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.

RESULTS:

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.

CONCLUSIONS:

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:

Neuron, Muscle, and Front-loading

Well, it’s been almost four months since I last updated this blog. The nice thing about the hypothesis of front-loading is that with the passing of time, and the acquisition of new data, the hypothesis becomes increasingly plausible. Consider this:

A previous sequencing of the genome of the Amphimedon queenslandica — a sponge that lives in Australia’s Great Barrier Reef — showed that it contained the same genes that lead to the formation of synapses, the highly specialized characteristic component of the nervous system that sends chemical and electrical signals between cells. Synapses are like microprocessors, said Kosik explaining that they carry out many sophisticated functions: They send and receive signals, and they also change behaviors with interaction — a property called “plasticity.”

“Specifically, we were hoping to understand why the marine sponge, despite having almost all the genes necessary to build a neuronal synapse, does not have any neurons at all,” said the paper’s first author, UCSB postdoctoral researcher Cecilia Conaco, from the UCSB Department of Molecular, Cellular, and Developmental Biology (MCDB) and Neuroscience Research Institute (NRI).

This time the scientists, including Danielle Bassett, from the Department of Physics and the Sage Center for the Study of the Mind, and Hongjun Zhou and Mary Luz Arcila, from NRI and MCDB, examined the sponge’s RNA (ribonucleic acid), a macromolecule that controls gene expression. They followed the activity of the genes that encode for the proteins in a synapse throughout the different stages of the sponge’s development.

“We found a lot of them turning on and off, as if they were doing something,” said Kosik. However, compared to the same genes in other animals, which are expressed in unison, suggesting a coordinated effort to make a synapse, the ones in sponges were not coordinated.
“It was as if the synapse gene network was not wired together yet,” said Kosik. The critical step in the evolution of the nervous system as we know it, he said, was not the invention of a gene that created the synapse, but the regulation of preexisting genes that were somehow coordinated to express simultaneously, a mechanism that took hold in the rest of the animal kingdom.

See? Evolution didn’t need to invent a new gene. Organisms without nervous systems had enough of the parts to make the synapse (the key component of the nervous system) and it was just a matter of time before something would trigger them to be expressed at the same time.

HT: Blas

If nervous tissue was front-loaded to exist, it would make sense to also front-load the appearance of muscle:

Introns continue to fit nicely in front-loaded evolution

In the past, I have raised the hypothesis that introns have a function – to facilitate the evolution of metazoan organisms. I raised the hypothesis here and defended it from criticism here.

A recent paper adds more support to this hypothesis:

Origin and evolution of spliceosomal introns.
Rogozin IB, Carmel L, Csuros M, Koonin EV.
Biol Direct. 2012 Apr 16;7(1):11.

Let’s go through the abstract.

Coyne vs. Shapiro

Jim Shapiro has been outlining his views on evolution over at the Huffington Post, including a posting entitled, What Is the Key to a Realistic Theory of Evolution?

Not surprisingly, Jerry Coyne does not like it and weighs in with a posting entitled, A colleague wrongfully disses modern evolutionary theory.

Let me focus on a key point of their disagreement.

Failure to replicate

This is not good:

A former researcher at Amgen Inc has found that many basic studies on cancer — a high proportion of them from university labs — are unreliable, with grim consequences for producing new medicines in the future.

During a decade as head of global cancer research at Amgen, C. Glenn Begley identified 53 “landmark” publications — papers in top journals, from reputable labs — for his team to reproduce. Begley sought to double-check the findings before trying to build on them for drug development.

Result: 47 of the 53 could not be replicated. He described his findings in a commentary piece published on Wednesday in the journal Nature.

Scientists Claim Brain Memory Code Cracked

Despite a century of research, memory encoding in the brain has remained mysterious. Neuronal synaptic connection strengths are involved, but synaptic components are short-lived while memories last lifetimes. This suggests synaptic information is encoded and hard-wired at a deeper, finer-grained molecular scale.

In an article in the March 8 issue of the journal PLoS Computational Biology, physicists Travis Craddock and Jack Tuszynski of the University of Alberta, and anesthesiologist Stuart Hameroff of the University of Arizona demonstrate a plausible mechanism for encoding synaptic memory in microtubules, major components of the structural cytoskeleton within neurons.

More here