Why do editors prune appealing afterthoughts and out of focus information to leave only the highly-scrutinized core of the research paper? ‘Appealing’ is the key word, that stuff has a life of its own and can literally beg you to add it to your papers. “Add me”, the factoid pleads, “and your work will make it into the news, will get discussed”.

Supplementary information may be capable of transmitting itself, regardless of its utility and accuracy. However, it may be under less selective pressure of reader scrutiny than the main findings. Should we worry about the quality of the information transmitted? Are there examples of runaway transmission?

I’ll try to provide an example, starting with a surprising re-uppopping of one of the earliest examples of a selfish element, supernumary or B-chromosomes, first reported by E.B. Wilson in Metapedius bugs in Science in 1907.

Selfish factoids can even infect Matt Ridley, probably the most accessible and informative science writer alive. I enjoyed reading his “Origins of Virtue– Human Instincts and the Evolution of Cooperation” but found this:

Chapter 1, footnote 29. “I am indebted to David Haig for the information that human beings have B chromosomes at the rate of 2-3 per cent of live births.”

Before rushing off to spread or apply this information and freak about its impact on genome-wide association studies for common diseases, I did a few reality checks.

Haig himself can’t resist transmitting B-chromosome factoids in a 1999 paper that is ostensibly about the origins of human autosomes. He performs some comparative paleocytology on our putative common ancestors, and (coolest of all) identifies them as the werepig and the weremouse.

“An extra ‘marker’ chromosome is detected in about one in 1000 prenatal diagnoses (refs), and a similar frequency is found among newborn infants (Gravholt and Friedrich 1995). "

That reference quotes the newborn frequency 0.7/1000.

So Ridley was exaggerating by a factor of forty-ish. But are there any risks associated with inheriting these chromosome “passengers”?

Lars Feuk and colleagues in Nature Reviews Genetics

“…structural abnormalities occur in about 1 out of 375 live births, with a quarter of these being unbalanced (Ref 37). The risk of congenital abnormalities that are associated with such variants is 6.7% for reciprocal translocations and inversions and 25.6% for all types of marker chromosome (Ref 12)”.

I’d be interested to know how this number was calculated, Ref 12 is Dorothy Warburton’s 1991 review in which she actually found abnormal phenotype associated with 10/68 nonsatellited marker chromosomes and 6/55 for satellited marker chromosomes identified de novo at prenatal diagnosis (10.9-14.7%).

M. D. Graf et al. also studied prenatally ascertained marker chromosomes and found “at least a 26% (28/108) risk for phenotypic abnormality for any non sex de novo supernumary marker chromosome”….“However, if high resolution ultrasound studies are normal, this risk reduces to 18%”.

Oliver Bartsch et al found 42 supernumary marker chromosomes of which 29 were de novo and 13 familial (10 of the resulting children with familial markers appeared unaffected) in 43,273 prenatal diagnoses. So Haig’s 1999 figure is still in the ball park. He concluded that human ‘markers’ are too infrequent to qualify as “fully fledged B chromosomes”.

They got wings tho’…..

Still, ‘marker chromosomes’ are a diagnosis by exclusion. The exclusion criteria vary, and ultimately, their detection is subject to the resolution limit of light microscopy. As Feuk and colleagues point out in their review, researchers can now detect variants well below that limit and all of us have several familial structural variants at birth. Some may indeed be very small marker chromosomes, but most are copy and structural variations in existing chromosomes. Given the caveats above, I won’t hazard a guess at the rate of de novo structural genome variants per live birth here, but will follow this area of the literature with great interest.

For more on human supernumaries, see Thomas Liehr’s site in Jena