I have been grievously mum in response to the many comments that readers have been sending to the Loom. My silence is not hostile--it is the result of way too much traveling, too much magazine writing, and the standard sleep deprivation that comes with life with two young daughters. In fact, reading comments is one of the favorite things I like about this blog. As a case in point, today Nick at talkdesign.org explored the link between the subject of two recent posts: the ongoing adaptation of bacteria to manmade pollutants and the ongoing pollution of biology education with creationist distractions: [snip] Well, I don't have a poem, but I would like to mention that the evolution of catabolic pathways is the perfect example of the evolution of "irreducible comlexity" in modern times, which as you will recall is exactly the thing that the Intelligent Design folks say can't evolve. (1) These catabolic pathways typically break down "xenobiotic" compouds that humans have only recently introduced into the environment (2) These compounds are typically environmentally persistent toxins. Sometimes they are pesticides or herbicides, or by-products of other nasty compounds like explosives. Much of the the research on the evolution of the degradation pathways is done by military-funded labs, because the military has a big problem with polluted ground on military bases where chemical weapons, explosives, etc. were stored. (3) The degradation pathways typically have multiple required proteins in the breakdown process. Often the compounds contain e.g. aromatic rings protected by tightly-binding atoms such as chlorine, and stripping off the chlorines and then breaking open the rings are all required before a non-toxic "eat-able" carbon chain is produced. Some example papers: * Copley, S. D. (2000). Evolution of a metabolic pathway for degradation of a toxic xenobiotic: the patchwork approach. Trends in Biochemical Sciences V25(N6): 261-265. Source: http://www.sciencedirect.com/science/journal/09680004 * Johnson, G. R., Jain, R. K. and Spain, J. C. (2002). Origins of the 2,4-Dinitrotoluene Pathway. Journal of Bacteriology 184(15): 4219-4232. Source: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12107140&dopt=Abstract * (Atrazine pathway evolution) Sadowsky, M. J., Tong, Z., de Souza, M. and Wackett, L. P., 1998. AtzC is a new member of the amidohydrolase protein superfamily and is homologous to other atrazine-metabolizing enzymes. J Bacteriol. 180 (1), 152-158. URL: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9422605&dopt=Abstract * (Atrazine pathway evolution) Seffernick, J. L. and Wackett, L. P., 2001. Rapid evolution of bacterial catabolic enzymes: a case study with atrazine chlorohydrolase. Biochemistry. 40 (43), 12747-12753. URL: http://pubs3.acs.org/acs/journals/doilookup?in_doi=10.1021/bi011293r The McAdams et al. Nature Reviews Genetics paper you linked to mentions studies like these, and also last year's paper in Nature by Lenski et al. that did a computer simulation of the evolution of an "irreducibly complex" system. McAdams et al. don't miss the chance to take a swipe at Intelligent Design: ==== These experiments are particularly valuable as they show how straightforward evolutionary mechanisms of mutation and selection can produce steady increases in organism complexity without invoking ‘intelligent design’. ==== So far, the ID folks seem to be saying that the computer simulation is irrelevant for [insert obscure hair-splitting here], and they seem to hope that if they completely ignore the studies on the evolution of catabolic pathways for xenobiotic compounds, the studies will just go away. I would not bet on their strategy over the long term. But then again, the ID folks appeal entirely to the public and avoid discussions with the relevant scientific experts like the plague, and their strategy seems be having some success lately. I'm glad that there are at least a few people like Carl Zimmer around to help get the word out. Nick [snip] Thanks for the connection and the sources, Nick.