Scotland researcher suspended during misconduct probe: report

Robert Ryan
Robert Ryan

A prominent researcher in Scotland has been suspended amidst a misconduct investigation at the University of Dundee.

According to The Scotsman, the allegations against Robert Ryan center around falsifying data and duplicating figures in his work about molecular bacteriology.

As the outlet reports:

The award-winning Wellcome Trust senior research fellow is at the forefront of global research which could lead to new treatments for cystic fibrosis and has received extensive public funding.

But it is alleged he used identical images across multiple papers, claiming they were different strains. In some cases, it is alleged the evidence was flipped or rotated, which could indicate an “intent to deceive”, according to one source.

The extent of the alleged misconduct is unclear, but the source indicated it is alleged to have spanned “a number of years” and involved numerous prestigious journals.

Six of Ryan’s papers have been cited at least 100 times, according to Thomson Reuters Web of Science.

A few of Ryan’s papers have been flagged on PubPeer; we’ve tracked down two corrections: One for a 2013 EMBO Journal paper, “A cyclic GMP-dependent signalling pathway regulates bacterial phytopathogenesis,” cited 18 times.  The correction notice was issued a few months after publication:

Since the publication of this article, the authors have noticed several errors that in any case do not affect the original conclusions presented. The authors apologize for any inconvenience caused.

The gel presented in panel A of Figure 2 suggests a slightly incorrect size for the purified CYC domain of XC_250. Panel E in the same figure incorrectly describes D28 as D41 (see below). The correct figure and legend are shown below. Source data for this figure is now available on the online supplementary information page.

The predicted critical amino acid sites of XC_0250 were reported incorrectly in the section ‘The cyclase domain of XC_0250 is active in cyclic GMP synthesis’, with D28 described as D41. The text should have read:

‘The two critical metal‐ion binding aspartates are conserved (D28 and D71) as well as an alanine (A150) residue that occupies a substrate‐specifying position. However, the transition state‐stabilizing asparagine and arginine residues are substituted by leucine (L157) and alanine (A161). The importance of both conserved and altered residues (D28, D41, D71, L73, A150, L157, A161) for the enzymatic activity of this domain was examined by assessing the effects of alanine or serine substitutions’.

And at a later point in the same section: ‘Several of these residues (D28, D71, A150, L157) are conserved in the R. centenum guanylyl cyclase (Supplementary Fig S1).’…Consistent with this, the alignment in Supplementary Fig S1 panel A incorrectly shows the position of D28. The correct figure and legend are available above.

And here’s the correction notice for “HD-GYP domain proteins regulate biofilm formation and virulence in Pseudomonas aeruginosa,” published in Environmental Microbiology in 2008 and cited 50 times. The correction notice was issued earlier this year, and cites a duplicated image:

…there was an image duplication within Figure 4C where the same image was mistakenly used to represent two different complemented bacterial strains. A corrected version of Figure 4 is given here. None of the conclusions of the paper are altered. We apologise to the readership of the Journal for this error and for any inconvenience caused.

Other papers by Ryan — such as “Cyclic di-GMP signalling in the virulence and environmental adaptation of Xanthomonas campestris” published in Molecular Microbiology in 2006 and cited 91 times — have also been questioned on PubPeer. Commenters have raised allegations about other papers, such as a 2012 PLOS ONE paper, and a 2010 paper in PNAS.

In 2013, Ryan was awarded the prestigious Society for General Microbiology’s Fleming Prize; the next year, he earned the Lister Prize fellowship, totaling 200,000 pounds over five years. Also in 2014, he received the RSE Patrick Neill Medal. Last year, he was selected to be an EMBO Young Investigator.

According to The Scotsman, Ryan has received more than $1 million in grant funding to support his research. The outlet reports that his lab has been disbanded, “with PhD students and staff scientists reallocated elsewhere.”

The Scotsman included a statement from the University of Dundee:

In a statement, the University of Dundee said: “There is an ongoing investigation into an allegation of research misconduct. In order not to prejudice in any way the outcome of that investigation, we are unable to comment further on it at this time.

“The university has clear policies relating to research misconduct, and any such allegations are thoroughly investigated.”

It added that a member of staff has been suspended pending the investigation being completed.

Professor Barry Plant, the co-ordinator of CFMATTERS, an EU-funded cystic fibrosis research consortium, provided a more specific quote to The Scotsman:

I can confirm that CFMATTERS is aware of his suspension. Any potential decisions regarding the project and Dr Ryan will be made in close collaboration with the EU Commission funders once the Dundee investigation is completed.

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10 thoughts on “Scotland researcher suspended during misconduct probe: report”

  1. It’s gutting that probably 95% of British biomedical researchers are no longer eligible for Wellcome funding, since they went all ‘Howard Hughes’ on us; it’s even more gutting if they’re giving considerable amounts of money to researchers who subsequently do things like this with the funding.

    1. “It’s gutting that probably 95% of British biomedical researchers are no longer eligible for Wellcome funding, since they went all ‘Howard Hughes’ on us”.

      Please explain what you mean by “gutting”. Also, ‘Howard Hughes’. These terms are not obvious.

    2. I don’t have their figures to hand but from memory of a presentation I saw last year, Wellcome give out about 0,5bn a year in funding of which ~85% is spent on UK research. I find it hard to believe that 5% of life science UK researchers are sharing upwards of 400million between themselves with with the other 95% looking on hungrily. Wellcome are quite strategic in their funding, but I think even they would argue only giving money to 5% of researchers would be poor value for money.

      I also don’t know what you mean by “going Howard Hughes”.

      1. They changed their funding structure; the vast majority of UK academics are no longer realistically eligible (they make personal awards (fellowships) and no longer fund project grants i.e. no RO1 equivalents, for those of you in the US). So, very similar to how HHMI fellows are funded.

        And whilst they fund a huge amount of science, the figures you quote fund research centres in no small part, so these funds are concentrated around very few epicentres.

        I hope this makes things a little clearer – apologies for being too colloquial:)

  2. The Welcome trust says
    “Investigator awards offer flexible awards typically up to £3m total for any duration of up to a maximum of seven years. Awards cover the direct costs of the research proposed, but the applicant’s salary must be provided by the host institution. The Wellcome Trust has now combined the senior and new investigator schemes into this one funding stream. To be eligible, applicants should be employed in an established academic post: a permanent, open-ended or long-term rolling contract, salaried by your host institution. You are also eligible if you have a written guarantee of an established academic post at your host institution, which you will take up by the start of the award.”

    And I too am curious how the above is “Howard hughes.”

  3. Just a note – Dr Ryan appears to have been completely scrubbed from the Dundee website, as though he doesn’t exist at all. Someone should follow up on this.

  4. Many of the work particularly with cyclic DiGMP associated phenotypes and quorum sensing are not repeatable even in their model organism Xanthomonas campestris by Ryan and Max Dow his mentor. Surprisingly the Axa21 story which Dr. Ronald lab retracted due to strain problem was repeated by Dr Ryan and his mentor Max Dow and their collaborators in animal pathogenic bacteria and they repeated the same story. I think that their work need to be repeated as many of their findings have different reports from other groups with not so high profile as Dr Ryan and his mentor and long time collaborator Max Dow published work.

    1. Thank you for your comments on Dr Ryan and Dow’s work. I have worked with both on and off for several years. I would very much like to know what phenotypes you are referring to in your post. I can assure you that the phenotypes associated with DSF and the Rpf cell-cell signaling system are solid and reproducible. They have been reported by numerous groups and strains confirmed and used by other groups. With regards the phenotypes observed in cyclic-di-GMP knockouts strains in Xanthomonas I again can assure you these been seen by a number of labs and the strains confirmed. In particular, phenotypes associated with HD-GYP and PilZ domain knockouts have been seen in most Xanthomonads with various degrees of potency. Importantly, the phenotypes are generally associated with virulence in plants and not seen in vitro making them difficult to detect.

      Finally, the major reason for the retraction of these papers from the Ronald laboratory were the absence of a specific effect of Ax21 on plant defence induction in rice lines carrying the Xa21 gene. In addition, it was shown that Ax21 secretion involved type II secretion and not the type I system encoded by rax genes, as initially thought. This was reported in a correction to one of these papers (the peerJ paper). It was not questioned whether the extracellular perception of Ax21 (or derived peptides) had a role in alteration of gene expression in Xanthomonas, as distinct from plants. In the experiments on Stenotrophomonas by the Ryan and Dow, there were no experiments on effects of peptides/proteins on plants and the mutation of a homolog of a gene encoding the type I secretion protein had only a slight effect on the Ax21 level. Importantly, these effects were measured indirectly as the effects of supernatants on the ax21 mutant in S. maltophilia. This point was raised in the peerJ paper, although without mentioning that the mutation still had significant signaling activity in the supernatant. Thus the conclusions seem to remain valid. This was discussed in detail at the last XGC meeting two years ago. I do think that if there are errors in the Stenotrophomonas article it will retracted.

      Why not contact the authors and ask for input? Or contact the Journal and ask to write a common?

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