Tyrosine kinases and front-loading

Back in 2002, a scientist who was skeptical of my front-loading hypothesis, asked me:

So the question arises: how much of the control machinery governing development in (for instance) metazoans could plausibly serve a useful role, and thus be maintained by selection, in unicellular organisms?

Then in 2005, another scientist who was skeptical of my front-loading hypothesis, was even more specific:

It seems to me that front-loading of genetic information makes the very strong prediction that we should find in the genomes of simple species remnants of genes whose functions are specific to complex species. If all of the genetic information to make vertebrates (for example) was front-loaded into the earliest bacterial species, followed by functional loss of information from the genomes of species that did not need particular genes, we should see remnants of at least some of those lost genes. Are there, for example, remnants of metazoan-specific genes found in the genomes of protozoa or bacteria? As far as I am aware, there are not. For instance, a search of genomes for a large class of metazoan-specific genes that encode tyrosine kinase receptors, a distinctly metazoan innovation (from the evolutionary perspective), reveals nothing in the way of related pseudogenes or gene remnants in any bacterial or protozoan genome. This is the sort of evidence that one would have to produce for the idea of front-loading to be taken seriously.

These quotes should help you to see that conventional evolutionary theory led scientists to predict that that tyrosine kinase receptors would be “a distinctly metazoan innovation” that co-evolved into existence alongside metazoa as such “control machinery governing development” in metaozoans would not be maintained in unicellular organisms.

Complex minimal complexity

According to this site:

In three papers published back-to-back in Science, they provide the first comprehensive picture of a minimal cell, based on an extensive quantitative study of the biology of the bacterium that causes atypical pneumonia, Mycoplasma pneumoniae. The study uncovers fascinating novelties relevant to bacterial biology and shows that even the simplest of cells is more complex than expected.

[…..]

A network of research groups at EMBL’s Structural and Computational Biology Unit and CRG’s EMBL-CRG Systems Biology Partnership Unit approached the bacterium at three different levels. One team of scientists described M. pneumoniae‘s transcriptome, identifying all the RNA molecules, or transcripts, produced from its DNA, under various environmental conditions. Another defined all the metabolic reactions that occurred in it, collectively known as its metabolome, under the same conditions. A third team identified every multi-protein complex the bacterium produced, thus characterising its proteome organisation.

“At all three levels, we found M. pneumoniae was more complex than we expected,” says Luis Serrano, co-initiator of the project at EMBL and now head of the Systems Biology Department at CRG.

So in what ways is this minimal cell more complex than expected?

Design Matrix reflections

Since it has now been two years since the publication of The Design Matrix, I thought I would take a brief moment to reflect before Turkey Day.

The SRP, Alu Elements, and Nudging

I’ve combined the essays about the signal recognition partcle, Alu elements, cytosine deamination, all connected by front-loading. All 11, 465 words of it.

Growth Control

If life truly is an example of carbon-based nanotechnology, then we would expect life processes to be permeated with control.  In essence, life processes would constitute a cybernetic system that responds to internal and external cues.

Take the process of cell growth, where a cell simply increases its size. One might be tempted to think such a simple process would be entirely passive, such that a cell in an environment with lots of nutrients would be able to build more cell parts and thus grow, while a cell that was being starved would not be able to build more cell parts and thus fail to grow.  Simple, right?

Not really.  It turns out that the seemingly simple process of cell growth is under a very sophisticated form of control.

Are those ears or a beak?

Over at the blog Uncommon Descent, there is an interesting discussion revolving around the views of Eugene Koonin who dethrones natural selection as the central mechanism of evolution.  I’ve discussed the implications of these views here and here.

Allen MacNeill, a biologist from Cornell University, summarized Koonin’s arguments as follows:

In other words, the evolving evolutionary synthesis of the 21st century is de-emphasizing adaptation.

Inefficient Selection

In The Design Matrix, I explain how the process of gene duplication, conventionally taken as a ‘brute given,’ is actually a mechanism of front-loading evolution given that it can carry designs far into the future.  Now we have evidence that gene duplication, in the correct context, actually functions as a nudge for the evolution of increased complexity:

10 Signs of Intellectual Honesty

I can never post this too much…

When it comes to just about any topic, it seems as if the public discourse on the internet is dominated by rhetoric and propaganda. People are either selling products or ideology. In fact, just because someone may come across as calm and knowledgeable does not mean you should let your guard down and trust what they say. What you need to look for is a track record of intellectual honesty. Let me therefore propose 10 signs of intellectual honesty.

Alu Behind Learning and Memory?

I’ve been wanting to comment on this article by Mattick and Mehler, but have just been too busy. Luckily, I just ran across a web article that borrows heavily from M&M’s article. I would encourage you to read the whole thing (if you can’t get your hands on M&M’s article, that is). Here are some excerpts:

Evolution Under Intrinsic Control

The appearance of antibiotic resistant bacteria has long been used as a classic example of Darwinian evolution in action. The general story works like this: take any population and there will be a certain amount of accumulated genetic variability as a consequence of a steady stream of random mutations. When the antibiotic is supplied, it interferes with some aspect of cell biology (cell wall synthesis, translation, transcription, etc.) Those few members of the population that just happen to possess a variation that makes them immune to the action of the antibiotic will survive and be favored by selection. Or at the very least, while the bacteria are exposed to the antibiotic, every new mutation that just happens to occur will become another opportunity to escape the insult.

A study by Floyd Romesberg and colleagues [1] has thrown a new and subtle twist into the story. The twist is this: in this case, mutations don’t “just happen” – bacteria make sure they happen. That is, the evolution of antibiotic resistance is not simply the passive process of selection screening through the available variability. On the contrary, bacteria respond to the insult by making sure there is a plentiful source of variability to screen.