Irreducible Complexity And The Bacterial Flagellum

Yes, I’ve been busy with Google Docs again. This time, a dismantling of the canards erected by Michael Behe with respect to “irreducible complexity” (including the fact that he didn’t even invent the concept) and the manner in which his attempt to erect the bacterial flagellum as the “poster child” for his bastardised version of “irreducible complexity” fell apart when actual biologists started work on the topic.

Enjoy the full account here:

And, once again, relevant peer reviewed scientific papers are cited for your pleasure. :slight_smile:


Some of the paper is above my level of education, but I assume that the irreducable complexity argument makes the assumption that a “partial flagellum” does nothing . . . so these partial components waste space and resources, while the actual fact is that the “partial flagella” was doing other tasks.

In humans, the inner ear functions to maintain balance and locomotion in addition to being essential for hearing, so the discreet components of the flagella were performing other (perhaps very different) functions in the bacterial cell before evolving together (more or less) into the flagellum motor.

Or this is how I understand the situation. I believe that I read somewhere that a partial flagella motor serves to push waste products out of the bacterial cell in Yersinia pestis . . . which causes bubonic plague, and that an understanding of the dynamics of this process explains why some antibiotics cure plague and why some do not.

Am I wrong, and/or do I misunderstand?

Basically, the hypothesis proposed by Pallen & Matzke, is that the bacterial flagellum arose stepwise from a simpler, antecedent system, possibly a system that had nothing to do with motility in the first place.

The papers in question destroy Behe’s assertions via a two pronged attack. First, by demonstrating that a flagellum can still function while missing several components. A particularly juicy find in one of those papers, centres upon the FliI and FliH proteins. Knock out the gene for FliI, and the whole process of flagellar biosynthesis crashes to a halt. But if you THEN knock out the gene for FliH, flagellar biosynthesis restarts, and the resulting flagellum works just as well as the original.

Next, the papers demonstrate that the genes for the various flagellar proteins aren’t some unique and ineffable construction arising from nowhere (oh, the irony of creationists asserting this …). Instead, the papers demonstrate that numerous homologies exist with other genes, indicating that the entire flagellar system arose via co-opting genes from another system, then adding some new features to result in a system with a new function.

And, lo and behold, it has been found subsequently, that a large part of the bacterial flagellum’s genes and proteins, were co-opted from a totally different system. Namely, the Type 3 Secretory System (T3SS). This is the system that allows some nasty pathogenic bacteria to inject lethal toxins into your cells.

The T3SS constructs a sort of hypodermic needle on the surface of pathogenic bacteria, and is found in such organisms as the bacteria responsible for typhoid fever, bubonic plague and cholera. Since the T3SS already contains features that would be readily reusable for the bacterial flagellum, biologists have been working on what evolutionary pathways would facilitate the relevant transition.

At some point, I’ll have to do a literature search, and see if that investigation has borne the requisite interesting fruit.


Thank you for clarifying.