The problem is, research keeps going on, and answers keep showing up.
"D R Lindberg (To Jim in Missouri): Here are a couple more of
those articles that you say do not exist..."
> Charles P: "I certify that this article exists."
> You might have noticed, Charles, that neither of the articles cited
by D R Lindberg actually explains how Darwinian evolution brought into
being the bacterial flagellum. Indeed, the first of the two articles
admits as much, saying that:
> "The bacterial flagellum has received attention as an exemplum of
biological complexity; however, how this complexity and diversification
have been achieved remains rather poorly understood. Although several
scenarios have been posited to explain how this organelle might have
been originated, the actual series of evolutionary events that have
given rise to the flagellum, as might be inferred from the
relationships of all genes that contribute to the formation and
expression of this organelle across taxa, has never been accomplished."
Still using the old creationist tricks, I see, copying from the problem
part of the article, rather than the results or observations, to pretend
that no one has any answers.
Look down a few paragraphs:
"Here, we take advantage of complete genome sequence data to trace the
history of each gene involved in the assembly and regulation of the
bacterial flagellum. Our results show that flagellum originated very
early, before the diversification of contemporary bacterial phyla, and
evolved in a stepwise fashion through a series of gene duplication,
loss and transfer events. In this article, we focus on the evolution of
the core set of flagellar genes that is uniformly present in all
flagellated bacteria. The later evolving and lineage-specific
components of the flagellar gene complexes remain to be addressed."
The remainder of the article is a detailed expansion of this.
> And it's hard to know what the second article says, as I couldn't
find anything more than the abstract, which spoke in glittering
generalities, for example:
> "The order and organization of flagellar genes have undergone
extensive shuffling and rearrangement among lineages, and based on the
phylogenetic distributions of flagellar gene complexes, the flagellar
gene operons existed as small, usually two-gene units in the ancestor of
Bacteria and have expanded through the recruitment of new genes and
fusion of gene units."
> Intoning such phrases as "extensive shuffling and rearrangement among
lineages" and "the recruitment of new genes and fusion of gene units"
is hardly enlightening if one wants to know how Darwinian evolution
brought the bacterial flagellum into being.
Imagine that! You might have to learn their language in order to
actually understand what they are saying!
Intoning phrases such as "fuselage," "stabilizers," "landing gear,"
"engine cowls, " "spoilers," and "flap track fairings" is hardly
enlightening if one wants to know how an aircraft is put together,
This comment leaves one wondering how you can be so sure that you know
exactly where their science is lacking when you aren't even interested
enough to learn a bit of the language.
Anyhow, for anyone interested, here is part of the relevant section of
To understand how the genes specifying the bacterial flagellar system
evolved and diversified, we previously analyzed the origins of the set
of structural genes that are ancestral to all flagellated bacteria (17
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-17> ). In this study, we focused
on the origins of the secondary flagellar systems, which are present in
several proteobacteria, as well as the formation and evolution of
flagellar gene operons. Despite the early origin and stable inheritance
of the core structural genes, flagellar gene complexes are subject to
extensive changes, promoted by both the gain and loss of individual
genes (and even entire flagellar systems), and the formation and
disruption of operon structures.
The primary and secondary flagellar systems within a cell can specify
different functions (swimming or swarming), display different expression
patterns (constitutional or conditional), and employ different motive
forces (sodium or proton) (3
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-3> , 14
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-14> ). But because the two
systems, when present in the same genome, have very similar sets of
structural genes, these functional differences are largely due to
changes in the regulation cascade of the systems (24
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-24> , 33
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-33> ). Our analyses revealed
that secondary systems originated twice from the duplication or
horizontal transfer of primary systems. The secondary systems present in
both the Beta- and Gammaproteobacteria appear to have originated from a
duplication of the entire flagellar gene complex in the nonenteric
gammaproteobacterial lineage, which was then transferred independently
to the Betaproteobacteria and to an ancestral lineage of enteric
bacteria. Whereas both the primary and secondary systems have been
sporadically maintained, this scenario suggests that the secondary
system was subsequently lost from most genomes.
Consistent with this history of an ancient duplication and horizontal
transfer and subsequent deletion of a flagellar gene complex are the
findings that there are two flagellar systems and that remnants of the
secondary system occur sporadically among strains of E. coli (33
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-33> ). This secondary system is
present in E. coli 042 but was deleted from E. coli K-12, which still
contains remnant copies of two boundary genes (fhiA and mbhB, which are
homologs of flhA and motB, respectively). Because the secondary system
of E. coli 042 clusters with those of the four Beta- and
Gammaproteobacteria that we investigated (see Fig. S2 in the
supplemental material) and is closest to that of Y. pseudotuberculosis,
the secondary system in E. coli seems to have originated early in the
enteric bacterial lineage and not by recent transfer events.
The primary flagellar system in B. japonicum is closely related to the
only flagellar system in Alphaproteobacteria group I, whereas its
secondary system is closely related to the flagellar system in
Alphaproteobacteria group II (Fig. 1
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#F1> ). Therefore, it is unlikely
that this secondary system originated from an intragenomic duplication.
The most likely scenario is that this secondary system resulted from
horizontal transfer from a species closely related to
Alphaproteobacteria group II, but it is possible that the ancestor of
all Alphaproteobacteria possessed a second flagellar system, like that
in B. japonicum, and that one system was subsequently lost in both
Alphaproteobacteria groups I and II. A recent study has shown that the
alphaproteobacterium Rhodobacter sphaeroides contains two flagellar
systems, which encode polar flagella (30
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-30> ). One of these systems is
ancestral to Alphaproteobacteria, whereas the other is homologous to the
primary system in Z. mobilis, which was shown previously to have
originated by lateral gene transfer from Gammaproteobacteria (17
Our results for the formation and disruption of flagellar operons are
consistent with those of whole-genome analyses (13
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-13> ), which showed that operons
and gene order are typically conserved among closely related organisms
and that the destruction of operons may be selectively neutral. Our
analyses revealed that the flagellar operons are most extensively
disrupted in Epsilon- and Alphaproteobacteria, but whether other operons
also show the most extensive disruption in these two lineages remains to
be investigated. Because the flagellar gene operons of E. coli have been
subject to extensive experimental verification, we performed this
analysis using the operon structures of E. coli as our frame of
reference. It is possible that in some organisms, the flagellar genes
form operons containing member genes different from those in E. coli
K-12 and that these flagellar operons are not as disassociated as they
appear. However, based on their phylogenetic relationships, E. coli and
the Gammaproteobacteria in general are the most recently derived
organisms and also have the most clustered flagellar gene complexes,
indicating a broad evolutionary trend toward increasing cluster size
through both the inclusion of new genes and the fusion of existing
Different models have been proposed to explain the driving forces and
mechanisms in the formation and maintenance of bacterial operons. Under
the "selfish operons" hypothesis (16
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-16> ), lateral gene transfer
promotes the formation of operons because clustered genes have a better
chance of being transferred together and functional in the new host.
Whereas there are certainly instances of lateral gene transfer of
flagellar systems, coamplification may also be a mechanism underlying
the creation of flagellar operons. According to this model, genes in
proximity to one another are more likely to be coamplified, and thus,
the tandem duplication of small gene clusters can create new gene
junctions and generate new regulatory schemes (32
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-32> ). As suggested by a recent
study, coregulation seems to be a major driving force in operon
formation and maintenance (31
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-31> ), in that the products of
adjacent flagellar genes often form protein complexes (e.g., flgBC,
flgKL, flhBA, fliMN, and fliPQR), and operons serve to regulate both the
timing and the amounts of the interacting proteins.
Our data also confirm the rapid changes in flagellar gene regulators
reported in previous studies (24
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-24> , 36
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-36> ). Although details of
flagellar gene regulation have not been fully elucidated, it is clear
that species have widely different regulation networks, as shown by the
variation in the numbers and types of the regulators harbored by
different genomes. For example, the master regulators, which control the
flagellar gene regulation cascade, differ among groups of bacteria. The
master regulators in E. coli, FlhC and FlhD, are present only in enteric
bacteria, and the master regulator FlaK in V. parahaemolyticus appears
to be limited to nonenteric Gammaproteobacteria. Such diversity is
consistent with the general pattern uncovered by genome-wide analyses:
transcription factors evolve much more quickly than their target genes,
and bacterial regulatory networks are extremely flexible (18
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-18> , 21
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-21> ). Many of the genes with
auxiliary roles in flagellar systems, such as the chaperone genes fliJ,
fliS, flgN, and flgJ, have sporadic distributions or are lineage
specific, although other genes, such as the chemotaxis genes, are shared
by Bacteria and Archaea (11
5a8b0fa-a5d9-4f26-88b0-2f347cbaee31#ref-11> ). Taken together, bacterial
flagellar systems have been formed with genes having very different
histories and have originated and evolved under a combination of
different evolutionary forces, including duplication, gene loss, and
lateral gene transfer.
> I'm grateful for the efforts D R has made to validate the claim made
by design theorists (and me) that the Darwinian literature provides no
detailed, testable accounts of how Darwinian evolution brought the
flagellum into being.
Again the galloping goalposts. Behe originally only required evidence
that this was possible. You seem to be demanding a billion or so years
old video recording showing it actually happening - one that anyone can
go back and make for themselves.
Interesting the picture your comments give of what you consider a fair
race. The obstacles you require from the Discovery Institute before
accepting their account are about three mm high (as seen in how quick
you are to offer excuses for Berlinski), whereas you demand that science
leap hurdles more than 16 miles high!
I understand that after the SARS outbreak a few years back, when
scientists went look for the source, they found a virus in a certain
species of Chinese bat that differed from the human SARS virus by a few
mutations. So the explanation considered most likely is that the bat
virus managed to make these few mutations that enabled it to infect
Similarly, the Type III Secretory System found in some bacteria is only
a few mutations away from the bacteria flagellum that Behe crows about.
So there appears to be no reason to suppose that it could not have made
a similar jump. As you can see from the illustrations here, the
similarities are pretty obvious:
The articles mentioned above are two of many that examine the various
mechanisms involved in greater detail.
When investigating something that took place in the past, it seems
logical to most people to work using the assumption that natural
processes worked the same way in the past as they do now so (unless we
have evidence to the contrary. While such explanations (probable
scenarios) may not be all that we would like, they seem satisfactory to
most, given the limitations of human powers.
But if one is determined not to accept anything, no possible evidence is
Which is what I originally saw as the problem with saying that Behe's
flagellum was falsifiable.
Nothing can be falsifiable to those who refuse to accept any conceivably
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