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Talk:Flaws in Richard Lenski Study (view source)
Revision as of 00:25, July 16, 2008
, 00:25, July 16, 2008→Expertise in Statistics
::Except that the growth pattern of the Cit+ cells in the third replay experiment demonstrated that there were no Cit+ cells in the cultures at the time of plating. Control plates with a mix of Cit- and Cit+ cells were done which showed rapid development of Cit+ colonies, whereas the experimental plates did not show any Cit+ colonies for at least 8 days and up to 28 days. If you believe that the plates became randomly contaminated during the course of the incubation, rather than at the initial plating, the post-plating contamination should have affected all generations equally, but it did not--[[User:Brossa|Brossa]] 12:46, 15 July 2008 (EDT)
::Except that the growth pattern of the Cit+ cells in the third replay experiment demonstrated that there were no Cit+ cells in the cultures at the time of plating. Control plates with a mix of Cit- and Cit+ cells were done which showed rapid development of Cit+ colonies, whereas the experimental plates did not show any Cit+ colonies for at least 8 days and up to 28 days. If you believe that the plates became randomly contaminated during the course of the incubation, rather than at the initial plating, the post-plating contamination should have affected all generations equally, but it did not--[[User:Brossa|Brossa]] 12:46, 15 July 2008 (EDT)
::Blount et al. discussed the unexpectedly low Cit+ conversion rate for the third replay set in the supplementary document. They have some speculations but don't know why it occurred. They are dealing with low probability events. I don't agree that the 'proper' interpretation is contamination. First, they isolated and tested each Cit+ isolate for the markers and sequences we've discussed on earlier Conservapedia pages. Second, the distribution of Cit+ isolates does not appear to be random: They correlate strongly with the later generations. If undetected contamination was random, it's unlikely the Monte Carlo resampling tests would reject the null hypothesis of the 'rare-mutation' hypothesis over the 'potentiated' hypothesis. As Brossa correctly notes, contamination would have affected all generations. Blount et al. write in the paper's supplement: "To facilitate handling and minimize possible confounding variables, we divided this third experiment into 20 blocks of 14 clones each. All of the clones within a block came from different generations, and the single ancestral clone was included in all 20 blocks."--[[User:Argon|Argon]] 20:01, 15 July 2008 (EDT)
::Blount et al. discussed the unexpectedly low Cit+ conversion rate for the third replay set in the supplementary document. They have some speculations but don't know why it occurred. They are dealing with low probability events. I don't agree that the 'proper' interpretation is contamination. First, they isolated and tested each Cit+ isolate for the markers and sequences we've discussed on earlier Conservapedia pages. Second, the distribution of Cit+ isolates does not appear to be random: They correlate strongly with the later generations. If undetected contamination was random, it's unlikely the Monte Carlo resampling tests would reject the null hypothesis of the 'rare-mutation' hypothesis over the 'potentiated' hypothesis. As Brossa correctly notes, contamination would have affected all generations. Blount et al. write in the paper's supplement: "To facilitate handling and minimize possible confounding variables, we divided this third experiment into 20 blocks of 14 clones each. All of the clones within a block came from different generations, and the single ancestral clone was included in all 20 blocks."--[[User:Argon|Argon]] 20:01, 15 July 2008 (EDT)
::: Good and detailed analyis and conclusion, Argon. I had no time to read everything in that detail, but i think you present exactly the arguments (contant background would favour rare mutation hypothesis) would be exactly the one i had in mind, so let's see how Mr. Schlafly will bend his own Monte-Carlo simulations to showing several 1000 times no mutation into accordance with any reasonable background explaining a significant number of counts in *some* samples --[[User:Stitch75|Stitch75]] 20:20, 15 July 2008 (EDT)
::: Good and detailed analyis and conclusion, Argon. I had no time to read everything in that detail, but i think you present exactly the arguments (contant background would favour rare mutation hypothesis) would be exactly the one i had in mind, so let's see how Mr. Schlafly will bend his own Monte-Carlo simulations to showing several 1000 times no mutation into accordance with any reasonable background explaining a significant number of counts in *some* samples --[[User:Stitch75|Stitch75]] 20:20, 15 July 2008 (EDT)
Is there anyone here with expertise in statistics who could give an analysis? [[User:Fyezall|Fyezall]] 16:15, 15 July 2008 (EDT)
:Hello Fyezall. I rearranged the position of your question to hopefully keep the conversations clearer. It boils down to this: The researchers found that mutant Cit+ strains arose over the course of time in their long term growth experiment. They wanted to learn something about how that strain acquired this ability. They wondered, 'Was this the result of a single, very low frequency mutation or did some other mutation have to precede it in earlier generations, followed by the final mutation(s) that allowed the cells to grow on citrate?'
:If the Cit+ change required a single mutation with a low but constant probability over time one would expect Cit+ mutations to be distributed across cells taken from any generation of the experiment. On the other hand, if a 'potentiating' mutation had to arise at some point in the cultures before the final Cit+ mutation could function, then one would expect the probability for Cit- cells to mutate to Cit+ cells would increase with samples of cells taken from later cultures.
:Blount ran the experiment and found that Cit+ mutants arose more frequently in cells taken from later generations in the culture. The Monte Carlo tests were used to assess how likely the pattern of results would fit the models. The statistical significance (smaller P-values mean greater significance), was calculated for each experiment and the combination of experiments. The numbers suggest the distribution of mutants was not randomly distributed across the experimental generations. This would argue against the single-mutation, constant, low-probability hypothesis. It appears that a pre-adaptive mutation had to have arisen first, followed by the mutation the finally allowed the cells to utilized citrate. Future work in Lenski's lab will focus on trying to identify the various mutations involved. Does that help?--[[User:Argon|Argon]] 20:25, 15 July 2008 (EDT)