Julia Shaw is a forensic psychologist. She is currently a senior lecturer in criminology at the London South Bank University (London, UK). Shaw is concerned that we are creating a culture where public outreach is being unfairly attacked. Read her Scientific American post at: The Perils of Public Outreach.

What scientists write in academic publications is generally intended for a scientific community, full of nuance and precise language. Instead, what scientists say and write in public forums is intended for lay audiences, almost invariably losing nuance but gaining impact and social relevance. This makes statements made in public forums particularly ripe for attack.

We find ourselves in a complicated space. On the one hand scientists are professionals, and want to keep the profession reputable. We want to make sure that ideas conveyed by scientists are accurate. On the other hand, if we censor the simplified or creative speech of scientists in public arenas, we have the potential to stifle important communication and debate.

Academic articles often take years to craft into something that colleagues and editors agree is worthy of being published. An interview for the media can take minutes, and is often an improvised attempt to convey a very complex issue on the spot.

If you put these two types of communications next to each other, “real” science is likely to slaughter popular science. It’s like taking a pen to a gunfight. And, it can be difficult for scientists who read each other’s comments in popular outlets to remember that an informal discussion of science should not, and cannot, stand on the same ground as a formal one.

Scientists must be careful to not police other scientists in a way that makes critical discussion impossible, and that dissuades dissemination.

Only then can we ensure that we can have real impact and continue to make science accessible.

The lead editorial in last week's issue of Nature (Dec. 8, 2016) urges us to Take the time and effort to correct misinformation. The author (Phil Williamson) is a scientist whose major research interest is climate change and the issue he's addressing is climate change denial. That's a clear example of misinformation but there are other, more subtle, examples that also need attention. I like what he says in the opening paragraphs,

Most researchers who have tried to engage online with ill-informed journalists or pseudoscientists will be familiar with Brandolini’s law (also known as the Bullshit Asymmetry Principle): the amount of energy needed to refute bullshit is an order of magnitude bigger than that needed to produce it. Is it really worth taking the time and effort to challenge, correct and clarify articles that claim to be about science but in most cases seem to represent a political ideology?

I think it is. Challenging falsehoods and misrepresentation may not seem to have any immediate effect, but someone, somewhere, will hear or read our response. The target is not the peddler of nonsense, but those readers who have an open mind on scientific problems. A lie may be able to travel around the world before the truth has its shoes on, but an unchallenged untruth will never stop.

Our data support these hypotheses, and we have generalized this idea over many different functional elements. The presence of conserved function encoded by conserved orthologous bases is a commonplace assumption in comparative genomics; our findings indicate that there could be a sizable set of functionally conserved but non-orthologous elements in the human genome, and these seem unconstrained across mammals.

Anyone who finds flaws should seek corrections with diplomacy and humility. A gloating sense of ‘gotcha’ does not help to provide constructive criticism; some ill-considered phrases have caused lasting damage. But many scientists use their blogs for credible, restrained, nuanced criticism, often engaging the authors whose works are criticized.

Sharing and discussion of scientific work has changed drastically in a world of blogs, online repositories and Twitter. The fact remains, however, that self-correction is at the heart of science. Critics — curated or not — should be courteous, but criticism itself must be embraced.

This is not news. We've known about this kind of data for 15 years and it's one of the reasons why many scientists over-estimated the number of humans genes in the decade leading up to the publication of the human genome sequence. The importance of the ENCODE project is that a significant fraction of the human genome has been analyzed in detail (1%) and that the group made some serious attempts to find out whether the transcripts really represent functional RNAs.

My initial impression is that they have failed to demonstrate that the rare transcripts of junk DNA are anything other than artifacts or accidents. It's still an open question as far as I'm concerned.

Despite what you may read, there is still a lot of junk DNA. The ENOCDE project does not "sound the death-knell for junk DNA." Our genomes are filled with fossils of genetic parasites, inactive genes, and other low-complexity, very repetitive sequence, and it's extremely clear that most of this stuff no functional role. Much of this sequence may be transcribed, but remember that the ENCODE evidence for most of this transcription is indirect - their direct measurements only detected transcripts for ~14% of the regions they studied. Even if much of it is transcribed, this mainly suggests that it is not worth expending energy to actively repress this transcription, since there are so many other controls in place to deal with unwanted transcripts in the cell.

There seems to be three possible interpretations for all these extra transcripts. One is that, even though we haven't detected a biological function, and evolution doesn't conserve them, they are actually specifically functional. This would be the "there is no junk DNA" take on matters. The opposite extreme would be an "it's all junk" view of it. From this perspective, the starting and stopping of transcription is just an inherently noisy process and doesn't do humans enough harm to create a selective pressure to improve it.

Somewhere between the two would be the view that few of these extra transcripts are useful in themselves, but it's useful having them present on the collective level. Reasons could include anything ranging from excess RNA performing some sort of structural function through to the random transcripts being a rich source of new genes.

Personally, I fall into the "it's all junk" end of the spectrum. If almost all of these sequences are not conserved by evolution, and we haven't found a function for any of them yet, it's hard to see how the "none of it's junk" view can be maintained. There's also an absence of support for the intervening view, again because of a lack of evidence for actual utility. The genomes of closely related species have revealed very few genes added from non-coding DNA, and all of the structural RNA we've found has very specific sequence requirements. The all-junk view, in contrast, is consistent with current data. We've wondered for decades how transcription factors can act specifically and at long distances despite their relatively weak specificity for DNA. This data answers that question simply: they don't.

This brings us to the ENCODE project, which was set up to provide a comprehensive look at how the human genome behaves inside cells. Back in 2007, the consortium published its first results after having surveyed one percent of the human genome, and the results foreshadowed this past week's events. The first work largely looked at what parts of the genome were made into RNA, a key carrier of genetic information. But the ENCODE press materials performed a sleight-of-hand, indicating that anything made into RNA must have a noticeable impact on the organism: "the genome contains very little unused sequences; genes are just one of many types of DNA sequences that have a functional impact."

There was a small problem with this: we already knew it probably wasn't true. Transposons and dead viruses both produce RNAs that have no known function, and may be harmful in some contexts. So do copies of genes that are mutated into uselessness. If that weren't enough, just a few weeks later, researchers reported that genes that are otherwise shut down often produce short pieces of RNA that are then immediately digested.

So even as the paper was released, we already knew the ENCODE definition of "functional impact" was, at best, broad to the point of being meaningless. At worst, it was actively misleading.

But because these releases are such an important part of framing the discussion that follows in the popular press, the resulting coverage reflected ENCODE's spin on its results. If it was functional, it couldn't be junk. The concept of junk DNA was declared dead far and wide, all based on a set of findings that were perfectly consistent with it.

Four years later, ENCODE apparently decided to kill it again.

... ENCODE remains a phenomenally successful effort, one that will continue to pay dividends by accelerating basic science research for decades to come. And the issue of what constitutes junk DNA is likely to remain controversial—I expect we'll continue to find more individual pieces of it that perform useful functions, but the majority will remain evolutionary baggage that doesn't do enough harm for us to eliminate it. Since neither issue is likely to go away, it would probably be worth our time to consider how we might prevent a mess like this from happening again.

The ENCODE team itself bears a particular responsibility here. The scientists themselves should have known what the most critical part of the story was—the definition of "functional" and all the nuance and caveats involved in that—and made sure the press officers understood it. Those press officers knew they would play a key role in shaping the resulting coverage, and should have made sure they got this right. The team has now failed to do this twice.

Here, we detail the many logical and methodological transgressions involved in assigning functionality to almost every nucleotide in the human genome. The ENCODE results were predicted by one of its authors to necessitate the rewriting of textbooks. We agree, many textbooks dealing with marketing, mass-media hype, and public relations may well have to be rewritten.

... So, what have we learned from the efforts of 442 researchers consuming 288 million dollars? According to Eric Lander, a Human Genome Project luminary, ENCODE is the “Google Maps of the human genome” (Kolata 2012). We beg to differ, ENCODE is considerably worse than even Apple Maps. Evolutionary conservation may be frustratingly silent on the nature of the functions it highlights, but progress in understanding the functional significance of DNA sequences can only be achieved by not ignoring evolutionary principles.

High-throughput genomics and the centralization of science funding have enabled Big Science to generate “high-impact false positives” by the truckload (The PLoS Medicine Editors 2005; Platt et al. 2010; Anonymous 2012a, 2012b; MacArthur 2012; Moyer 2012). Those involved in Big Science will do well to remember the depressingly true popular maxim: “If it is too good to be true, it is too good to be true.”

We conclude that the ENCODE Consortium has, so far, failed to provide a compelling reason to abandon the prevailing understanding among evolutionary biologists according to which most of the human genome is devoid of function. The ENCODE results were predicted by one of its lead authors to necessitate the rewriting of textbooks (Pennisi 2012a, 2012b). We agree, many textbooks dealing with marketing, mass-media hype, and public relations may well have to be rewritten.

Kellis says that ENCODE isn't backing away from anything. The 80% claim, he says, was misunderstood and misreported. Roughly that proportion of the genome might be biochemically active, he explains, but some of that activity is undoubtedly meaningless, leaving unanswered the question of how much of it is really 'functional'. Kellis also argues that focusing on the portion of the genome that is shaped by natural selection can be misleading. For example, he says, genes that cause Alzheimer's disease or other late-in-life disorders may be largely immune to evolutionary pressure, but they are still definitely functional.

In the social-media age, scientific disagreements can quickly become public — and vitriolic. A report from the ENCODE (Encyclopedia of DNA Elements) Project consortium proposes a framework for quantifying the functional parts of the human genome. It follows a controversial 2012 Nature paper by the same group that concluded that 80% of the genome is biochemically functional (Nature 489, 57–74; 2012). Dan Graur, who studies molecular evolutionary bioinformatics at the University of Houston in Texas and is a vocal ENCODE critic, weighed in on this latest report. ENCODE's “stupid claims” from 2012 have finally come to back to “bite them in the proverbial junk”, Graur wrote on his blog. The targets noticed. “Some people seek attention through hyperbole and mockery,” says the report's first author Manolis Kellis, a computer scientist at the Massachusetts Institute of Technology in Cambridge. “We should stay focused on the issues.”

This is just the latest skirmish in an ongoing battle. In a scathing 2013 article, Graur and co-authors argued that the ENCODE researchers had essentially ignored evolutionary evidence that suggests that only 2–15% of the genome was under pressure from natural selection (D. Graur et al. Genome Biol. Evol. 5, 578–590; 2013).