It has been widely advertised that nylon eating genes evolved after 1940. I have no problem with that claim in principle since new antibiotic and malaria resistances have evolved since 1940. Even though I can easily accept the possibility of post-1940 nylon-eating evolution in principle, where is the slam dunk evidence that this is actually the case? Did a significant portion of the ability for bacteria to digest nylon take place after 1940 (or 1935 when nylon was first created)?
Andreas Wagner’s book,The Arrival of the Fittest has been mentioned many times (just try a site search as I’ve just done) since it was published. Petrushka pointed it out in a comment
For anyone interested in whether RMNS can create stuff, I recommend a relatively new book, Arrival of the Fittest. I just bought the Kindle version an haven’t finished, but it has a lot to say about how goldilocks mutations occur.
Much later Mung writes:
Reminds me of petrushka, who is always plugging Andreas Wagner’s Arrival of the Fittest, but will never post an OP on it for discussion.
So I’ve taken the hint and bought the book at last. I can see why people have recommended it. Continue reading
Last week, George Church talked at the school where I take part-time evening classes. I provide a link to that talk. He talked about re-engineered codons (something I’m grateful to Rumraket for introducing me to), stem cell research, human animal chimeras, aging therapies, human genome re-engineering, and just a little bit about ENCODE. Though I have ethical concerns about human/animal chimeras, and human genome re-engineering (like what happens if you mess up), Church goes into the technologies and raises questions as to what our world may look like in the not too distant future. Not that I’m trying to make a point about ID or God by linking this video, but it shows how rapidly we may be forced to deal with certain issues.
I personally don’t have too much problem with GMO foods. After all, my YEC friend John Sanford created the gene gun through which a large fraction of genetically engineered crops on the planet were made at one time. But one thing that bothers me is genetically engineered bacteria. Church discussed super bacteria created for research applications. I can imagine an accident where germs are created accidentally that become really hard to kill and we basically have an apocalypse. Maybe that will be the fulfillment of prophecy by Jesus, “there will be famines and pestilence”.
Here is the video (with Francis Collins speaking at the start):
Here is a description of the talk:
Attached is Larry Moran’s exit exam for biochemistry and molecular biology. Exit Exam for Biochemistry.
I probably will not get a lot of these right on the first try, but it is a good learning experience. When I don’t know the answer, I can look it up, so this is a good chance to review important concepts.
I will provide answers I think Professor Moran wants students to give, and then I’ll provide my own answers which I think he might dock points for if he were grading. I always try to give the answer the professor is expecting even if I disagree. It shows that I am trying to understanding of what he was trying to teach. It’s not a confession of belief on my part.
21.How much of your genome is functional?
Answer I think Larry is expecting:
10%, because of the limits mutational load imposes on a genome the size of a human’s and their reproductive excess. But even the 10% number is likely high since the Muller Limit of 1 mutation/person/generation might allow even less than 10% function for the human genome.
It is a little known fact that scientists who argue that the paleontological record of life is hundreds of millions of years old, when confronted with astrophysical facts, must eventually rely heavily on the hypothesis of finely tuned, large scale global warming. The problem is known as the Faith Young Sun Paradox. A few claim they have solved the paradox, but many remain skeptical of the solutions. But one fact remains, it is an acknowledged scientific paradox. And beyond this paradox, the question of Solar System evolution on the whole has some theological implications.
Astrophysicists concluded that when the sun was young, it was not as bright as it is now. As the sun ages it creates more and more heat, eventually incinerating the Earth before the sun eventually burns out. This is due to the change in products and reactants in the nuclear fusion process that powers the sun. This nuclear evolution of the sun will drive the evolution of the solar system, unless Jesus returns…
The National Institute of Mental Health (NIMH) of the National Institutes of Health (NIH) sponsored the work of John Calhoun on social behaviors. Here were the results of one of his experiments:
On July 9th, 1968, eight white mice were placed into a strange box at the National Institute of Health in Bethesda, Maryland. Maybe “box” isn’t the right word for it; the space was more like a room, known as Universe 25, about the size of a small storage unit. The mice themselves were bright and healthy, hand-picked from the institute’s breeding stock. They were given the run of the place, which had everything they might need: food, water, climate control, hundreds of nesting boxes to choose from, and a lush floor of shredded paper and ground corn cob.
This is a far cry from a wild mouse’s life—no cats, no traps, no long winters. It’s even better than your average lab mouse’s, which is constantly interrupted by white-coated humans with scalpels or syringes. The residents of Universe 25 were mostly left alone, save for one man who would peer at them from above, and his team of similarly interested assistants. They must have thought they were the luckiest mice in the world. They couldn’t have known the truth: that within a few years, they and their descendants would all be dead.
The extent of variation present in human populations and the consequences of genetic load seem to be topics of perennial interest here (see, for example, recent comments in the Evolution Visualized thread). Recent issues of Nature have published a flurry of papers aimed at getting a better handle on just how much genetic diversity is likely to exist among humans. One notable paper from last August is the following:
In this study, Monkol Lek and many, many colleagues sequenced the exomes–i.e., the portion of DNA sequences that code for proteins along with some accompanying untranslated regions–of more than 60,000 people. The results were pretty spectacular. The paper is incredibly dense, but here are some highlights:
- The authors found more than 7 million reliably identified variants. Most were single base pair substitutions, but the variants also include more than 300,000 insertions/deletions.
- On average, 1 out of every 8 nucleotides is variable. However, the overwhelming majority of variants are rare. That is they are found in only a single or a few individuals
- The frequency of different kinds of variants is proportional to both the rate at which they occur as well as the extent to which they are likely to be deleterious. This is not at all surprising, but it’s neatly demonstrated. For example, 63.1% of all possible CpG transitions (i.e., a cytosine adjacent to a guanine that mutates to a thymine) were observed, while only 3% of possible transversions were present. CpG transitions are among the most common type of substitution in mammals, while transversions are less frequent. Likewise, the proportion of possible synonymous variants that were actually observed was much higher than the proportion of possible nonsynonymous variants that were observed, which is consistent with the generally accepted notion that nonsynonymous mutations are usually subject to stronger purify selection than synonymous mutations.
- They identified almost 180,000 different protein truncation variants (PTVs), which are protein-coding genes predicted to be shortened due to an introduced stop codon, a frameshift, or removal of a critical splice site. Amazingly (to me at least), the average genome in their dataset includes 85 PTVs in the heterozygous state and almost 35 PTVs in the homozygous state.
- They identified more than 100 variants previously thought to contribute to disease phenotypes that are present at anomalously high frequencies in human populations (> 1%). Based on the fact that the evidence of pathogenicity for most of these variants is actually extremely weak, the authors suggest that these variants are most likely benign.
There is a lot more in the paper that’s worth chewing over, so give it a read. This is easily the largest dataset of its type ever generated, but it has limitations. The sampling is heavily biased toward Europeans, and there is likely some variation missing, especially in Central and Middle Eastern Asia.
I imagine that within a few years, we’ll have datasets of similar size consisting of high-coverage, whole genome sequences, which will no doubt show even larger amounts of genomic variation. It’s an exciting time to be interested in biology!
Larry Moran, Dan Graur and other garbologists (promoters of the junkDNA perspective), have argued SINES and ALU elements are non-functional junk. That claim may have been a quasi-defensible position a decade ago, but real science marches forward. Dan Graur can only whine and complain about the hundreds of millions of dollars spent at the NIH and elsewhere that now strengthens his unwitting claim in 2013, “If ENCODE is right, Evolution is wrong.”
Larry said in Junk in Your Genome: SINES
The Lenski lab has just published a new paper in Nature that looks at the dynamics of genome evolution in E. coli populations over the course of the LTEE. Here is the abstract:
Adaptation by natural selection depends on the rates, effects and interactions of many mutations, making it difficult to determine what proportion of mutations in an evolving lineage are beneficial. Here we analysed 264 complete genomes from 12 Escherichia coli populations to characterize their dynamics over 50,000 generations. The populations that retained the ancestral mutation rate support a model in which most fixed mutations are beneficial, the fraction of beneficial mutations declines as fitness rises, and neutral mutations accumulate at a constant rate. We also compared these populations to mutation-accumulation lines evolved under a bottlenecking regime that minimizes selection. Nonsynonymous mutations, intergenic mutations, insertions and deletions are overrepresented in the long-term populations, further supporting the inference that most mutations that reached high frequency were favoured by selection. These results illuminate the shifting balance of forces that govern genome evolution in populations adapting to a new environment.
I’m assuming the whole thing is pay-walled, but a pre-print copy (which may or may not be identical to the final version) is freely available here.
I’ve only read the abstract thus far, but the paper seems likely to touch on a variety of topics that folks here like to discuss. Have at it!
A prominent ID supporter at UD, gpuccio, has this to say:
My simple point is: reasoning in terms of design, intention and plans is a true science promoter which can help give new perspective to our approach to biology. Questions simply change. The question is no more:
how did this sequence evolve by some non existent neo darwinian mechanism giving reproductive advantage?
why was this functional information introduced at this stage? what is the plan? what functions (even completely unrelated to sheer survival and reproduction) are being engineered here?