Talk:Adaptive mutation
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irrelevance of orthogenesis
editI deleted the stuff about orthogenesis, which adds nothing to the article. Here is the justification. If you want to add it back, prove me wrong.
"Orthogenesis" refers to a disputed, poorly defined, antiquated idea in the history of evolutionary thought. The idea itself is disputed because most present-day authors have a mistaken understanding based on the caricatures used in Synthesis propaganda, where orthogenesis (and all other alternatives to neo-Darwinism) is treated as a kooky idea based on mystical inner urges. This makes it easy to dismiss, without doing any actual thinking or research. You can't get your history from Ernst Mayr. He is a partisan.
The reality of history is never so stupid or so simple. Scholarly articles on this topic include Popov [1] and Ulett [2]
In these scholarly accounts, orthogenesis is mostly the idea that the course of evolution is channeled so strongly by development that it is the main determinant of form, and selection for a functional fit with the environment has only a small role. This was the view of Eimer, for instance, the one person whose name is most strongly associated with the term "orthogenesis" historically.
Once you understand this is what orthogenesis means in actual history, then it will become clear that referencing "orthogenesis" adds nothing to this article. This article is about a dispute that was launched in 1988 by Cairns, et al. It is a contemporary debate about mutation, not some ancient debate about Lamarck or orthogenesis.
When I have time, I will try to add some more to the content of the article. I am a scientist who works on mutation in evolution (I also study history and I have published peer-reviewed work on the history of science), and I was very familiar with this topic when it was hot back in the early 1990s. Dabs (talk) 02:19, 4 December 2022 (UTC)
References
- ^ I. Popov (2009). "The problem of constraints on variation, from Darwin to the present". Ludus Vitalis. 17: 201–220.
- ^ M. A. Ulett (2014). "Making the case for orthogenesis: The popularization of definitely directed evolution (1890–1926)". Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences. 45: 124–132. doi:https://doi.org/10.1016/j.shpsc.2013.11.009.
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Definition
editThe section "Definition" has little connection with cited literature. Ivan Pchelin (talk) 16:50, 19 November 2020 (UTC)
Directed mutagenesis
editThis should be merged with directed mutagenesis. 136.142.169.66 (talk) 17:37, 17 March 2010 (UTC)
As far as I can understand, the two topics barely have things in common Ivan Pchelin (talk) 16:54, 19 November 2020 (UTC)
Rosenburg 2012 Research
editA section could be added based on these sources.
http://www.ncbi.nlm.nih.gov/pubmed/23041320
Mutation hotspots and showers occur across phylogeny and profoundly influence genome evolution, yet the mechanisms that produce hotspots remain obscure. We report that DNA double-strand breaks (DSBs) provoke mutation hotspots via stress-induced mutation in Escherichia coli. With tet reporters placed 2 kb to 2 Mb (half the genome) away from an I-SceI site, RpoS/DinB-dependent mutations occur maximally within the first 2 kb and decrease logarithmically to ∼60 kb. A weak mutation tail extends to 1 Mb. Hotspotting occurs independently of I-site/tet-reporter-pair position in the genome, upstream and downstream in the replication path. RecD, which allows RecBCD DSB-exonuclease activity, is required for strong local but not long-distance hotspotting, indicating that double-strand resection and gap-filling synthesis underlie local hotspotting, and newly illuminating DSB resection in vivo. Hotspotting near DSBs opens the possibility that specific genomic regions could be targeted for mutagenesis, and could also promote concerted evolution (coincident mutations) within genes/gene clusters, an important issue in the evolution of protein functions.
http://www.ncbi.nlm.nih.gov/pubmed/23224554
Mechanisms of DNA repair and mutagenesis are defined on the basis of relatively few proteins acting on DNA, yet the identities and functions of all proteins required are unknown. Here, we identify the network that underlies mutagenic repair of DNA breaks in stressed Escherichia coli and define functions for much of it. Using a comprehensive screen, we identified a network of ≥93 genes that function in mutation. Most operate upstream of activation of three required stress responses (RpoS, RpoE, and SOS, key network hubs), apparently sensing stress. The results reveal how a network integrates mutagenic repair into the biology of the cell, show specific pathways of environmental sensing, demonstrate the centrality of stress responses, and imply that these responses are attractive as potential drug targets for blocking the evolution of pathogens. — Preceding unsigned comment added by 184.153.187.119 (talk) 04:28, 30 January 2013 (UTC)
Von Borstel
editOther experiments should be considered, such as von Borstel and his research with yeast. An overview can be found here:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989722/ — Preceding unsigned comment added by Becca.a.sanders (talk • contribs) 03:06, 9 October 2013 (UTC)