He is also the senior author on a paper I blogged about last week—the one where some journalists made a big deal about junk DNA when there was nothing in the paper about junk DNA [How to Turn a Simple Paper into a Scientific Breakthrough: Mention Junk DNA].
Dan Graur contacted him by email to see if he had any comment about this misrepresentation of his published work and he defended the journalist. Here's the email response from Axel Visel to Dan Gaur.
I’m not sure about the sources of individual journalists (although I did speak to some of them), but generally speaking I think it’s a valid strategy for general media to use a provocative and widely recognized term in a title to capture the attention of their audience, as long as they set the record straight in the text.That reply is astonishing on many levels. First, scientists should not condone the use of provocative titles that have to be corrected in the text. Second, no knowledgeable scientist ever said that all noncoding DNA was junk. Third, it is not true that the majority of press reports conveyed the point of the paper. The point of the paper was that some more mouse enhancers have been putatively identified. They account for about 0.001% of the genome. This is a miniscule percentage of the entire genome and a tiny percentage of the known amount of functional noncoding DNA.
When I talk to general audiences (or journalists) about my research, I generally explain that the function of most of the non-coding portion of the genome was initially unclear and many people thought of it as “junk DNA”, but that it has become clear by now that many parts of the non-coding genome are functional - as we know from the combined findings of comparative genomics, epigenomic studies, and functional studies (such as the mouse knockouts in our paper).
As far as I can tell, the majority of general news reports appropriately conveyed the point of this paper, i.e. that at least those non-coding sequences we looked at here are indeed not “junk”.
Theme Genomes & Junk DNADan Graur rightly complains about Axel Visel's improper use of the term "noncoding DNA" [Dear Card Carrying #ENCODE members: Please Remember That Junk DNA is Not a Synonym for Noncoding DNA] and I want to emphasize this point. It's about time we banned the use of "noncoding DNA" because it really doesn't serve any useful purpose. In most cases it's used as a strawman synonym for "junk DNA" or a synonym for DNA with no known function.
I've said it many times but it bears repeating. A small percentage (about 1.4%) of our genome encodes proteins. There are many other interesting regions in our genome including ...
- ribosomal RNA genes
- tRNA genes
- genes for small RNAs (e.g spliceosome RNAs, P1 RNA, 7SL RNA, linc RNA etc.)
- 5' and 3' UTRs in exons
- SARs (scaffold attachment regions)
- origins of DNA replication
- regulatory regions of DNA
- transposons (SINES, noncoding regions of LINES, LTRs)
- defective transposons
Given all this, under what circumstances does the term "noncoding DNA" mean anything significant? Here's an excerpt from Axel Visel's webpage. Does his use of "noncoding DNA" mean anything that's useful?
Research InterestsLook at that list up above. Does that look like non-annotated regions to you? Transposons and defective transposons alone account for more than 50% of the annotated genome. Introns account for 40% of the annotated genome—although this is probably an overestimate. Regulatory regions have been part of annotated human genome sequences for thirty years. The discovery of a few more transcription factor binding sites in remaining parts of the genome that were not previously annotated is not exactly breaking news.
The sequence of the human genome has been known for over a decade, but well-defined functional annotations exist mainly for the small portion of the genome that encodes proteins. In sharp contrast, the 98% non-coding regions of the genome remain poorly annotated. Examples from gene-centric studies have provided strong evidence that the non-coding portion of the genome harbors distant-acting transcriptional enhancers and have shown that these regulatory sequences are critical for normal embryonic development.