protein evolution: turning wrenches into hammers, J. Creation 25(2):14–17, 2011. Return to text.
  12. A few researchers are doing just this. Their results all show overwhelmingly impossible odds for naturalistic formation of even basic subsets of biology, like single proteins or gene regulators. See, for example, Behe, M., Experimental Evolution, Loss-of-function mutations, and the first rule of adaptive evolution, Quart. Rev. Biol. 85(4):419–444, 2010; Finnigan, G.C. et al., Evolution of increased complexity in a molecular machine, Nature 481(7381):360–364, 2012; Bridgham, J.T., Ortlund, E.A. and Thornton, J.W., An epistatic ratchet constrains the direction of glucocorticoid receptor evolution, Nature 461(7263):515–519, 2009; Axe, D., Estimating the prevalence of protein sequences adopting functional enzyme folds, J. Mol. Biol. 341(5):1295–1315, 2004; Axe, D., The limits of complex adaptation: an analysis based on a simple model of structured bacterial populations, Bio-Complexity 2010(4):1–10, 2010. Return to text.

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