The points in purple are objections raised by Ambur et al. to the hypothesis that the main function of DNA uptake by competent bacteria is acquisition of DNA as a nutrient:
These points are typical of those raised when the goal is to dismiss the nutrient hypothesis rather than to carefully consider all the issues.
(i) As yet, there is no clear evidence that the integration of nucleotides
taken up by transformation become routed into DNA metabolism.
Yes.
Competence has mainly been studied in mucosal commensals, where investigations
of metabolism are difficult. In these
organisms absence of evidence is not evidence of absence.
(ii) The presence of exogenous DNA does not appear to induce
competence in any transformable species.
Yes,
but I don’t see why this is more relevant for the nutrient hypothesis than for
other hypotheses. (Also, Vibrio does use
chitin as a signal for competence; its presence indicates biofilms and abundant
DNA.)
(iii) Competence in streptococci, like S. pneumoniae, is induced
for only a short time period during exponential growth when other resources are
highly abundant.
Because
laboratory growth conditions for human commensals and pathogens are so
different from natural growth conditions, lab cultures are very poor guides to
what matters in the real world. That’s
why our work focused on understanding the regulatory machinery.
(iv) Transported DNA is heavily protected against nuclease
digestion within the cell, potentially enabling transported fragments to remain
intact as a substrate for recombination.
And
yet most competent bacteria take up all DNAs they encounter, and DNA that cannot
be recombined is efficiently degraded. The
proteins that protect the DNA are also common in non-competent species and so
must function outside of transformation.
(v) The hypothesis does not explain why several competent species
only take up DNA from close relatives due to conserved DNA uptake sequences (USS
and DUS) despite the fact that non-homologous DNA could be used as a source of nucleotides
for direct use or degradation.
On
the flip side, almost all competent bacteria take up DNA indiscriminately, so DNA’s
benefit can’t depend on its information content. For these exceptions, we have hypothesized that sequence-dependent
uptake constraints exist in these species, and have shown that these create molecular drive that causes uptake sequences to
accumulate in genomes at frequencies and distributions corresponding to those seen in real genomes with DUS and USS.