For the non-biologists, a bacterial transposon is a region of DNA, usually five to twenty thousand bases (‘letters of DNA’) long that can move around (transposition). Many bacterial plasmids–mini-chromosomes that can move from bacterium to bacterium–carry transposons. In bacterial, transposons usually carry other genes along with those responsible for the jumping around, such as antibiotic resistance. So tracking transposons is an important part of understanding how antibiotic resistance evolves.
Which brings us to Our Looming Bacterial Transposon Crisis–and it has to do with the phrase “tracking transposons.” Different transposons have been assigned numbers, Tn1, Tn2, and so on (most microbiologists aren’t really very creative in the naming of things). Decades ago, microbiologists began a transposon registry so all of the different transposons could be kept straight. The founders of the registry handed out numbers to different biologists (e.g., Dr. Joe Schmoe would have been assigned Tn501-Tn550).
That doesn’t mean the numbers were actually used, however, so it’s unclear if we’re missing assigned transposons. Unfortunately, a fair number of the original ‘title holders’ are… dead. That makes it somewhat difficult to determine if a number was used. We know that Tn1-Tn4865 were allotted, but we have no idea, other than scanning old literature, if they were used (Tn5000 and on are pretty traceable, and Tn6000 and on are assigned by a database). But it gets worse (you didn’t think I was going to write better, did you?).
Many of the older transposons were characterized before DNA sequencing was cheap and (relatively) easy. So often, a transposon had smaller pieces sequenced, such as the antibiotic resistance gene and the ends of the transposon. The rest of the transposon might have been characterized by DNA hybridization and restriction mapping. If you don’t know what those are (and you’ve still stuck with this post this far), don’t worry: what that means is we don’t have the full DNA sequence for the transposon. In some cases, these transposons occurred in ‘important’ bacterial isolates that have since had their genomes sequenced, and we can reconstruct what the transposon sequence should be. But in too many cases, the strain is poorly described, if it even exists anymore, and there is no genome sequence. In other words, there are transposons in the literature that are ‘dead’–we can’t reconstruct their sequences, even though a lab described them in one or more papers.
All that effort, and it’s utterly useless in the genomics era. It might not be a Looming Crisis, but it’s a problem.