by Evolution News and Views 
It’s a struggle out there. You have to be fit to survive. When the pressure is on, nature favors the ones who can take the heat.
It’s a theme that has been drummed into our heads since school. It’s a cultural meme. Social Darwinists used it to justify atrocities — see the new documentary The Biology of the Second Reich . Today’s kinder, gentler Darwinists downplay the violence in the struggle for existence, yet the fact as they see it is inescapable: environmental circumstances select random genetic mutations that confer fitness, i.e., survival, by allowing organisms to adapt.
That in a nutshell explains the development of complex life forms. We’re assured there are gobs of evidence for it, too.
Looking into a recent paper in PNAS  about evolutionary fitness tradeoffs, you have to feel sorry for a team of five evolutionists from UC Irvine who did their level best to produce clear evidence for the favored story. They began with a startling revelation:
Despite the centrality of adaptation to evolution, surprisingly little is known about the diversity of mutations that contribute to adaptation or about their phenotypic and fitness effects (1). There are, in fact, only a few well-known examples linking genotype, phenotype, and adaptation in nature (2-4). (Emphasis added.)
Those references are worth a glance. Reference (1) is to H. Allen Orr (2005), “The genetic theory of adaptation: a brief history,”where he states, “Here I survey the history of adaptation theory, focusing on the rise and fall of various views over the past century and the reasons for the slow development of a mature theory of adaptation.”
References (2-4) surely must represent what, in the authors’ opinions, constitute the best “well-known examples linking genotype, phenotype, and adaptation in nature.” What are they? #2 is about stickleback fish that gained or lost body armor, but the authors admit, like these ones do, that “the genetic and molecular basis of morphological evolution is poorly understood.” #3 is about mice with varying coat colors due to a single mutation that allows light-colored mice to survive better on light backgrounds and dark-colored mice to survive better on dark backgrounds (a kind of “peppered mice” story). #4 is about a gene in butterflies that affects wing pattern mimicry. So these are their best examples linking genes to adaptation. What became of Darwin’s finches and peppered moths?
Moving right along, the UC Irvine team next offers an excuse for this lack of evidence:
In nature, this connection is often complicated by factors such as varying selection pressures or underlying genetic heterogeneities. Although the task is difficult, the general inability to connect phenotype to genotype in the context of environmental adaptation has been a major failing in the field of evolution.
So they are here to fix that epic fail. After listing four complicating factors in their study, they say this in the last sentence of the paper:
Given the breadth of these complexities in a well-controlled experimental system, it is no wonder that the mapping of genotype, phenotype, and fitness continues to be a daunting task in natural populations.
In a moment we will see what they did and what went wrong, but first pause to be astonished. This is the theory that is so well-established by mountains of evidence, we are constantly told, that any criticism of it must be stifled as ignorant, and only this theory must be allowed to be considered scientific. They have just told us otherwise. “Surprisingly little is known” about it, and the best examples they could produce are all instances of trivial variations among existing species. If they had better examples, they surely would have brandished them proudly instead of giving excuses about how hard it is to find genetic evidence for adaptation.
The Experimental Test
Their experiment should have been ideal for testing the genetics of adaptation: 2,000 generations of E. coli bacteria subjected to heat. “In total, we performed >800 fitness competitions, making this one of the largest studies of its kind.” The games are on! Evolve or perish! Long live the fittest!
Their “large-scale experiment” started with an “ancestral strain” of E. coli bacteria that they replicated 115 times and subjected to high temperatures (42.2 °C, or 108 °F) for 2,000 generations. “At the end of the experiment, fitness was measured at 42.2 °C for a single clone from each of 114 lineages; on average, fitness increased ∼40% during the yearlong experiment” (meaning, there were still some that hadn’t died of heat exhaustion).
The hunt was on for genetic mutations that conferred ability to take the heat. “We sequenced the genome of these 114 clones, identifying 1,258 mutations relative to the ancestral genome,” they say. To decide which mutations most likely had something to do with fitness, they identified two “adaptive pathways,” both affecting RNA polymerase (RNAP). Clones could survive with one or the other mutation, but not the two together: “mutations in the two pathways were strongly negatively associated.” (This is called negative epistasis; more on that later).
Their challenge of linking genetic mutations to fitness, though, was only beginning.
Our thermal stress experiment has identified many putatively beneficial mutations that lead to higher fitness under thermal stress. However, we still do not know the phenotypic consequences of these mutations or their relationship with fitness. Do the apparently distinct adaptive pathways converge on similar phenotypes? Or might the two pathways … lead to alternative phenotypic solutions to a common selective pressure?
Here we begin to address these questions by measuring a complex phenotype: the magnitude of fitness tradeoffs across a thermal gradient. Evolutionary tradeoffs, which are defined as reduced fitness in a nonselected environment, are of great interest in their own right; they are widely observed and frequently assumed to govern and constrain trait evolution.
The operative word there is “assumed.” For example, all these mutations may have been neutral, with no phenotypic consequences. Or, mutations for better survival in heat might have had negative consequences for surviving cold (an evolutionary trade-off), with no overall gain in fitness. “Whatever the cause, tradeoffs have rarely been linked to specific genetic variants” — another embarrassing revelation.
In this ideal setup (one of the largest of its kind, remember), they were not even looking for a glamorous innovation, like a wing or an eye. Just connecting a particular mutation to a functional phenotype would have been rated a great success, even if all it meant was shifting the germ’s optimum temperature range by a few degrees. Trade-offs notwithstanding, so what if the fittest germ in the hot tub would shiver in the cold bath? They would at least be able to connect “genotype, phenotype and adaptation” together — the kind of evidence neo-Darwinians need and want.
They found that half the clones shifted their thermal range upward by a few degrees (losing ability to survive cold — the trade-off), and others survived the heat without losing ability to survive cold. Then they found two independent mutations in the RNAP gene that appear relevant to those shifts, as long as they don’t occur together. Success? Not so fast.
For one thing, they don’t know why those mutations had that effect. They suggested that they might slow RNAP down when its tendency under heat stress is to speed up, thus improving its likelihood to finish a protein synthesis, but this was not clear. Also, to their surprise, the ancestral strain could sometimes bounce back from doom through the “Lazarus effect” (resurrection from the dead) — but they don’t know how that effect works.
Surprisingly, however, wa [absolute fitness] of the ancestor was negative (wa = −0.290) but not significantly <0.00 at 45.0 °C (Table S2 and Fig. S1). This unexpected behavior was caused by the occasional sudden recovery of populations whose densities had initially declined markedly, a phenomenon known as the “Lazarus effect”.
So how is Lazarus coming out of the grave? They don’t know. Maybe there is some “preadaptation” to heat in these bacteria:
At the upper end of the thermal niche, most (>95%) of the clones persist at 45 °C, signaling an expansion of their niche at least 2 °C beyond that of the ancestor (Fig. 1B). This observation contrasts with a previous study in which only one of six 42 °C-adapted lines expanded their upper thermal limit but suggests a degree of “preadaptation” to temperatures beyond the clones’ immediate experience. Above 45 °C the analyses become complicated by the Lazarus effect, in which declining populations suddenly recover, presumably due to major effect mutations. Indeed, the ancestral clone, which is habituated to laboratory conditions of 37 °C, does not persist at 43 °C but often recovers at 45 °C (Fig. S2). We do not yet know the molecular processes underlying the Lazarus effect, but two seem possible: either the fitness effects of mutations change as a function of the intensity of stress or the mutation rate increases under high stress (33, 34). We do not yet know which of these two mechanisms predominates.
Complicating matters even more are things like “negative epistasis” (mutations that counteract each other) and “antagonistic pleiotropy” (unintended consequences of a “beneficial” mutation on other parts of the genome).
In short, it was hard to find anything beyond a “suggestion” or a “scenario” that these bacteria improved their fitness in any way by genetic mutations, other than the gross observation that some of the clones managed to survive at 45 °C. But even the ancestor could do that sometimes through the “Lazarus effect.” The authors also ignored the possibility that E. coli have ways to generate their own mutations under stress. That would be supportive of intelligent design, as would the notion that bacteria contain “a degree of preadaptation” to temperatures beyond their immediate experience.
Some experiment. What we learn from this paper is that under ideal conditions, with the best methods, scientists have a devil of a time trying to establish neo-Darwinian theory in a scientifically rigorous way. A look at their references shows a debt to Lenski’s methods that similarly produced paltry results  on one of the longest-running experiments in history trying to demonstrate evolution in a lab.
Is this a theory that deserves to rule the world?
Read the Full Article Here .