Very interesting and timely paper.
I agree that it’s interesting, but is there any particular reason why it’s timely?
Totally fascinating hypothesis.
The trick (the challenge) would be to test it.
So two cancer researchers from Cambridge publishes an open access paper in Science that could help in cancer research. DI’s Paul Nelson writes a piece in Evolution News that includes a lovely video from a Disney movie. Thanks to Paul and others at DI for the insightful analysis and their fine work on curing cancer. 
Will DI fund experiments to test the hypothesis?
Great article @pnelson. Seems like it would hard for even the most hardened of ID critics to fault that article. 
Oh, Patrick – seriously.
Science can’t have fun? Those WALL-E robots are cute.
I meant what I said above: this is an utterly fascinating (as in, excellent, fruitfully counterintuitive, thought-provoking) hypothesis, and I GENUINELY would like to figure out how to test it. Next week, I’ll see Doug Axe at Biola, and will discuss the paper with him, in re possible avenues for testing.
To Josh: ditto my comments here to Patrick. Ideas like the one linked in the OP are the reason I love biology. Well, one of the reasons, anyway.
Science research is fun. You and others at DI should try it sometime. The trill of discovering something new and useful is great. Ask @nlents, @swamidass, Coyne, and Lenski about it.
It’s not that counter-intuitive.
DNA error detection and correction mechanisms use energy. The more thorough the mechanisms, the more energy is used. That energy must be obtained from somewhere, and could be used elsewhere. Since not all replication errors have a noticeable effect, there must be a point at which the cost of the energy used on error detection and correction exceeds the benefit.
There’s also the issue that organisms with 100% efficient DNA mutation correction mechanisms can’t evolve in response to changing environments or colonisation of new ones, so have increased risk of extinction.
If I am reading the hypothesis correctly, the authors are proposing that excessive DNA damage, and more specifically the repair of such damage, requires an excessive amount of cellular resources, which might compromise overall survivability. If that is really the case, I am a bit skeptical. This is because I am not convinced that the repair of DNA damage really can take up very much of the overall energy budget of the cell.
To illustrate my opinion, recall that the eukaryotic cell is constantly initiating non-productive transcription events - probably millions of times over the life of a cell. Even if the same cell has to repair a comparable number of DNA damage events (not likely, IMO, but I honestly don’t know the scope of such events), it would not make any bigger dent in the overall energy budget than does inappropriate transcription.
Then there is the matter of the deliberate production of thousands or millions of long mRNAs that are destined for rapid degradation. By my way of thinking, the energy that goes into making and degrading these far exceeds the possible costs of repair of DNA damage.
my 2c…
This objection makes sense to me, but I wonder if perhaps the energy budget is not the only metric that matters. Could the time investment also be a factor? For example, might too much repair of DNA damage lead to dis-regulation of the cell cycle, and/or slow down the expression of important genes?
Something along these lines seems to be what’s implied in the image that accompanies the article:
In addition, one of the papers cited (Breivik and Gaudernack 2004) present a mathematical model that also suggests that the time factor is key:
As demonstrated by Fig. 3, an elongation of replication time will necessarily decrease the average cost of non-lethal errors. Slow growth makes each error statistically cheaper, and repair relatively more expensive. Any growth-inhibiting environment, regardless of mutagenicity, may thus transform the evolutionary potential of a repair mechanism from positive (Fig. 4A) to error rate-dependent (Fig. 4B) and all the way to constitutively negative (Fig. 4C).
It’s not intuitively clear to me the extent to which growth and division rates are the key factors that determine cell survival, but I could imagine cases in which they would be.
Hey @pnelson, how about getting into the debate on this at the adult’s table? You don’t need to stay at the kid’s table watching.
Thanks for the invite, Patrick, but I’m preparing for the Evangelical Philosophical Society discussion on theistic evolution upcoming Wednesday (11/20) in San Diego, and Phil Johnson’s memorial symposium in Berkeley on Saturday (11/23).
However, I will leave this nice casserole from Michael Lynch at the adult’s table, to enliven the festivities. I’d love to see some calculations like these, but with respect to DNA repair:
Will the Evangelical Philosophical Society be doing anything on Theistic Gravity anytime soon? Theistic ancient Genomes would be a good topic as well. As well as Theistic Paleontology. By the way, what is Evangelical Philosophy?
Having grown up in Minnesota, I’m contractually obligated to inform you that this is actually a hotdish, not a casserole. 
I grew up in Minnesota too (north Minneapolis and Golden Valley), so I have NO EXCUSE for the mislabelling. 
Hotdish it is.
Patrick, you made that joke before, and it wasn’t funny the first time. But if you really want to know something about the EPS, their 2019 conference program (jointly with the Evangelical Theological Society) is available here:
https://www.etsjets.org/2019_program
It’s a big file (64+MB), so beware. Click on the first link. I think you’ll find some topics that would interest a non-theist like you, just as I know (from experience) that conference presentations at skeptics and atheist meetings often deeply interest me.
“Opposition is true friendship.” William Blake (1757-1827)
Thanks. The 2020 program on “Christianity and Islam” isn’t that interesting to me as the world is going secular rapidly but the 2021 program on “Wealth and Poverty” is very interesting given that we live in a global secular economy.
Trying to sum up, Lynch and Marinov state that, when it comes to the cumulative cost of a gene (sc) to fitness:
“The major contribution that pushes sc past the drift barrier in eukaryotes is the cost of translation. Most values of sDNA and sRNA in multicellular species are below the threshold for efficient selection.”
As I am wont to repeat, the business of life is the ribosome. This small excerpt conveys this message nicely, IMO.
When it comes to DNA damage and repair, it would be interesting to know how much research has been put into the effects of these processes on the parts of genomes that encode ribosomal RNAs. This may be where a correlation, inverse or otherwise, between DNA repair and cell survival lies.