I recently published an article on the marvelous design and engineering which undergirds the bacterial chemotaxis system. Since then, a notorious atheist who posts regular videos on YouTube under the alias “C0nc0rdance“, as well as “agentorange20” (under the latter, he identifies himself as Zachary Moore), has posted a rebuttal. This is a brief response to that rebuttal.
The extent to which two-component regulatory systems, or the chemotaxis system in particular, are irreducibly complex lay beyond the remit of my previous article, the purpose of which was to highlight the clear engineering analogues. With many of these signalling systems, there is an element of redundancy, with feedback and overlapping systems so as to make things stable and robust to error. As a result, there are often multiple versions that can still get the job done. Such systems are well designed — and detectably so — but there is no requisite for them to be irreducibly complex. However, it is my opinion that some subcomponents of the chemotaxis system may possibly be legitimately described as irreducibly complex (more on this to follow).
Such associated design and engineering principles associated with this system are obvious to those who are not pushing a materialist agenda. For example, one paper published in May of this year stated that,
Describing this pathway mathematically as a dynamical system can be facilitated by using tools from control theory. For example, it has been shown that the adaptation mechanism in the E. coli model is a particular example of integral control, a feedback system design principle used in control engineering to ensure the elimination of offset errors between a system’s desired and actual signals, irrespective of the levels of other signals.
One can discuss the clear design hallmarks pertinent to the system without even talking about the problems with the evolutionary account. The paper continues,
One of the different pathway configurations that is possible in this system has similarities to a feedback architecture commonly found in engineering control systems termed cascade control, which is usually employed when the process to be controlled can be split into a slow ‘primary’ sub-process ( in Figure 1) and a faster, secondary sub-process ( in Figure 1). […] In fact, cascade control is employed as a design principle in several engineering systems such as aircraft pitch control and industrial heat exchangers.
Moore raises four complaints with regards this system and irreducible complexity. Two of those complaints are relevant only to common descent (and not the grander thesis of neo-Darwinism that unguided mutation/selection are adequate to account for the system). Since ID is consistent with both common and uncommon descent, I will address the two points which are relevant to the adequacy of respective explanations.
Moore’s first complaint is that not all bacteria have the full pathway which I described. Before getting into the specifics, it is worth noting that irreducible complexity, as defined by Michael Behe in Darwin’s Black Box, does not entail that no simpler systems which perform the same job exist. In fact, Behe made this quite explicit. On page 43, Behe wrote,
To feel the full force of the conclusion that a system is irreducible complex and therefore has no functional precursors, we need to distinguish between a physical precursor and a conceptual precursor. The trap described above is not the only system that can immobilize a mouse. On other occasions my family has used a glue trap. In theory, at least, one can use a box propped open with a stick that could be tripped. Or one can simply shoot the mouse with a BB gun. These are not physical precursors to the standard mousetrap, however, since they cannot be transformed, step by Darwinian step, into a trap with a base, hammer, spring, catch and holding bar.
Similarly, it makes no sense to say that an automobile does not require an engine because one can use a bicycle! In like-manner, there are simpler ways to construct a flagellum. But that does not entail that a given flagellar system is not irreducibly complex. In the specific case which concerns us here, there may be alternative chemotaxis systems — but that does not nullify the irreducible complexity for the specific example that I described.
Another misconception which warrants clarification is the view that, for a system to be irreducibly complex, all of its subcomponents must be indispensable for the system’s overall functioning. But this is not the case. Contrary to this common misconception, irreducible complexity only requires that a subset of a given system’s components be indispensible.
Now, as Moore correctly notes, there is a significant amount of variation on chemotaxis systems. The pathway is best understood in the Gammaproteobacteria: a class of bacteria which includes E. Coli (the most extensively studied example) and Salmonella enterica. It is this class to which my previous discussion of the chemotaxis system pertained. A substantially less amount of data is available for other species of bacteria. Although individual genes bear homology to their Gammaproteobacteria counterparts, the pathways are somewhat mechanistically different. Furthermore, while general features of excitation remain conserved among bacteria and archaea, many of the more specific features are fairly diverse. One considerably more complex system than that of E. Coli is that of Bacillus subtilis (which you can read about here or here).
In E. coli, as discussed previously, chemoeffectors bind to the receptors and cause a conformational change in the methyl accepting chemotaxis proteins (MCPs). This conformational change is detected by CheA and CheW. This subsequently causes a change in the rate of autophosphorylation of CheA. CheA-P transfers phosphate groups to CheB and CheY. When CheY-P interacts with the switch, tumbling is induced. CheB-P acts as a methylesterase to remove methyl groups from the MCPs genearating methanol. CheR acts as a methyltransferase and methylates the MCPs. CheB thus brings about adaptation to the simuli by modifying the degree of methylation of the MCPs such that the rate of CheA autophosphorylation returns to the level it was at prior to the stimulus. CheZ acts to destroy the chemotactic signal by dephosphorylating CheY. In B. subtilis, the core control strategy for signal processing is very similar. However, B. subtilis possesses two additional feedback loops which provide an added layer of regulation. Moreover, although the proteins involved in both organisms are the same, the network structures are somewhat different.
So, in what ways are the pathways different between E. coli and B. subtilis? Rao et al. (2004) illustrate this with the aid of the following diagram:
The figure legend reports,
(A) E. coli. (B) B. subtilis. Both organisms respond to extracellular signals by regulating the activity of the CheA histidine kinase. CheA is coupled to transmembrane receptors (MCP) by an adaptor protein CheW. Chemoattractants, by binding the receptor, inhibit CheA in E. coli (red line) (Borkovich et al. 1989) and stimulate CheA in B. subtilis (green line) (Garrity and Ordal 1997). CheA phosphorylates CheY. Phosphorylated CheY binds to the flagellar motor and increases the frequency of tumbles in E. coli (Cluzel et al. 2000) and runs in B. subtilis (Bischoff et al. 1993). Phosphorylated CheY is also predicted to inhibit the receptor complex in B. subtilis (dashed line). Both organisms tune the sensitivity of CheA to ligands by reversibly methylating the receptors using the CheR methytransferase and CheB methylesterase (Zimmer et al. 2000; Sourjik and Berg 2002b). Phosphorylation of CheB by CheA increases its methylesterase activity nearly 100-fold (Anand and Stock 2002). CheA activity is proportional to the degree of receptor methylation in E. coli. In B. subtilis, CheA activity depends on which residue is methylated, akin to a binary switch. E. coli possesses a phosphatase, CheZ, not present in B. subtilis, that enhances the rate of CheY dephosphorylation. B. subtilis possesses three chemotaxis proteins not found in E. coli: CheC, CheD, and CheV. CheC is a negative regulator of receptor methylation and homologous to the CheY-binding domain (P2) in CheA (Rosario et al. 1995; Rosario and Ordal 1996). CheD is a positive regulator of receptor methylation and also deamidates specific residues on the receptor (Kristich and Ordal 2002). CheV is a CheW-response regulator fusion. CheV is functionally redundant to CheW and is predicted to negatively regulate receptor activity (dashed line) (Rosario et al. 1994; Karatan et al. 2001).
So, yes, there are alternative ways in which different bacteria undergo chemotaxis, even with the same or similar components (for further information on the various chemotaxis systems, I refer readers to this paper). But having an alternative — even a simpler — means to accomplish a goal does not entail that you have a possible physical precursor which can be transformed step-by-Darwinian-step into the particular system which I described. The key defining characteristic of an irreducibly complex system is that multiple, co-ordinated and non-adaptive changes are required to attain novel utility. It is in achieving this end that the Darwinian mechanism is notoriously hopeless. As Michael Behe himself explains in response to John McDonald on the mousetrap
The second mousetrap (above) has a spring and a platform. One of the extended arms stands under tension at the very edge of the platform. The idea is that if a mouse in the vicinity jiggles the trap, the end of the arm slips over the edge and comes rushing down, and may pin the mouse’s paw or tail against the platform. Now, the first thing to notice is that the arms of the spring are in a different relationship to each other than in the first trap. To get to the configuration of the spring in the second trap from the configuration in the first, it seems to me one would have to proceed through the following steps: (1) twist the arm that has one bend through about 90° so that the end segment is perpendicular to the axis of the spring and points toward the platform; (2) twist the other arm through about 180° so the first segment is pointing opposite to where it originally pointed (the exact value of the rotations depend on the lengths of the arms); (3) shorten one arm so that its length is less than the distance from the top of the platform to the floor (so that the end doesn’t first hit the floor before pinning the mouse). While the arms were being rotated and adjusted, the original one-piece trap would have lost function, and the second trap would not yet be working.
Moore also cites a 2009 paper by Schlesner et al. which concludes that “in the archael domain, previously unrecognized archaea-specific Che proteins are essential for relaying taxis signaling in the flagellar apparatus.” They also report,
Using protein-protein interaction analysis, we have identified three proteins in Halobacterium salinarum that interact with the chemotaxis (Che) proteins CheY, CheD, and CheC2, as well as the flagella accessory (Fla) proteins FlaCE and FlaD. Two of the proteins belong to the protein family DUF439, the third is a HEAT_PBS family protein. In-frame deletion strains for all three proteins were generated and analyzed as follows: a) photophobic responses were measured by a computer-based cell tracking system b) flagellar rotational bias was determined by dark-field microscopy, and c) chemotactic behavior was analyzed by a swarm plate assay. Strains deleted for the HEAT_PBS protein or one of the DUF439 proteins proved unable to switch the direction of flagellar rotation. In these mutants, flagella rotate only clockwise, resulting in exclusively forward swimming cells that are unable to respond to tactic signals. Deletion of the second DUF439 protein had only minimal effects. HEAT_PBS proteins could be identified in the chemotaxis gene regions of all motile haloarchaea sequenced so far, but not in those of other archaeal species. Genes coding for DUF439 proteins, however, were found to be integral parts of chemotaxis gene regions across the archaeal domain, and they were not detected in other genomic context.
So certain previously unrecognized Che proteins (which are specific to the archea domain) are essential for relaying chemotaxis signalling in archea. But the relevance of this to the present discussion is not entirely clear.
Moore also asserts that removing a single component rarely disrupts function. Contrary to this assertion, however, genetic knockout experiments reveal that knocking out single genes usually does disrupt function. As Rao et al. (2004) report,
E. coli and B. subtilis bias their motion towards favorable conditions with nearly identical behavior by adjusting the frequency of straight runs and reorienting tumbles. Both pathways (summarized in Figure 1 and Table 1) share five orthologous proteins with apparently identical biochemistry. How these individual orthologs contribute to the overall function, however, is different, as illustrated when synonymous orthologs are deleted in each organism. Deletion of the CheY response regulator causes E. coli to run exclusively and B. subtilis to tumble exclusively (Bischoff et al. 1993). When the CheR methyltransferase is deleted in E. coli, the cells are incapable of tumbles and only run. Likewise, when the CheB methylesterase is deleted, E. coli cells are incapable of runs and only tumble. In B. subtilis, cells still run and tumble when either CheB or CheR is deleted, though they no longer precisely adapt (Kirsch et al. 1993a, 1993b). Remarkably, both genes complement in the heterologous host. Deletion of the CheW adaptor protein in E. coli results in a run-only phenotype, whereas there is no change in phenotype for the synonymous deletion in B. subtilis. When the genes involved in regulating methylation are deleted (cheBR in E. coli and cheBCDR in B. subtilis), E. coli does not adapt (Segall et al. 1986), whereas B. subtilis either oscillates or partially adapts when exposed to attractants (Kirby et al. 1999). These differences demonstrate that the pathways are different even though they involve homologous proteins.
It seems that there are multiple systems, which could be argued to be irreducibly complex, in operation here. The CheY response regulator, for example, is an indispensable component, as illustrated in genetic knockout experiments where E. coli is seen to run exclusively and B. subtilis to tumble exclusively. Similar results are found when one knocks out the CheR methyltransferase in either E. coli or B. subtilis. CheW is indispensable to the system in E. coli, but not in B. subtilis. When you delete the genes involved in regulating methylation, the adaptation system in E. coli is completely lost, though only partially lost in B. subtilis.
I recommend that Dr. Moore re-read Michael Behe’s two books, Darwin’s Black Box and The Edge of Evolution for the ID perspective on the properties of irreducibly complex systems. Furthermore, I would stress once again that the case for design is not merely contingent on a negative complaint about the inadequacy of Darwinism. Rather, it is the observation that there are real engineering hallmarks in biological systems which forcefully compel the conclusion of intelligent design. Increasingly, we are learning that system evolvability requires the occurrence of multiple co-ordinated changes to facilitate novel utility and functional innovation. That is perhaps the biggest and most fundamental hurdle that the neo-Darwinian synthesis must overcome.