University press releases are a major source of science misinformation

Here's an example of a press release that distorts science by promoting incorrect information that is not found in the actual publication.

The problems with press releases are well-known but nobody is doing anything about it. I really like the discussion in Stuart Ritchie's recent (2020) book where he begins with the famous "arsenic affair" in 2010. Sandwalk readers will recall that this started with a press conference by NASA announcing that arsenic replaces phosphorus in the DNA of some bacteria. The announcement was treated with contempt by the blogosphere and eventually the claim was discproved by Rosie Redfield who showed that the experiment was flawed [The Arsenic Affair: No Arsenic in DNA!].

This was a case where the science was wrong and NASA should have known before it called a press conference. Ritchie goes on to document many cases where press releases have distorted the science in the actual publication. He doesn't mention the most egregious example, the ENCODE publicity campaign that successfully convinced most scientists that junk DNA was dead [The 10th anniversary of the ENCODE publicity campaign fiasco].

I like what he says about "churnalism" ...

In an age of 'churnalism', where time-pressed journalists often simply repeat the content of press releases in their articles (science news reports are often worded vitrually identically to a press release), scientists have a great deal of power—and a great deal of responsibility. The constraints of peer review, lax as they might be, aren't present at all when engaging with the media, and scientists' biases about the importance of their results can emerge unchecked. Frustratingly, once the hype bubble has been inflated by a press release, it's difficult to burst.

Press releases of all sorts are failing us but university press releases are the most disappointing because we expect universities to be credible sources of information. It's obvious that scientists have to accept the blame for deliberately distorting their findings but surely the information offices at universities are also at fault? I once suggested that every press release has to include a statement, signed by the scientists, saying that the press release accurately reports the results and conclusions that are in the published article and does not contain any additional information or speculation that has not passed peer review.

Let's look at a recent example where the scientists would not have been able to truthfully sign such a statement.

A group of scientists based largely at The University of Sheffield in Sheffield (UK) recently published a paper in Nature on DNA damage in the human genome. They noted that such damage occurs preferentially at promoters and enhancers and is associated with demethylation and transcription activation. They presented evidence that the genome can be partially protected by a protein called "NuMA." I'll show you the abstract below but for now that's all you need to know.

The University of Sheffield decided to promote itself by issuing a press release: Breaks in ‘junk’ DNA give scientists new insight into neurological disorders. This title is a bit of a surprise since the paper only talks about breaks in enhancers and promoters and the word "junk" doesn't appear anywhere in the published report in Nature.

The first paragraph of the press release isn' very helpful.

‘Junk’ DNA could unlock new treatments for neurological disorders as scientists discover how its breaks and repairs affect our protection against neurological disease.

What could this mean? Surely they don't mean to imply that enhancers and promoters are "junk DNA"? That would be really, really, stupid. The rest of the press release should explain what they mean.

The groundbreaking research from the University of Sheffield’s Neuroscience Institute and Healthy Lifespan Institute gives important new insights into so-called junk DNA—or DNA previously thought to be non-essential to the coding of our genome—and how it impacts on neurological disorders such as Motor Neurone Disease (MND) and Alzheimer’s.

Until now, the body’s repair of junk DNA, which can make up 98 per cent of DNA, has been largely overlooked by scientists, but the new study published in Nature found it is much more vulnerable to breaks from oxidative genomic damage than previously thought. This has vital implications on the development of neurological disorders.

Oops! Apparently, they really are that stupid. The scientists who did this work seem to think that 98% of our genome is junk and that includes all the regulatory sequences. It seems like they are completely unaware of decades of work on discovering the function of these regulatory sequences. According The University of Sheffield, these regulatory sequences have been "largely overlooked by scientists." That will come as a big surprise to many of my colleagues who worked on gene regulation in the 1980s and in all the decades since then. It will probably also be a surprise to biochemistry and molecular biology undergraduates at Sheffield—at least I hope it will be a surprise.

Professor Sherif El-Khamisy, Chair in Molecular Medicine at the University of Sheffield, Co-founder and Deputy Director of the Healthy Lifespan Institute, said: “Until now the repair of what people thought is junk DNA has been mostly overlooked, but our study has shown it may have vital implications on the onset and progression of neurological disease."

I wonder if Professor Sherif El-Khamisy can name a single credible scientist who thinks that regulatory sequences are junk DNA?

There's no excuse for propagating this kind of misinformation about junk DNA. It's completely unnecessary and serves only to discredit the university and its scientists.

Ray, S., Abugable, A.A., Parker, J., Liversidge, K., Palminha, N.M., Liao, C., Acosta-Martin, A.E., Souza, C.D.S., Jurga, M., Sudbery, I. and El-Khamisy, S.F. (2022) A mechanism for oxidative damage repair at gene regulatory elements. Nature, 609:1038-1047. doi:[doi: 10.1038/s41586-022-05217-8]

Oxidative genome damage is an unavoidable consequence of cellular metabolism. It arises at gene regulatory elements by epigenetic demethylation during transcriptional activation1,2. Here we show that promoters are protected from oxidative damage via a process mediated by the nuclear mitotic apparatus protein NuMA (also known as NUMA1). NuMA exhibits genomic occupancy approximately 100 bp around transcription start sites. It binds the initiating form of RNA polymerase II, pause-release factors and single-strand break repair (SSBR) components such as TDP1. The binding is increased on chromatin following oxidative damage, and TDP1 enrichment at damaged chromatin is facilitated by NuMA. Depletion of NuMA increases oxidative damage at promoters. NuMA promotes transcription by limiting the polyADP-ribosylation of RNA polymerase II, increasing its availability and release from pausing at promoters. Metabolic labelling of nascent RNA identifies genes that depend on NuMA for transcription including immediate–early response genes. Complementation of NuMA-deficient cells with a mutant that mediates binding to SSBR, or a mitotic separation-of-function mutant, restores SSBR defects. These findings underscore the importance of oxidative DNA damage repair at gene regulatory elements and describe a process that fulfils this function.

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