PNAS has a curious correction in a recent issue. A group from Toronto and Mount Sinai in New York, it seems, had been rather too liberal in their use of text from a previously published paper by another researcher — what we might call plagiarism, in a less charitable mood.
To paraphrase Beyoncé: If you like it, better put some quotation marks around it. But we’re pretty sure she meant before, not after, the fact.
The article, “Structural basis for substrate specificity and catalysis of human histone acetyltransferase 1,” had appeared in May 2012, in other words, some 17 months ago. It has been cited twice, according to Thomson Scientific’s Web of Knowledge.
As the notice states:
BIOCHEMISTRY Correction for “Structural basis for substrate specificity and catalysis of human histone acetyltransferase 1,” by Hong Wu, Natasha Moshkina, Jinrong Min, Hong Zeng, Jennifer Joshua, Ming-Ming Zhou, and Alexander N. Plotnikov, which appeared in issue 23, June 5, 2012, of Proc Natl Acad Sci USA (109:8925–8930; first published May 21, 2012; 10.1073/pnas.1114117109).
The authors note that the review article by M. R. Parthun (ref. 11) provided an excellent summary of the structure and biochemical function of HAT1 as a histone acetyltransferase, and served as background introduction for our study. As such, description of some of the specific biochemical functions of HAT1 was not appropriately noted in our article and should be cited and quoted in the following sections:
On page 8925, left column, second paragraph, lines 11–15, “In vitro, HAT1 specifically acetylates Lys5 and Lys12 of free (nonnucleosomal) histone H4, and “this specificity is entirely consistent with the pattern of acetylation found on newly synthesized histone H4” from many organisms (11).”
On page 8925, left column, second paragraph, lines 18–22, “The p46/48 protein “is a WD40 repeat protein” involved in “a wide variety of chromatin-modifying complexes” (11). In yeast, “the association of HAT2 with HAT1 increases the catalytic activity of” HAT1 “by a factor of 10 and appears to function by increasing” HAT1 binding to histone H4 (2, 11).”
On page 8925, right column, first full paragraph, lines 8–10, ““Once in the nucleus, the HAT1–HAT2 H3–H4 complex becomes associated with the histone chaperone/chromatin assembly factor HIF1 to form the NuB4 complex” (11).”
On page 8930, left column, first full paragraph, lines 1–9, “Because of the important role of HAT1 in chromatin assembly, “a number of studies have begun to link HAT1 to” different types of human cancer (11). “The levels of HAT1” have been found “to increase substantially in liver tumors” (11, 29). Also, “HAT1 mRNA and protein levels are elevated in primary and metastatic human colon cancer tissues” (11, 30). In addition, immunohistochemical studies show that HAT1 is primarily nuclear in normal cells, but the localization of HAT1 largely shifted to cytoplasm in the tumor tissues (11, 30).”
Additionally, Campos, et al. (ref. 12) should be quoted in the following section:
On page 8925, right column, first full paragraph, lines 10–16, “In human cells, “the sNASP chaperone binds H3.1–H4 heterodimers and presents the H4 carboxyl domain to RbAp46,” which “recruits HAT1 activity. After acetylation of histone H4, the complex is stabilized and the histones” are transferred to the ASF1B chaperone. “ASF1B associates with importin-4, and the histones are then transported into the nucleus” (12).”
Parthun is Mark Parthun, a professor at Ohio State University. It was he who brought the misused text to PNAS’s attention. He tells us:
I read this paper with great interest because my lab also studies the Hat1 enzyme. While reading this, a number of the passages in the Introduction and Discussion sections started to sound very familiar. These passages were familiar because they were plagiarized from a review article I had published earlier (Parthun, M.R. Oncogene 26:5319–5328, 2007). I also found some sentences that were plagiarized from another manuscript from another lab (Campos, et al, NSMB 2010). I brought this plagiarism to the attention of the editors at PNAS and suggested that this manuscript be retracted. After more than a year, PNAS published a correction (http://www.pnas.org/content/110/45/18339.full). This correction lists all of the passages that were plagiarized and simply says that they should have had quotation marks around them. This seems like a woefully inadequate response. PNAS has essentially made plagiarism irrelevant because if you are caught, all you have to do is retroactively say that you should have used quotations. Is this a common practice with journals. I hope not because I think this represents a serious step in the erosion of scientific ethics.
We asked Daniel Salisbury, a PNAS editor, why the journal opted to correct rather than retract the paper. This was his reply:
In light of recent concerns from the author of the plagiarized text, we are following up with the PNAS authors’ institution.
Parthun, who said he received a similar message, was not impressed:
My problem with his response [is] that they are simply passing the buck. I would have thought that PNAS had the ultimate responsibility for the manuscripts that it publishes. I don’t understand why they need Mount Sinai to tell them when something is improper.
To which we say, we agree.
We’ve emailed Plotnikov for comment and will update this post if we hear from him. Meanwhile, although we think there might be room in science publishing for correcting improperly attributed text, an instance of multiple examples of frank plagiarism such as this probably isn’t the test case.