Reduction and Elimination in Philosophy and the Sciences

Are Lamarckian Explanations Fully Reducible to Darwinian ones?
The Case of “Directed Mutation” in Bacteria
Davide Vecchi, Vienna, Austria
One of the striking features of the debate on directed
mutation is that it was largely based on semantical
quibbles generated by the idiosyncrasies on the
interpretation of the crucial terms “random”, “directed”,
“Darwinian” and “Lamarckian”. I am not claiming that this is
an atypical situation in science. On the contrary, it is quite
ubiquitous. But, of course, only part of the controversy
rotated around semantics. The rest was about substantive
scientific and philosophical issues.
The official Neo-Darwinian line on bacterial mutation
crystallised in the 40s and 50s thanks to Luria’s and
Delbrück’s and then the Lederberg’s “crucial” experiments.
For those who thought that Duhem had established once
and for all that there cannot be crucial experiments, it is
sufficient to take a look at D. Futuyma’s “Evolution”
textbook, where such experiments are presented as the
ultimate and definitive demonstration that genuine directed
mutation in bacteria cannot happen. According to the
“received view” bacterial mutation is not a Lamarckian
response to need; mutants arise at a constant rate during
growth, independently of any selection pressure and
environmental influence.
The Modern-Synthesis had hardened too much by
discounting possible Lamarckian phenomena and
processes in one stroke, by trivialising the Lamarckian
position and by simplifying too much the Darwinian picture
of bacterial evolution. A classic Kuhnian paradigm was
build.
The odd thing is that Delbrück himself readily
admitted in 1946 that the fluctuation test had limited scope,
as it could not rule out the existence of adaptive
mechanisms of mutation, the reason being that the
selective pressure applied to bacteria in the test was too
strong. Experimental anomalies contradicting the received
view accumulated in the 40 years or so that climaxed with
Cairns et al. 1988 paper. But such anomalies were simply
written off as mere noise by referring to the crucial
experiments. The story is quite interesting and also quite
typical of science. History was edited and falsity
transcribed in the biology textbooks by omitting crucial
details, by referring to supposedly crucial experiments of
limited scope, by using obscure terminology. But
eventually the bubble burst. The Lamarckian idea of
directed mutation was suddenly back from limbo, and
thanks to just one authoritative paper published in an
authoritative journal.
The “received view” on bacterial mutation was
based on a series of tenets that started to be assessed
independently. Some tenets can be deemed central to the
Neo-Darwinian view, while others are possibly more
peripheral. The central tenet is that mutations are not more
likely to be beneficial than not. Lenski and Mittler (1993)
provide possibly the clearest definition:
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We define as directed a mutation that occurs at a
higher rate specifically when (and even because) it
is advantageous to the organism, whereas comparable
increases in rate do not occur either (i) in the
same environment for similar mutations that are not
advantageous or (ii) for the same mutation in similar
environments where it is not advantageous.
Other tenets of the Neo-Darwinian view included the auxiliary
hypotheses that mutations are never environmentally
induced, that mutations are solely due to replication errors,
that mutation rates are constant, that mutations do not
target specific parts of the genome, and that mutations are
due to the breakdown of the cellular machinery of DNA
repair.
Even though the partial “blindness” of bacterial
mutational response to need has been substantially
vindicated, all the other tenets of the Neo-Darwinian view
have been partly or totally rejected. What can safely be
said is that there has been a softening of the Neo-
Darwinian perspective in many respects (Brisson 2003).
The softening is so extensive that one can sensibly ask
whether to call the emerging view on adaptive
mutagenesis “Neo-Darwinian” instead of “Lamarckian”
makes sense at all (Jablonka and Lamb 2005).
One of the most intriguing explanatory models of
adaptive mutagenesis, generally considered to be
essentially correct (cf. e.g. Foster 2004), is the
hypermutable state hypothesis (HSH). The HSH was
originally proposed by Hall (1988) and provides an
explication of the puzzling fact that some process seems to
generate purely beneficial mutations in the genes under
selection that allow environmentally stressed cells in
stationary phase to resume growth. The main idea of the
HSH is that most bacteria under stress-induced conditions
are mutationally inert, but that an unspecified but relatively
small number of cells enters an hypermutable state. Those
bacteria that do not mutate appropriately die (are selected
against), so that their deleterious and neutral mutations
are wiped out and un-retrievable, while those striking a
“lucky jackpot” resume growth and reproduce, while the
beneficial mutations carried become heritable by escaping
the correction mechanisms (e.g. mismatch repair editing,
or MMR).
Focusing on HSH, we can now ask a number of
specific questions. Consider that the history of the
discovery of phenomena of apparently directed generation
of variation is always surrounded by a first attempt to
resurrect the ghost of Lamarck, followed by a call for
restraint and a process of “Darwinisation” of the
phenomenon. I will now assess whether such second level
reaction is justified in the case of HSH. Can we explain
HSH in purely Darwinian terms? The HSH surely provides
a selective explanation of the supposedly Lamarckian
phenomenon of “preferential mutation” first highlighted by
Cairns et al. But the HSH does not fully vindicate a Neo-
Darwinian perspective at all, given that most auxiliary
hypotheses surrounding the view have been rejected or
substantially revised. Clearly HSH does not rely on the
hypothesis of constant mutation rates (cells that enter the
hypermutable state can mutate at rates 800 times higher
than normal), nor on the hypothesis that mutations do not
happen in stationary phase (in fact, mutations accumulate
in stationary phase, that is, in that period of the bacterium
life cycle, somehow equivalent to development, when it
does not replicate), nor on the hypothesis that