Hell hath no fury as a scientific community that finds traces of intelligent design in a peer-reviewed journal.
Last month, a paper ran in the online version of the journal Proteomics rejected the endosymbiotic origin of mitochondria and instead attributed the complexity of the cell to the handiwork of a “mighty creator.”
The resulting revolt — on blogs, in newspapers, and in online chatrooms — was of biblical proportions as researchers inside and outside the proteomics field described their puzzlement at how the article made it passed peer review and into the pages of the respected journal.
Allegations of plagiarism also were leveled against the authors of the article.
This week, Proteomics said it will retract the article, titled “Mitochondria, the missing link between body and soul: Proteomic prospective evidence,” which had appeared in the Jan. 23 online edition.
“The article has been retracted due to some overlap of passages with several previously published articles,” Wiley-VCH, which publishes Proteomics, said in a statement this week.
In the statement, Michael Dunn, the editor of Proteomics and a professor at University College Dublin Conway Institute of Biomolecular & Biomedical Research, said: “We are fully aware of the considerable interest that the article by Warda and Han has engendered, as well as the controversial viewpoints expressed by the authors. Clearly human error has caused a misstep in the normally rigorous peer-review process that is standard practice for Proteomics and should prevent such issues arising.”
The authors of the retrospective study, Mohammad Warda and Jin Han, both of Inje University in South Korea, did not respond to e-mail requests for interviews.
In an e-mail to PZ Myers, whose blog Pharyngula has been flooded with letters and comments about the article, Han apologized for the article and said he had asked that the article be retracted.
In his e-mail to Myers, Han said that he made “serious error[s]” but doesn’t directly address the issues of creationism or plagiarism.
“Based on this good experience, I will study science and prepare a manuscript with caution,” Han says in his e-mail.
Myers, an associate professor of biology at the University of Minnesota, Morris, told ProteoMonitor that while the content of the paper and its scientific merit have been savaged by the research community, the bigger concern is the breakdown in the peer-review process that should have caught red flags and ultimately rejected the article.
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“We are fully aware of the considerable interest that the article by Warda and Han has engendered, as well as the controversial viewpoints expressed by the authors.” |
“The main reaction is that everyone is concerned about what happened in peer review with this paper,” said Myers. “It’s clear it had to have broken down somewhere, and it’s not clear at all where that happened, whether we had a lazy reviewer who just rubber stamped it, or whether there was something more devious where somebody inserted text after it had been approved by a reviewer, or whether there was something that was just off-the-wall weird like elves sneaking into the printing presses and changing it.”
Myers conceded that he is not a proteomics researcher and has never submitted a paper to Proteomics and so has no knowledge of its peer-review process.
Still, Myers said he is “unsatisfied” with just a retraction of the paper without an explanation of how it got into the journal in the first place.
“What broke down in peer review?” he asked. ”I'm mostly wondering about the principle of peer review as implemented at Proteomics, and what holes in their procedures exist that allow such a bad paper to slip through.”
Dunn, “didn't address that, nor did he explain what steps were being take to prevent it happening again,” Myers said.
Dunn declined to comment for this article.
Foresaken
In their article, Warda and Han write that the focus of their retrospective study was to cover “first the mitochondrial proteome/genome interplay” believed to play a role in a host of diseases.
They then say that the paper seeks to explore the relationship between mitochondria and different cytoskeleton proteins, as well as other cellular organelles. Finally, the role of mitochondria in apoptosis and the “mitochondrial contribution in intercellular communication mediated by gap junctions are also described.”
In their abstract the authors state the paper will “disprove the endosymbiotic hypothesis of mitochondrial evolution that is replaced in this work by a more realistic alternative.”
According to the paper, “Instead of sinking in a swamp of endless debates about the evolution of mitochondria, it is better to come up with a unified assumption that all living cells undergo a certain degree of convergence or divergence to or from each other to meet their survival in specific habitats. Proteomics data greatly assist this realistic assumption that connects all kinds of life. More logistically, the points that show proteomics overlapping between different forms of life are more likely to be interpreted as a reflection of a single common fingerprint initiated by a mighty creator than relying on a single cell that is, in a doubtful way, surprisingly originating all other kinds of life.”
Their contention that intelligent design, not evolution, spawned mitochondria, left the scientific community reeling.
Someone identified only as Dr. Spencer, posting a comment on the blog PIMM-Partial Immortalization, said, “The specifics for the process of how mitochondria arose to be part of most extant eukaryotic cells are still being discussed, as indeed are some of the finer points of evolution itself. But no respectable, sane biologist disputes the reality, the fact, of biological evolution [or] that mitochondria (and chloroplasts) trace their origins to free-living bacteria that, through an obviously complex series of processes over about a billion years, became integrated into the complex ‘machine’ we call the eukaryotic cell.”
“DS,” a graduate fellow working in an undisclosed proteomics lab, was more blunt. Writing in his blog, A Drunken Walk Through Science, DS said that “Basically they tried to claim that there was zero evidence for an intermediate between a bacterial endosymbiont and mitochondria, which is untrue.”
Warda and Han were also accused by many of their peers of plagiarism. John McDonald, a professor of biology at the University of Delaware, points out similarities in Warda and Han’s paper to four other papers by different authors, including himself. In some instances, passages in the Proteomics article are virtually verbatim with other papers.
In one instance, Warda and Han write in their paper, “Oxidative stress is caused by an imbalance between the pro-oxidant and anti-oxidant systems, which may cause reversible and/or irreversible modifications on sensitive proteins leading to structural, functional, and stability modulations.”
In a 2006 article appearing in the European Journal of Pharmacology, D. Allan Butterfield and his colleagues write, “Oxidative stress is caused by an imbalance in the prooxidant and antioxidant systems. Oxidative stress may cause reversible and/or irreversible modifications on sensitive proteins leading to structural, functional, and stability modulations.”
“How this got published in Proteomics is beyond me,” Andrew McArthur, a bioinformatics consultant, writes in his blog. “My objection is not to the religious belief expressed but to this misuse of a scientific journal.”