This page exists so nobody has to take the article on trust. Every quotation below was read out of a downloaded file — a publisher PDF converted with
pdftotext -layout, a locally stripped HTML page, or in one case an OCR of rendered page images — and none was obtained through an AI summarising tool. Where a source could not be opened, that is stated.
The dispute over Lenski's experiment is unusually quotable, and unusually often quoted badly. What follows is grouped by claim rather than by author, so that the two sides can be read against each other on the same question.
On the scale of the experiment
Blount, Borland & Lenski 2008, PNAS 105:7899-7900, Abstract and Introduction:
"No population evolved the capacity to exploit citrate for >30,000 generations, although each population tested billions of mutations."
"During that time, each population experienced billions of mutations, far more than the number of possible point mutations in the ≈4.6-million-bp genome. This ratio implies, to a first approximation, that each population tried every typical one-step mutation many times. It must be difficult, therefore, to evolve the Cit+ phenotype, despite the ecological opportunity."
Lenski, Rose, Simpson & Tadler 1991, American Naturalist 138:1318, under the heading "Culture Conditions." Read off OCR'd page images, then checked character by character against a 2× crop of the page, because the available scan has no text layer and the OCR mangles superscripts:
"The culture medium used in all experiments was Davis minimal broth ... supplemented with 2 × 10-6 g thiamine hydrochloride and 0.025 g glucose per liter, which permits a stationary phase bacterial density of about 5 × 107 cells per mL. Culture volume was 10 mL maintained in 50-mL Erlenmeyer flasks set in a shaking incubator at 37°C and 120 rpm. Cultures were propagated daily by transferring 0.1 mL of each culture into 9.9 mL of fresh medium. ... The resulting 100-fold daily growth of each bacterial population represents ~6.64 generations of binary fission."
Van Hofwegen, Hovde & Minnich 2016, J. Bacteriol. 198:1022 — the comparison the article argues against:
"To date, the Lenski LTEE cultures exceed 63,000 generations, equivalent to over 1 million years of human evolution."
Good et al. 2017, Nature 551, on why those generations are not drift:
"With an effective population size of Ne ~ 107, new mutations would require Δt ~ 0.1 Ne ~ 106 generations to reach the 10% detection threshold by genetic drift alone. Thus, the mutations in Fig. 1 must have reached observable frequencies through the direct or indirect action of natural selection."
On whether Cit+ is new information
Van Hofwegen, Hovde & Minnich 2016, J. Bacteriol. 198:1022, the last two sentences of the Importance statement:
"We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved."
and in the Discussion:
"because this adaptation did not generate any new genetic information and required expanded expression of only two existing transporters (citT and dctA), generation of E. coli Cit+ phenotypes in our estimation does not warrant consideration as a speciation event."
Lenski & Blount 2016, Telliamed Revisited, replying:
"The claim that 'no new genetic information evolved' is based on the fact that the bacteria gained this new ability by rearranging existing structural and regulatory genetic elements. But that's like saying a new book—say, Darwin's Origin of Species when it first appeared in 1859—contains no new information, because the text has the same old letters and words that are found in other books."
"In an evolutionary context, a genome encodes not just proteins and patterns of expression, but information about the environments where an organism's ancestors have lived and how to survive and reproduce in those environments ... So when natural selection—that is, differential survival and reproduction—favors bacteria whose genomes have mutations that enable them to grow on citrate, those mutations most certainly provide new and useful information to the bacteria."
Behe 2019, Darwin Devolves, chapter 7 — the same point in Behe's own vocabulary:
"In my QRB classification scheme the mutation would be counted as modification-of-function—because no new functional coded element was gained or lost, just copied."
"Interesting as it is, the ambiguous citrate mutation that started the hoopla is a sideshow. The overwhelmingly important and almost completely unnoticed lesson is that genes are being degraded left and right, both when they directly benefit the bacteria and when they do so indirectly in support of another mutation. The occasional particularly noticeable modification-of-function or gain-of-FCT mutation can't turn back the tide of damaging and loss-of-FCT ones."
Lenski 2019, Telliamed Revisited, on what that classification requires:
"In other words, Behe won't count any newly evolved function as a gain of function unless some entirely new gene or control region 'poofs' into existence. But that's not how evolution works—unless you believe, as Behe apparently does, that God or some other 'intelligent agent' intervened to insert new genetic information into various lineages during the course of history. (Suffice it to say that I don't regard this as a scientifically useful hypothesis, because I don't think it can be tested.) Evolutionary biology doesn't require that new genes poof into existence. Instead, old genes and their products are coopted, modified, and used in new ways—a process called exaptation."
On the mechanism of the citrate mutation
Blount et al. 2012, Nature 489 — the module:
"All 9 sequenced Cit+ genomes have two or more tandem copies of a 2933-bp segment that includes part of the citrate fermentation (cit) operon. ... The amplification joined upstream rnk and downstream citG fragments, producing an rnk-citG hybrid gene expressed from the upstream rnk promoter."
— and the reporter test that shows the unamplified gene really is silent in oxygen:
"The native citT regulatory region showed no expression (above background) in any strain, indicating that citT is normally silent under oxic conditions."
— and the measured value of the first step:
"In the same medium used in the LTEE, ZDB595 experienced a lag of >60 hours after glucose depletion, followed by a short period of abortive and inconsistent growth on citrate. These data imply that the initial Cit+ type was too weak to allow exploitation of citrate under the daily-transfer regime of the LTEE. Nonetheless, ZDB595 had a small (1.0%) but significant competitive advantage over ZDB30 in the same environment (n = 10, t = 3.09, two-tailed P = 0.0128)."
Quandt et al. 2014, PNAS 111:2217, Abstract — the sentence that changed the story:
"Surprisingly, strains containing just the citT and dctA mutations fully use citrate, indicating that earlier mutations thought to have potentiated the initial evolution of Cit+ are not required for expression of the refined version of this trait. Instead, this metabolic innovation may be contingent on a genetic background, and possibly ecological context, that enabled citT mutants to persist among competitors long enough to obtain dctA or equivalent mutations that conferred an overwhelming advantage."
Read the second sentence as carefully as the first. Barrick's lab is not retiring contingency; it is moving it from mutational access to competitive persistence, which is where Leon et al. 2018 later finds it.
Quandt et al. 2015, eLife 4:e09696, Figure 4 legend — the sentence that complicates the stepwise claim in the other direction:
"these competitions show that the citT mutation would be highly deleterious to fitness if it evolved in a genetic background without the gltA1 mutation. In contrast, the citT mutation is neutral or possibly slightly beneficial to fitness when the gltA1 mutation is present."
— and, in the Results proper, closing the subsection "Initial citrate synthase mutation potentiated Cit+ evolution":
"Epistatic interactions between gltA1 and the citT mutation in this evolved genetic background prevented a massive fitness defect that would have almost certainly led to the rapid extinction of any newly evolved Cit+ cells before this rudimentary trait could be refined to the advantageous Cit++ phenotype by further mutations."
Purdom 2008, "A Poke in the Eye?", Answers in Genesis, 30 June 2008, section "A Creationist Perspective," before the mechanism was known:
"Since E. coli already possess the ability to transport and utilize citrate under certain conditions, it is conceivable that they could adapt and gain the ability to utilize citrate under broader conditions. This does not require the addition of new genetic information or functional systems (there are no known 'additive' mechanisms). Instead degenerative events are likely to have occurred resulting in the loss of regulation and/or specificity."
Purdom 2012, "Bacteria Evolve 'Key Innovation' or Not?", Answers in Genesis blog, 8 November 2012, paragraph 4, after the mechanism was known:
"There was a definite loss of regulation as the original citT gene was only expressed under low oxygen levels."
Carter 2011, updated 2025, "Can mutations create new information?", section "Degraded information":
"aerobic citrate digestion by bacteria (which involves the loss of control of the normal anaerobic citrate digestion)"
Batten 2008, addendum prepared March 2016, Creation Ministries International, the source Carter cites, conceding the mechanism and keeping the label:
"While the existing controls and the citrate transporter gene were not actually broken, the transporter gene was duplicated (copied) to a different location away from the existing control sequence such that the production of the transporter is no longer suppressed in the presence of oxygen. ... So the ability of the cell to control the production of the citrate transporter was indeed broken (the cell is no longer able to turn off the production of the transporter)."
Blount et al. 2012's reporter test is the check on all three: the native citT control region "showed no expression (above background) in any strain," including a weakly Cit+ clone. The original switch was not broken; a copy of the gene acquired a different one.
Behe 2012, "Rose-Colored Glasses: Lenski, Citrate, and BioLogos," Evolution News, 13 November 2012, paragraphs 12-14, on how his Edge of Evolution counts mutations:
"Only required deleterious and neutral mutations count against the limit to Darwinian evolution."
"Thus, unlike Venema, I count perhaps three to four mutations — the original duplication placing the oxygen-tolerant promoter near the citT gene, plus several rounds of duplication of that region."
"If, before Lenski's work was done, someone had sketched for me a cartoon of the original duplication that produced the metabolic change, I would have assumed that would be sufficient — that a single step could achieve it. The fact that it was considerably more difficult than that goes to show that even skeptics like myself overestimate the power of the Darwinian mechanism."
On whether the delay required contingency
Blount, Borland & Lenski 2008, PNAS 105:7899, the 2008 hypothesis:
"This potentiating change increased the mutation rate to Cit+ but did not cause generalized hypermutability. Thus, the evolution of this phenotype was contingent on the particular history of that population."
— with the honest statement of how weak the estimate was:
"The potentiated genetic background thus increases the mutation rate to Cit+ at least 2-fold, and probably much more."
— and the caveat on the largest experiment:
"Although the third experiment was the largest, it was the least significant, owing primarily to the production of two Cit+ mutants by a 20,000-generation clone. We also used the Z-transformation method to combine the probabilities from our three experiments, and the result is extremely significant (P < 0.0001) whether or not the experiments are weighted by the number of independent Cit+ mutants observed in each one."
Van Hofwegen, Hovde & Minnich 2016, J. Bacteriol. 198:1033 and 1032, in that order:
"This indicates that the 33,000 generations to potentiate the evolutionary resources for the Cit+ phenotype do not reflect a direct requirement but merely experimental conditions."
"First, potentiated and actualized cells were routinely diluted away by the LTEE daily 1:100 dilution transfers. Cells with an amplified citT gene had only a brief advantage in the use of citrate once glucose was expended and were likely lost with each daily dilution/transfer into fresh glucose-containing media due to the fitness cost of the maintenance of multiple gene copies."
Roth & Maisnier-Patin 2016, J. Bacteriol. 198:1009 and 1011 — two mainstream Salmonella geneticists agreeing, in the same issue:
"Thus, the delay may not reflect the necessity of a nonselective potentiation event (the 'historical contingency') but may rather be due to selective events with a low probability of serial transfer."
"The transitory nature of simple amplifications may explain why the posited simple duplications were not apparent in sequences of cells from early tubes from the LTEE—they may have been lost during nonselective growth prior to sequencing."
Lenski & Blount 2016, replying — and this is the part of their reply that has not aged well:
"Roth and Maisnier-Patin's suggestion that our idea of 'historical contingency' may require reinterpretation reflects a false dichotomy between historical contingency, on the one hand, and the effects of different selection schemes, on the other. The fact that evolution might be fast and not contingent on genetic background (though the evidence of Van Hofwegen et al. is, at best, ambiguous in this regard) in one set of circumstances has no bearing on whether it is contingent in another set of circumstances."
Leon, D'Alton, Quandt & Barrick 2018, PLoS Genetics 14:e1007348, Abstract — the resolution, from Lenski's own scientific descendants. Note that the paper's title keeps the word contingent: Innovation in an E. coli evolution experiment is contingent on maintaining adaptive potential until competition subsides. Contingency is relocated here, not abolished:
"We found that there was already a slight fitness benefit for this mutation in the original ancestor of the evolution experiment and in other early isolates. However, evolution of citrate utilization was blocked at this point due to competition with other mutations that improved fitness in the original niche. Subsequently, an anti-potentiated genetic background evolved in which it was deleterious to evolve rudimentary citrate utilization. Only later, after further mutations accumulated that restored the benefit of this first-step mutation and the overall rate of adaptation in the population slowed, was citrate utilization likely to evolve."
— and, from the Discussion (pp. 12-13), their explanation of why direct selection is a different experiment:
"this difference in environmental conditions relative to the glucose-limited transfer regime of the LTEE, in which cells are in stationary phase for only ~16–18 hours each day, dramatically increases the fitness benefit of evolving the rudimentary Cit+ phenotype. Therefore, these stark conditions are expected to completely mask and overwhelm the dependency on potentiating genetic and population factors found in the LTEE. Activating citT expression would be universally beneficial in any genetic background in these types of experiments."
On "twelve generations"
Van Hofwegen, Hovde & Minnich 2016, J. Bacteriol. 198:1022, Abstract — the headline:
"Potentiation/actualization mutations occurred within as few as 12 generations, and refinement mutations occurred within 100 generations."
The same paper, page 1027, giving the protocol behind that number:
"After inoculation (9 × 105 to 7 × 106 CFU/ml), the turbidity of the cultures rose to an OD600 of 0.02 to 0.03 overnight, or the equivalent of approximately six generations based on plate count. These cultures were maintained for 7 days in stationary phase, after which cells were inoculated into fresh media at a 1:100 dilution, similarly to Lenski's LTEE but with deliberately extended time spent in stationary phase to enrich for the desired Cit+ phenotype. ... All but one E. coli Cit+ strain were recovered within two to five weekly transfers, representing 12 to 30 generations."
Lenski & Blount 2016, converting it back into days:
"the fastest time that Van Hofwegen et al. saw for the Cit+ function to emerge was 19 days (from their Table 1), and in most cases it took a month or two. While that's a lot faster than 15 years, it's still much longer than typical 'direct selections' used by microbiologists where a readily accessible mutation might confer, for example, resistance to an antibiotic after a day or two."
On the probability arithmetic
Van Hofwegen, Hovde & Minnich 2016, J. Bacteriol. 198:1033 — note the qualifying clause:
"The frequency of the occurrence of both amplification/promoter capture (citT) and a point mutation (dctA) in the same cell under nonselective conditions is on the order of 1 in 1014. This is almost exactly the number of cells Lenski screened to find Cit+, and the frequency Hall predicted for his Cit+ mutation."
Emphasis added.
Minnich & Hovde 2025, J. Physiol. 603:1326, the same argument nine years later with its components broken out:
"the combined probability of getting both aerobic CitT expression and the dctA point mutation suppressing the need of dcuS is ∼1 × 10-14. This figure is derived from: (i) gene amplifications are the most common mutations in bacteria ... and we estimate that getting aerobic expression of CiT via gene amplification/recombination in the order of ∼1 × 10-5; and (ii) a point mutation to suppress dcuS- is in the range of 1 × 10-9 to 10-10. The fact that the LTEE Cit+ mutation was acquired after 33,000 generations (∼1 × 1014 cells, see Pennesi, 2013) likewise argues against contingency."
Blount, Borland & Lenski 2008, PNAS 105 — the only direct measurement of that first rate, which is seven or eight orders of magnitude lower than the estimate above:
"With no more than three mutations among the 8.4 × 1012 cells tested here and in the third replay experiment, the upper bound on the ancestral mutation rate to Cit+ is 3.6 × 10-13 per cell per generation. To the best of our knowledge, this value is the lowest upper bound ever reported for a mutation rate that has been experimentally measured."
On the strain
Quandt et al. 2014, PNAS 111 — the finding Minnich builds on, published by Barrick's lab:
"Unlike most strains of E. coli K-12, the ancestral strain of E. coli B used in the LTEE cannot use C4-dicarboxylates. This difference has been attributed [to] an inactivating mutation in the gene for DcuS, the sensor kinase in the DcuSR two-component system that regulates genes involved in C4-dicarboxylate transport and utilization."
Minnich & Hovde 2025, J. Physiol. 603:1326, the argument built on it:
"Had he chosen E. coli K12, rather than E. coli B (Lenski's starting strain which lacks a functional key gene in its genetic deck), it is likely that all 12 flasks would rapidly have become Cit+ and we would not be arguing about contingency and the requirement of rare and necessary non-repeatable antecedent mutations."
On loss of function
Cooper, Schneider, Blot & Lenski 2001, J. Bacteriol. 183:2834, Abstract:
"Twelve populations of Escherichia coli B all lost D-ribose catabolic function during 2,000 generations of evolution in glucose minimal medium. ... These Rbs- mutants were all about 1 to 2% more fit than the progenitor. A fluctuation test revealed an unusually high rate, about 5 × 10-5 per cell generation, of mutation from Rbs+ to Rbs-, which contributed to rapid fixation."
Cooper & Lenski 2000, Nature 407:
"Sixteen of the 64 informative substrates showed parallel decay in the first 10,000 generations. ... In fact, nine substrates showed parallel decay after only 2,000 generations, at which time none of the populations had yet evolved a mutator phenotype. Average total catabolic function declined by 32% (from 1 to 0.68) in the first 10,000 generations, but declined only 15% (from 0.68 to 0.58) between 10,000 and 20,000 generations."
Tenaillon et al. 2016, Nature 536:
"In total, we found 14,572 point mutations; 500 insertions of IS (insertion sequence) elements; 726 deletions and 1132 insertions each ≤50 bp (small indels); and 267 deletions and 45 duplications each >50 bp (large indels). After 50,000 generations, average genome length declined by 63 kbp (~1.4%) relative to the ancestor."
"six populations (Ara–1, Ara–2, Ara–3, Ara–4, Ara+3 and Ara+6) had 96.5% of the point mutations, having evolved hypermutable phenotypes caused by mutations that affect DNA repair or removal of oxidized nucleotides."
Behe 2019, Darwin Devolves, chapter 7 — the conclusion drawn from those tables:
"After fifty thousand generations of the most detailed, definitive evolution experiment ever conducted, after so much improvement of the growth rate that descendant cells leave revived ancestors in the dust, after relentless mutation and selection, it's very likely that all of the identified beneficial mutations worked by degrading or outright breaking the respective ancestor genes. And the havoc wreaked by random mutation had been frozen in place by natural selection."
Lenski 2019, Telliamed Revisited — conceding most of it, and then not:
"Indeed, the LTEE environment is so extremely simple that one might reasonably expect the bacteria would evolve by breaking many existing functions. ... And just as one would expect, the bacteria have diminished or lost various abilities during the LTEE. For example, all 12 populations lost the ability to use another sugar, called ribose, and they gained a small but measurable competitive advantage as a result."
"The LTEE fits the bill for Behe because it's just about the best case possible to showcase his rule. But just as loss of sight in cave-dwelling organisms is a special case that won't tell us how eyes evolved, one must be careful when extrapolating from this experiment to evolution writ large."
On fine-tuning versus degradation
Maddamsetti et al. 2017, Genome Biol. Evol. 9:1078 — the evidence Behe cites and then discounts:
"only 5 of the 57 genes, all with negative essentiality scores (yijC, malT, yabB, ybaL, and yeeF), have nonsense mutations in any of the nonmutator genomes ... This line of evidence therefore supports the hypothesis that some of the beneficial mutations in the LTEE modulate protein function, rather than knocking it out."
"Ten of the 57 genes that showed gene-level parallel evolution also show parallelism at the amino-acid level."
Behe 2019, Darwin Devolves, endnote 15 to chapter 7. His answer to that evidence is a single endnote, and here it is in full:
"More recent investigation by Lenski's lab suggests that mutations in a small minority (10 of 57) of selected E. coli genes may not completely break them but rather, as they put it, 'fine-tune' them (probably by degrading their functions): 'In some cases, adaptive mutations appear to modify protein functions, rather than merely knocking them out' (R. Maddamsetti et al., 'Core Genes Evolve Rapidly in the Long-Term Evolution Experiment with Escherichia coli,' Genome Biology and Evolution 9 [2017]: 1072–83)."
He has read the paper and quotes its abstract accurately. The whole of the counter-argument is the four words in the parenthesis.
Lenski 2019, naming the hidden premise:
"if one assumes the ancestral state of a gene is perfect, then there's no room for improvement in its function, and the only possible functional changes are degradative. ... that assumption breaks down when an organism encounters a new environment, where the optimal state of a protein might differ from what it was before."
Quandt et al. 2015, eLife 4:e09696, Abstract — the one case where the enzymology was measured, and it will not sit still for either side:
"The first gltA mutation, which increases CS activity by disrupting NADH-inhibition of this enzyme, is beneficial for growth on the acetate and contributed to preserving the rudimentary Cit+ trait from extinction when it first evolved. However, after Cit+ was refined by further mutations, this potentiating gltA mutation became deleterious to fitness. A second wave of beneficial gltA mutations then evolved that reduced CS activity to below the ancestral level."
On fitness, and whether it can rise forever
Lenski et al. 2015, Proc. R. Soc. B 282:20152292, Abstract:
"Here, we examine whether the previously estimated power-law model predicts the fitness trajectory for an additional 10 000 generations. To that end, we conducted more than 1100 new competitive fitness assays. Consistent with the previous study, the power-law model fits the new data better than the hyperbolic model. ... our results imply that both adaptation and divergence can continue indefinitely—or at least for a long time—even in a constant environment."
The same paper, giving both models so a reader can check the arithmetic:
"The best fit of the hyperbolic model gave w = 1 + 0.7007 t/(t + 4431), where w is the grand-mean fitness relative to the ancestor and t is time in generations. This equation predicts grand-mean fitness values relative to the ancestor of 1.6308, 1.6437 and 1.6525 at 40 000, 50 000 and 60 000 generations, respectively. For the power-law model, the best fit yielded w = (0.00515 t + 1)0.0950, which predicts values of 1.6597, 1.6951 and 1.7246 at the same time points."
Behe 2007, The Edge of Evolution, chapter 7, subsection "Lab Star," at about 30,000 generations:
"Breaking some genes and turning others off, however, won't make much of anything. After a while, beneficial changes from the experiment petered out."
His endnote 26 cites de Visser and Lenski 2002 for this, which reported that the rate of improvement "has declined substantially over this period," a slowing rather than a stop.
Sanford 2014, Genetic Entropy, 4th edition, chapter 11, section 2b, "Reexamination of the famous Lenski experiment":
"Over a period of a few decades, a strain of E. coli bacteria became slightly better-adapted to an artificial nutrient medium. This is not unexpected or remarkable in any way."
"Over hundreds of years, Lenski's 'evolving' strains of bacteria must logically go extinct (if they could be maintained in the artificial environment that long). Nearly-neutral deleterious mutations will inevitably cause the bacterial genome to 'rust out'"
On the "death spiral"
Blount et al. 2020, eLife 9:e55414 — the numbers Behe uses, in full:
"On average, 10.7% of the LTEE ancestral cells grown in DM25 were scored as dead in stationary phase. By contrast, when grown in the same DM25 medium, 29.6% and 39.9% of cells were scored as dead for the Cit+ clones isolated from LTEE population Ara–3 at 33,000 (CZB151) and 50,000 generations (REL11364), respectively. We observed similarly high proportions of dead cells for both clones in DM0 as well (33.1% and 44.2% for CZB151 and REL11364, respectively)."
— and the qualifications in the same paper's Discussion, which Behe's article does not quote:
"we observed extensive cell death in Cit+ clones, and the level of mortality varied considerably even between replicate assays for reasons that we do not understand."
"most evolved clones show no significant increase in fitness, and some are less fit than their ancestor, even in the environment where they evolved."
Behe 2020, "Citrate Death Spiral," Discovery Institute:
"Let me emphasize: the only result from the decades-long, 50,000-plus generation E. coli evolution experiment that even seemed at first blush like it had a bit of potential to yield a novel pathway in the bacterium has resulted instead in spectacular devolution."
On what the experiment was for
Lenski 2019, Telliamed Revisited — the most useful sentence in the whole exchange, from either side:
"The LTEE was designed (intelligently, in my opinion!) to be extremely simple in order to address some basic questions about the dynamics and repeatability of evolution, while minimizing complications. It was not intended to mimic the complexities of nature, nor was it meant to be a test-bed for the evolution of new functions."
Blount, Borland & Lenski 2008, PNAS 105 — the question they asked and did not answer:
"Will the Cit+ and Cit– lineages eventually become distinct species?"
Lenski & Blount 2016, on why that question has no short answer:
"In short, speciation is not an event. ... In our first paper on the citrate-using E. coli that arose in the LTEE, we clearly emphasized that becoming Cit+ was only a first step on the road to possible speciation."
Quotations checked and rejected
"Even after 64,000 generations, only the Ara–3 population has evolved that new ability." This one is genuine — it is Lenski's, on Telliamed Revisited, 20 February 2016 — but it is often cited as though it were current. The experiment has since passed 82,000 generations, and no published statement covering the later interval has been located either way. Cite it with its date attached.
Minnich & Hovde's internal citation "Pennesi, E. (2013)" is a misspelling of Elizabeth Pennisi's Science news feature "The man who bottled evolution." Their reference list also gives Blount's co-author as "Borland, Z. D." where the paper has C. Z. Borland. Neither error affects their argument; both are noted so that a reader chasing the citation is not sent to a dead end.
Claims that a peer-reviewed rebuttal of Van Hofwegen et al. 2016 exists. None was found. Lenski and Blount answered on a blog three days after the accepted manuscript posted; no journal comment followed. The scientific reply came as new data — Leon et al. 2018 — rather than as a correction. Anyone who says the Minnich paper was refuted in the literature should be asked for the citation.
No source could be located for the frequently repeated claim that the LTEE has been "running continuously without a single missed day." Lenski's own 1 April 2020 post records that the lines were frozen on 9 March 2020 for the pandemic, and Blount et al. 2008 records that contaminated populations are restarted from the most recent frozen sample. The experiment's continuity is remarkable; it is not literally unbroken.