Knots are part of our everyday life. In some cases they can be very useful as in climbing or sailing whereas in some others they can be a nuisance, as we experience each time we try to disentangle extension cables or garden pipes.
Like extension cables, long biological filaments such as DNA can be highly self-entangled and the presence of knots may have detrimental effects in several cellular process such as transcription, replication and recombination. Fortunately there exist enzymes such as topo-isomerases which control the topological state of the DNA by cutting, disentangling and resealing DNA strands continuously.
On the other hand, within very small viruses, where there is space only for the DNA itself, knots inevitably accumulate because of the tight confinement. Yet their presence does not prevent the virus to infect the hosting cell by translocating its DNA through a small hole. So how could these viruses have highly knotted DNA and still be infective?
To gain insight into this puzzling problem we analysed the data on viral DNA packaging and knotting offered by beautiful experiments on bacteriophages. In particular, starting from the abundance of certain knot types (torus knots) and the shortage of others (twist knots) we established that the aligning tendency of contacting DNA strands plays a major role in leading the spatial organisation and knotting of the packaged DNA. By explicitly modelling this aligning interaction we found that it favours ordered DNA spools which, during the ejection process, experience a lower effective topological friction than more disordered entangled structures. We also find that torus knots exit the bacteriophage easily; while complex knots or twist knots slow down and may stall ejection.
The Colloquium will be followed by coffee and biscuits from 2:00pm.