The executive board of the Leibniz Association in Germany has reprimanded the director of its institute on aging for “grossly negligent scientific misconduct.”
Besides a written reprimand, the executive board has removed Karl Lenhard Rudolph’s “passive voting rights” in association committees, and excluded the institute under his leadership from receiving funds from a multi-million Euro internal funding competition, both for a period of three years.
The executive board identified problems in eight out of 11 reviewed papers, published between 2001 and 2016; it has asked Rudolph to retract one and issue errata for the others. The papers — some of which have been discussed on PubPeer — appear in journals such as Cell, Nature Cell Biology, and the EMBO Journal, and have been collectively cited 552 times, according to Clarivate Analytics’ Web of Science.
Rudolph is the director of one of the 91 independent research institutions that make up the Leibniz Association. He told us he is putting the position of Director of the Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) in Jena “on hold” while he investigates the allegations:
The commission states that there is no evidence for data fabrication or manipulation by me. I will rigorously investigate all criticized mistakes and will correct these by publications in the scientific journals. At the same time, I will install measures to prevent the occurrence of such mistakes in my group in the future. This process is ongoing and will be reported to the Leibniz Association by November 1st, 2017. In this period, I put the position as a Scientific Director of the Institute on hold to take my responsibility as scientist to the full extent. With this step I wish protect all co-workers in my group and at institute aiming to prevent damage to the development of the Institute.
Here’s more from the Leibniz statement:
-Eight of the 11 scientific publications reviewed contain errors in data representation. These errors include improper duplication of parts of images, unmarked edits when electronically compiling parts of images, presentation of incorrect parts of images, improper selection when presenting results and inadequate loading controls for what are known as ‘Western blots’ on separate gels. Prof. Dr Rudolph is primarily responsible for six of these publications as corresponding author / senior author; he is jointly responsible as co-author for the presentation of criticised data in another publication.
-In eight of the reviewed publications, it was not possible to submit data documentation corresponding to the requirements for good scientific practice with relevant trial protocols and primary data (lab books).
-In four of the reviewed publications, experiments were not sufficiently checked for their reproducibility in accordance with the rules of good scientific practice.
As a result, the executive board has excluded FLI from receiving a type of intramural funding for three years:
Based on the recommendations of the Review Board, the Executive Board has decided to adopt measures including a written reprimand directed at Prof. Dr Rudolph on the grounds of grossly negligent scientific misconduct, the withdrawal of his passive voting rights for Leibniz Association committees for three years and the exclusion of the FLI under Prof. Dr Rudolph’s leadership from Leibniz Association competition proceedings for three years.
The statement confirmed Rudolph’s claim that the executive board did not find evidence that he personally manipulated data; a longer statement from the institution concludes “his breach of the duty of supervision as working group leader and primary author to be grossly negligent:”
While the Review Board does not see any specific indications that data was fabricated or that data manipulation was carried out directly or initiated by Prof. Dr Rudolph, it considers there to be proof of insufficient documentation of the steps and results of the experiments in question in the form of protocols and primary data collection, insufficient quality control that should have ensured the validity and reproducibility of all of the results of this experimental work, inadequate supervision when preparing the publications and insufficient supervision of researchers within the working group. All of these violations arose because Prof. Dr Rudolph neglected his duty of supervision as working group leader (and the main senior author) over a period of more than five years.
A spokesperson for Leibniz sent us a list of the 11 papers, but declined to indicate which one was recommended for retraction.
Rudolph told us:
I would like to clarify that the Leibniz statement says that a retraction should occur according to the recommendation of the commission. The commission [states] “it should be considered if a [retraction] needs to be conducted”. I am in the process of investigating this…
The Leibniz spokesperson explained how the investigation came about:
The Ombudsperson of Leibniz Association received hints of an external expert. There also was a discussion on the Website https://pubpeer.com/ about several of the papers in question. Furthermore Dr. Rudolph himself informed the review board about the external allegations.
Regarding the funding ban, the spokesperson explained that FLI was excluded from the Leibniz Competition:
The Leibniz Association Competition is an internal funding program meant to stimulate strategic objectives of the organization. Around 30 Million of Leibniz’s basic funding go to the competition. Institutes can apply annually for different funding schemes…A proposal from FLI under Dr. Rudolph’s leadership will not be accepted in this internal competition for three years.
Since Rudolph said he has put the position of Scientific Director “on hold” until November, we asked if FLI would be eligible for consideration for the 2018 competition, for which researchers have already submitted applications:
There is no final decision on the matter yet. It is still being examined.
One of the 11 papers — published in 2012 by Cell — received an erratum in 2014, citing problems with western blots:
It has come to our attention that the actin loading control for the BATF western blots depicted in Figures 3C and 4C of the article above are from different exposures of the same western blot. Although appropriate actin controls were performed for the experiments presented in Figures 3C and 4C, because the error occurred at the stage of data collection, we cannot provide an image of the correct control bands for the data presented in 4C. The magnitude and impact of this error do not affect the published conclusions. We apologize for any confusion the error may have caused.
The 2012 paper “A differentiation checkpoint limits hematopoietic stem cell self-renewal in response to DNA damage” has been cited 153 times.
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Curr Biol. 2001 Jun 26;11(12):962-6.
Rescue of a telomere length defect of Nijmegen breakage syndrome cells requires NBS and telomerase catalytic subunit.
Ranganathan V1, Heine WF, Ciccone DN, Rudolph KL, Wu X, Chang S, Hai H, Ahearn IM, Livingston DM, Resnick I, Rosen F, Seemanova E, Jarolim P, DePinho RA, Weaver DT.
Author information
1
Center for Blood Research, 200 Longwood Avenue, Boston, MA 02115, USA.
https://pubpeer.com/publications/AAC96A54E54A2403C6504DE7968A45#
Figure 2. http://imgur.com/cXNDJT2
This is clearly a duplication of the lane in the EtBr staining which is not acceptable and should be corrected. The experiment in question should be repeated or deleted from the publication and conclusions. A repetition might be difficult after 16 year but maybe possible.
That said, how can this now be blamed on Rudolph KL who is fourth author on the publication which did not even come from the lab in which he was in at the time (DePinho lab). Is is proven that he is responsible for the duplication of the lanes?
I get the feeling that there is a witch hunt going on here! If we want scientific integrity we have to ask for this from all sides including the people that analyse the cases afterwards.
I knew something is going to happen when I read on pubpeer sometime ago. A common author in 4 of the listed papers has secured a good position here http://www.sps.tsinghua.edu.cn/en/team/team/2016/0814/54.html Very unfortunate!
That would make the second director of a Leibniz institute to be sanctioned.
http://retractionwatch.com/?s=bulfone-paus
2017 correction.
EMBO J. 2015 Mar 4;34(5):624-40. doi: 10.15252/embj.201490700. Epub 2015 Jan 21.
Wnt activity and basal niche position sensitize intestinal stem and progenitor cells to DNA damage.
Tao S1, Tang D2, Morita Y2, Sperka T2, Omrani O2, Lechel A3, Sakk V3, Kraus J4, Kestler HA5, Kühl M6, Rudolph KL7.
Author information
1 Leibniz Institute for Age Research – Fritz Lipmann Institute e.V. (FLI), Jena, Germany Institute of Biochemistry and Molecular Biology, Ulm University, Ulm, Germany International Graduate School in Molecular Medicine Ulm, Ulm University, Ulm, Germany.
2 Leibniz Institute for Age Research – Fritz Lipmann Institute e.V. (FLI), Jena, Germany.
3 Cooperation Group between the Leibniz Institute for Age Research, Ulm University, Ulm, Germany.
4 Medical Systems Biology Unit, Ulm University, Ulm, Germany.
5 Leibniz Institute for Age Research – Fritz Lipmann Institute e.V. (FLI), Jena, Germany Medical Systems Biology Unit, Ulm University, Ulm, Germany.
6 Institute of Biochemistry and Molecular Biology, Ulm University, Ulm, Germany [email protected] [email protected].
7 Leibniz Institute for Age Research – Fritz Lipmann Institute e.V. (FLI), Jena, Germany Research Group on Stem Cell Aging, Jena University Hospital (UKJ), Jena, Germany [email protected] [email protected].
2017 correction notice.
http://emboj.embopress.org/content/36/19/2920
The authors state that it came to their attention that the figure legends of two figures were not sufficiently detailed in the original version of the manuscript.
The figure legend of Fig 1E and F should read:
A single representative FACS plot was chosen to illustrate (E) the gating of LGR5hi and LGR5lo populations within the population of LGR5+ (GFP‐positive) intestinal cells and (F) the gating of LGR5hi‐high, LGR5hi‐low, LGR5lo‐high, and LGR5lo‐low populations. The same FACS plot is displayed in (E) and (F).
The figure legend of Fig 6C should read:
Representative Western blots of cell lysates for the expression of phospho‐p53 and cleaved caspase‐3 (each n = 3; see Source Data for this figure). Samples from a single experiment were divided into identical portions and probed for phospho‐p53 or cleaved casp3. The expression control of beta‐actin was conducted on the second aliquot of the samples and was run in parallel on a separate gel.
The corrections do not affect the original conclusions presented. We apologize for the lack of detail and any inconvenience it may have caused.
Editorial Note
These changes were based on the results of an investigation of the Leibniz Association. All authors agree with this correction.
© 2017 The Authors. Published under the terms of the CC BY NC ND 4.0 license
2017 correction.
EMBO J. 2015 May 12;34(10):1371-84. doi: 10.15252/embj.201490070. Epub 2015 Mar 27.
Telomerase abrogates aneuploidy-induced telomere replication stress, senescence and cell depletion.
Meena JK1, Cerutti A2, Beichler C3, Morita Y1, Bruhn C1, Kumar M4, Kraus JM5, Speicher MR3, Wang ZQ1, Kestler HA6, d’Adda di Fagagna F7, Günes C8, Rudolph KL8.
Author information
1 Leibniz Institute of Age Research, Fritz Lipmann Institute e.V., Jena, Germany.
2 IFOM Foundation-FIRC Institute of Molecular Oncology Foundation, Milan, Italy.
3 Institute of Human Genetics, Medical University of Graz, Graz, Austria.
4 Institute of Experimental Cancer Research, University of Ulm, Ulm, Germany.
5 Medical Systems Biology Unit, Ulm University, Ulm, Germany.
6 Leibniz Institute of Age Research, Fritz Lipmann Institute e.V., Jena, Germany Medical Systems Biology Unit, Ulm University, Ulm, Germany.
7 IFOM Foundation-FIRC Institute of Molecular Oncology Foundation, Milan, Italy Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche, Pavia, Italy.
8 Leibniz Institute of Age Research, Fritz Lipmann Institute e.V., Jena, Germany [email protected] [email protected].
2017 correction notice.
http://emboj.embopress.org/content/36/19/2922
The authors state that errors occurred during formatting of Fig 2B and Supplementary Fig 3C during the submission process of the original manuscript. The histogram of Fig 2B was mistakenly duplicated in Supplementary Fig S3C. The corrected histogram of Supplementary Fig S3C is shown below. In addition, Fig 2B contains two labeling errors of P‐values, originating from mistakes in the labeling during the graphical assembly of the figure: The P‐value for OSBPL3‐shRNA vs. scrambled shRNA should read 0.0218 instead of 0.0216, and the P‐value for GJB3‐shRNA vs. scrambled shRNA should read 0.0011 instead of 0.0012. The corrected Fig 2B is shown below. For the experiments shown in Fig 2B and Supplementary Fig S3C, a total number of 74–174 cells was analyzed in 3–14 vision fields per cell line.
Further, γH2AX staining of IMR90 cells mentioned in the results section (page 1373, last sentence “… telomerase‐negative BJ and IMR90 fibroblasts exhibited a strong accumulation of DNA damage (staining positive for both γH2AX and 53BP1) at early passage after shRNA transduction (Fig 2A, C and D, Supplementary Fig S3A and B)…” was not depicted in the paper, and the 53BP1 staining was performed only on the BJ cells. To correct for this mistake, the text and data presentation of the result section on the description of DNA damage foci (page 1373, last sentence, and page 1374, first paragraph) is specified as follows: “The experiments on IMR90 cells were conducted only for γH2AX staining. These results are now provided in Supplementary Fig S8”.
The description and presentation of Western blot results in Fig 1D (page 1372, first paragraph on the right column) is corrected as follows: The depicted analyses of p‐p53, p‐p38, and GAPDH in Fig 1D (see also the corresponding Source Data file in the original article) were all analyzed from the same blot. A repeat of the p‐p53 Western blot was run on a separate gel using the same protein lysates and loading buffer (see Source data for Figure 1D below).
The Western blot for p21 in Fig 1D and the corresponding beta‐actin control were run in parallel with the same protein lysates and the same loading on 2 separate gels; the gel probed for beta‐actin was not shown in the original source data file of Fig 1D. The gel was also used to repeat the analysis of p‐p38 expression (see Source data for Figure 1D below). Results of p21 induction were confirmed by immunofluorescence analysis (see Fig 1E and Supplementary Fig S2H–K of the original manuscript).
The corrections do not affect the original conclusions presented. The authors apologize for the mistakes and any inconvenience they might have caused.
Editorial Note
These changes were based on the results of an investigation by the Leibniz Association. All authors agree with this correction.
© 2017 The Authors. Published under the terms of the CC BY 4.0 license