At UcD, a poster named DLH, presents an ‘argument’ which is hard to distinguish from an April Fool’s joke (especially given its publication date).
Having apparently browsed the abstract of a paper, DLH concludes that:
Researchers have discovered two proteins essential for reproductive cells to latch onto each other and then to fuse. Changing at least one of these proteins appears to prevent species from interbreeding. This appears to open up a way to stop malaria. A new species would appear to require at least two changed genes, one for the protein change and the other for the matching protein docking change. What is the probability of these simultaneous changes occurring by random mutation & natural selection - versus - this being a key/lock design with complex specified information? Such simultaneous changes appear to be pushing Behe’s limits of Darwinism.
Let’s explore the obvious answer as well as the findings of the paper in more detail. Although I refuse by principle to link to UcD postings, this one has earned the highly coveted link from PandasThumb.
In a commentary Gene blocking could help quash malaria the paper is described as follows:
In a study to be published in the April 14 issue of the journal Genes and Development, and available now, researchers from UT Southwestern have found that sexual reproduction begins with two genetically different steps: First, two reproductive cells must latch onto each other with one protein, and secondly, they must fuse their membranes to form a single cell using a different protein.
So far so good. However, the same article explains:
Although the study involved only single-celled organisms, Dr. Snell said that the use of two different proteins in the two-step fertilization process may be the case in all species. The gene controlling whether egg and sperm can bind would be unique to each species, while the gene for the second step—fusing into a single cell—could be more universal. For example, the researchers found that HAP2, the gene that controlled whether cells fused, is also present in agriculturally important crops such as corn and wheat.
For the parasite that causes malaria, fusion is controlled by a gene not found in mammals, so blocking this step might prove effective in stanching the spread of the disease without harming humans, Snell said.
So what did the researchers do? Wonder about whether the system could have evolved or was ‘irreducibly complex’? No, they took a far more applied approach
The British researchers found that blocking HAP2 in Plasmodium cells stops the fusing step. When mutant Plasmodium organisms lacking HAP2 were injected into mice, mosquitoes that bit the mice did not become infected with Plasmodium and therefore could not spread the infection to other mice. This indicates that without HAP2, Plasmodium could not reproduce in a mosquito’s gut, a vital step in the cycle of infection.
From the abstract our friend at UcD proposes:
From Janjie’s et al. abstract:
“HAP2 is essential for membrane merger”
“yet Chlamydomonas minus and Plasmodium hap2 male gametes retain the ability, using other, species-limited proteins, to form tight prefusion membrane attachments with their respective gamete partners.”
From these facts and the ID paradigm, following are two proposed ID hypothesis to pursue (as posited by a design engineer):
ID hypothesis 1: The membrane merger including HAP2 essential for such “male”-”female” cell merger are irreducibly complex.
ID hypothesis 2: This “male”-”female”protein & docking site are part of a species specific reproduction - barrier system that is a species specific irreducibly complex system.
Submitted for further evidence to support and/or refine these hypotheses.
Let’s look at the abstract in question:
The cellular and molecular mechanisms that underlie species-specific membrane fusion between male and female gametes remain largely unknown. Here, by use of gene discovery methods in the green alga Chlamydomonas, gene disruption in the rodent malaria parasite Plasmodium berghei, and distinctive features of fertilization in both organisms, we report discovery of a mechanism that accounts for a conserved protein required for gamete fusion. A screen for fusion mutants in Chlamydomonas identified a homolog of HAP2, an Arabidopsis sterility gene. Moreover, HAP2 disruption in Plasmodium blocked fertilization and thereby mosquito transmission of malaria. HAP2 localizes at the fusion site of Chlamydomonas minus gametes, yet Chlamydomonas minus and Plasmodium hap2 male gametes retain the ability, using other, species-limited proteins, to form tight prefusion membrane attachments with their respective gamete partners. Membrane dye experiments show that HAP2 is essential for membrane merger. Thus, in two distantly related eukaryotes, species-limited proteins govern access to a conserved protein essential for membrane fusion
The overview article explains the relevance:
If the first step in reproduction, binding of egg and sperm, is controlled by a single gene per species, then the binding step would serve as a gatekeeper to prevent incompatible cells from getting close, Dr. Snell said. Evolutionarily, this scheme makes sense, he said, because it would take only a mutation in the single gene that controls egg-sperm binding to create a new species.
So what is the excitement all about?
It starts with the plant Arabidopsis and a gene called HAP2 which is a sterility gene. Remember that plants reproduce sexually and ‘sperm cells’ develop which are transported to the ‘egg’ where it fertilizes. HAP2 is a gene found in eukaryotes, including mammals, although as I understand it, the gene has evolved its function.
Based on the finding that a mutation in the HAP2 gene in a plant could induce infertility, the researchers set out to find a similar gene in Chlamydomonas, a unicellular green alga. To the surprise of the researchers, the gene identified showed it to encode a homolog of HAP2. The researchers decided to do additional searches for HAP2 and found them in a large variety of genomes
Our results showing that Chlamydomonas HAP2 mutants were fully motile and fully capable of flagellar adhesion demonstrated that the protein functions directly in the interactions between minus and plus gametes at a step in fertilization after initial gamete recognition. Moreover, we found that in addition to being present in the human malaria parasite P. falciparum (Mori et al. 2006), HAP2 was also present in the rodent malaria parasite P. berghei (Fig. 1G), in which sexual development is most amenable to experimentation. We therefore chose this species to ask if HAP2 functioned directly in gamete interactions in an organism that is only very distantly related to plants and green algae.
From an evolutionary perspective this is a very valid question. Since the malaria parasite reproduces both asexually and sexually, it provides for an interesting testing ground. The researchers replaced all the protein coding sequences of HAP2 and found that
Consistent with this sexual stage-specific transcription, examination of mice infected with hap2 clones showed that the parasites underwent normal asexual develop- ment in erythrocytes. Neither the rate of gametocyte formation nor the sex ratio was affected, and gametocytes were able to emerge from their host cells and differentiate into gametes when exposed to activating conditions (data not shown). To test for a role of HAP2 in fertilization, we first allowed female Anopheles mosquitoes to feed on mice infected with hap2 parasites and 10d later used phase contrast microscopy to examine the walls of midguts from the mosquitoes for the presence of oocysts. As shown in Figure 2E, whereas oocysts were plentiful in midguts of control mosquitoes allowed to feed on mice infected with wild-type P. berghei (Fig. 2E, left panel of photomicrograph and bar graph), we failed to detect oocysts in the mosquitoes that were fed on mice infected with hap2 parasites (Fig. 2E, right panel of photomicrograph and bar graph). Thus, HAP2 is required for transmission of P. berghei to mosquitoes.
Based on the conserved similarities between the plant, the alga and the plasmodium, the researchers proposed that
Divergence of the prefusion attachment genes could contribute to establishment of barriers to fertilization that might lead to speciation. The functional separation of membrane adhesion and subsequent events resulting in fusion between two different membranes may thus be the way in which many eukaryotes reconcile two opposite evolutionary needs, on the one hand, to ensure reproductive isolation through rapidly changing gamete recognition mechanisms, and, on the other hand, to preserve the machinery for the biophysically complex process of membrane fusion.
Two steps, one involving a well conserved HAP2 gene and the process of membrane fusion and one involving gamete recognition mechanisms which can evolve rapidly.
The work supported the ‘working model’ for gamete fusion, and provided the much needed genetic evidence.
Although the working model for gamete fusion has been that prefusion attachment and membrane fusion per se depend on separate sets of gene products, the model was not supported by genetic evidence because no mutants were available that allowed adhesion and blocked fusion in any organism. Our results assigning HAP2 function to a step in the gamete membrane fusion reaction after close (10-nm) prefusion attachment is the first gene disruption-based evidence that the gamete membrane fusion reaction depends on at least two separate sets of proteins that function at discrete steps in the reaction.
In other words, evolutionary theory provided for much of the foundations for the research and exciting new findings, showing that evolutionary science is scientifically fruitful as opposed to for instance Intelligent Design which remains scientifically vacuous. Science has expanded its understanding of the role of HAP2, provided a new approach to deliver a solution to the Malaria problem, provided genetic evidence for the hypothesis of gamete fusion and finally provided us with a much needed source of entertainment when the results were evaluated by ID proponents.
What is so fascinating is how amateurs at UcD base a ID hypothesis on their reading of an abstract. As an amateur myself, reading the articles referencing the research as well as the abstract caused me significant concern as to the accuracy of the comments by DLH and with the help of the actual article, it was relatively straightforward to determine that my causes for concern were well founded.
I hope to discuss the paper, which outlines how real science is done, in a future posting. For now I sign off