Not gain.
Darwinism, as taught in school, is the claim that natural selection acting on random mutation generates huge levels of information, not noise. Here is what really happens:
Ann Gauger of the Biologic Institute here:
Microbiologist Ralph Seelke and I published a paper in 2010 where we demonstrated that cells always, or nearly always, take the easiest road to success. Given a choice between a simple two-step path leading to repair of two genes needed to make tryptophan, versus a one-step path that eliminated expression of the those genes, only one out of a trillion cells went down the path toward making tryptophan, even though that path would ultimately be much more beneficial. Why did this happen?
The genes to be repaired were overexpressed — too much of their products were made. Because one of the genes was broken in two places, no tryptophan could be made. Thus both genes were expensive to keep around. It was easier for the cell to break the useless genes than to repair them — one step instead of two — and the cells, having no foresight, took that path. Some of those cells deleted the genes, thus losing the information needed to make tryptophan for good.
…
In fact, that is what we observed. Nearly all the cells inactivated the genes (only one out of a trillion didn’t). Some of the cells even deleted the genes, thus losing the capacity to make tryptophan for good. Darwinian evolution travels by the shortest road, without regard for where it’s headed. And if the shortest road is to break an existing function — to lose information — that’s the path it chooses. More.
That clearly has implications for understanding cancer. The cancer cell is defective as a useful cell, but highly fit when lethal, due to dumped information:
Cancers develop when one or more normal functions in a cell are disrupted or broken. The ironic thing is that for the cancer cells, this breaking increases their fitness, their rate of growth and cell division, and thus is beneficial — to them. Normal constraints have been removed, allowing uncontrolled growth.
In that sense, cancer is a form of devolution. We looked at devolution here: Devolution: Getting back to the simple life:
Most of the time, when we think of evolution, we mean mechanisms for the growth of complex new information. After all, entropy (the tendency for disorder to increase over time) can satisfactorily explain loss of information. Yet, in the history of life, some forms survive while — or even by — losing information (devolution).
Which may not be good news for other parts of the life form or ecosystem.
See Talk to the fossils: Let’s see what they say back for more ways evolution can actually happen.
Here’s the abstract:
New functions requiring multiple mutations are thought to be evolutionarily feasible if they can be achieved by means of adaptive paths-successions of simple adaptations each involving a single mutation. The presence or absence of these adaptive paths to new function therefore constrains what can evolve. But since emerging functions may require costly over-expression to improve fitness, it is also possible for reductive (i.e., cost-cutting) mutations that eliminate over-expression to be adaptive. Consequently, the relative abundance of these kinds of adaptive paths–constructive paths leading to new function versus reductive paths that increase metabolic efficiency–is an important evolutionary constraint. To study the impact of this constraint, we observed the paths actually taken during long-term laboratory evolution of an Escherichia coli strain carrying a doubly mutated trpA gene. The presence of these two mutations prevents tryptophan biosynthesis. One of the mutations is partially inactivating, while the other is fully inactivating, thus permitting a two-step adaptive path to full tryptophan biosynthesis. Despite the theoretical existence of this short adaptive path to high fitness, multiple independent lines grown in tryptophan-limiting liquid culture failed to take it. Instead, cells consistently acquired mutations that reduced expression of the double-mutant trpA gene. Our results show that competition between reductive and constructive paths may significantly decrease the likelihood that a particular constructive path will be taken. This finding has particular significance for models of gene recruitment, since weak new functions are likely to require costly over-expression in order to improve fitness. If reductive, cost-cutting mutations are more abundant than mutations that convert or improve function, recruitment may be unlikely even in cases where a short adaptive path to a new function exists. (Public access) Pdf
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