Tag Archives: evolution

Nick Lane Lecture

Enjoy this lecture, as it echoes many of the points i have made on this blog:

Amoeba now support front-loading evolution


I told you tyrosine kinases were old. It has now been discovered in amoeba, along with machinery to help front load the emergence of the immune system:

From Clarke M et al., Genome of Acanthamoeba castellanii highlights extensive lateral gene transfer and early evolution of tyrosine kinase signaling.  Genome Biol. 2013 Feb 1;14(2):R11

BACKGROUND: The Amoebozoa constitute one of the primary divisions of eukaryotes encompassing taxa of both biomedical and evolutionary importance, yet its genomic diversity remains largely unsampled. Here we present an analysis of a whole genome assembly of Acanthamoeba castellanii (Ac) the first representative from a solitary free-living amoebozoan.


Ac encodes 15,455 compact intron rich genes a significant number of which are predicted to have arisen through interkingdom lateral gene transfer (LGT). A majority of the LGT candidates have undergone a substantial degree of intronization and Ac appears to have incorporated them into established transcriptional programs. Ac manifests a complex signaling and cell communication repertoire including a complete tyrosine kinase signaling toolkit and a comparable diversity of predicted extracellular receptors to that found in the facultatively multicellular dictyostelids. An important environmental host of a diverse range of bacteria and viruses, Ac utilizes a diverse repertoire of predicted pattern recognition receptors many with predicted orthologous functions in the innate immune systems of higher organisms.


Our analysis highlights the important role of LGT in the biology of Ac and in the diversification of microbial eukaryotes. The early evolution of a key signaling facility implicated in the evolution of metazoan multicellularity strongly argues for its emergence early in the Unikont lineage. Overall the availability of an Ac genome should aid in deciphering the biology of the Amoebozoa and facilitate functional genomic studies in this important model organism and environmental host.

Remind me again why I am supposed to be wrong about the hypothesis of front-loading evolution?

Is evolution predictable? To a surprising extent the answer is yes.

In chapter 7 of The Design Matrix, I have a section entitled, “Unpredictably Predictable.”  The basic argument is summarized in the last sentence of that chapter:

Even though evolution is supposed to be inherently unpredictable, as we can see, it has occurred within a very predictable biological matrix.

Evolution is not some random “free-for-all” where anything that just happens to work will eventually be selected for.  Evolution is a biological process that is constrained and thus channeled by the composition and arrangement of life’s machinery.

I then spell out one aspect of this evolution in a section entitled, “Designed to Redesign.”  Here I talk about the essential role that gene duplication plays in the function we call “evolution”:

It is a beautiful solution for a front-loading designer. In one process, we both propagate the original design and set things up to unpack secondary designs without erasing the original design. Stability and change, all in one package. As an added bonus, the infl uence of contingency is dampened. It does not matter if some or many gene duplication events drift off in unintended fashion (most will merely tweak the original function or decay away). Th e beauty of gene duplication is that it explores sequence space while retaining and propagating the original sequence. As long as the original sequence is essentially retained somewhere, someplace, evolution gets to “try again” over and over and over in its rigged search for some future design. In other words, if a designer wanted a secondary design to unpack itself in an animal cell, duplication of the original sequence is bound to happen in all cells, including animal cells. When it eventually occurs in an animal cell, the stage is set to unpack the secondary design. If it fails, we need only wait until the next round of duplication and mutation occurs. It is the intelligent use of chance.

Over five years later, a paper has appeared in the journal Science that adds even more plausibility to my perspective.  Enjoy:

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A humbling reversal?

I have long noted that the case for non-teleological evolution was stronger in the past than it is in the present.  Consider this tiny example.

Below is a figure from Eukaryotic Evolution: Getting to the Root of the Problem (Simpson and Roger, Current Biology, Vol. 12, R691–R693, October 15, 2002).

The figure on the left is the eukaryotic phylogenetic tree from 1993 and before.  Simpson and Roger explain it as follows:

A decade ago, phylogenies based on small subunit ribosomal (r)RNA sequences provided an intuitively appealing evolutionary tree of eukaryotes. Complex eukaryotes, including animals, fungi, plants and most algae, emerged as a broad radiation usually called the ‘eukaryotic crown’ [1]. Below this ‘crown’, more bizarre, and generally simpler, organisms diverged in a ladder-like succession. The small subunit rRNA tree was ‘rooted’ with mitochondrion-lacking unicellular eukaryotes such as diplomonads, parabasalids and microsporidia forming the basal branches (Figure 1a).

Yes, this was intuitively appealing from a non-teleological, neo-darwinian viewpoint.

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Evolution Follows the Path of Least Resistance

Over at Jerry Coyne’s blog, biologist Greg Mayer wrote:

One of the most important lessons of comparative anatomy is that evolution usually proceeds by the modification of pre-existing structures (or, stated more precisely, the modification of the pre-existing developmental programs that produce those structures). Certain changes are easier to evolve because the developmental system can be modified to produce them—evolution follows the developmental path of least resistance. In terms of the skeleton of vertebrates, this means that most evolutionary changes are reduction, fusion, loss, lengthening, shortening, thickening,  and narrowing of bones. Evolution uses what’s already there, and rarely do wholly new structures arise.  (from “Tinkering with elephants’ feet”)

All of this is true, yet we can proceed beyond this conventional thinking and ask a couple of questions:

WHY does evolution follow the developmental path of least resistance?

WHAT are the implications of evolution following the developmental path of least resistance?

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Evolutionary Thought Experiment

Let me provide you with a little evolutionary thought experiment.  Stephen J. Gould once noted that “evolution is a bush, not a ladder.”  Quite true.  Consider the following representation:


Notice that the evolution of mammals does not entail a straight shot from some ancestral chordate to mammal.  On the contrary, the evolution of mammals also involves the evolution of sharks, bony fish, frogs, snakes, and birds along the way.  What’s more, the bush shows a nesting pattern, where the tetrapods, for example, nest together to the exclusion of all other chordates.  This is because the tetrapods derive from an ancestral tetrapod state that was not shared by the other chordates.  In fact, the following arrangement makes this more clear.

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Genetic Switch for Limbs and Digits Found in Primitive Fish

From here:

Genetic instructions for developing limbs and digits were present in primitive fish millions of years before their descendants first crawled on to land, researchers have discovered.

Genetic switches control the timing and location of gene activity. When a particular switch taken from fish DNA is placed into mouse embryos, the segment can activate genes in the developing limb region of embryos, University of Chicago researchers report in Proceedings of the National Academy of Sciences. The successful swap suggests that the recipe for limb development is conserved in species separated by 400 million years of evolution.

“The genetic switches that drive the expression of genes in the digits of mice are not only present in fish, but the fish sequence can actually activate the expression in mice,” said Igor Schneider, PhD, postdoctoral researcher in the Department of Organismal Biology and Anatomy at the University of Chicago and lead author on the paper.

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