Monday 3 July 2023
Pre:Darwinian design.
The Design of the Seminal Fluid and Sperm Capacitation
In a previous article, I discussed the ways in which sperm cells exhibit irreducible complexity. Here, I will discuss the importance of the seminal fluid and how it contributes to the irreducibly complex core of components needed for successful reproduction. I will then consider the process of sperm capacitation, the mechanism that prepares the sperm cells for successful fusion with the egg.
The Seminal Fluid
As I mentioned in my previous article, between two hundred and five hundred million sperm, surrounded by seminal fluid, are released with each ejaculation. Such huge numbers are necessary in order to have a significant chance of fertilizing the egg, since many hazards confront the sperm cells as they swim through the uterus and uterine tubes. Following ejaculation, millions of the released sperm cells will either flow out of the vagina, or else die in its acidic environment. Sperm cells also need to pass through the cervix and opening into the uterus, which requires passage through the cervical mucus. Though the mucus is thinned to a waterier consistency during the fertile window, making it more hospitable to sperm, millions of sperm cells will nonetheless die attempting to make it through the mucus. Furthermore, the female reproductive tract has immune defenses that protect against pathogens. These defenses can also target and destroy foreign cells like sperm. Antibodies may recognize sperm as foreign invaders and lead to their inactivation or elimination. There are also tiny cilia in the fallopian tube that propel the egg towards the uterus. Some of the remaining sperm will become trapped in the cilia and die. Only a small handful of the original sperm cells will make it as far as the egg. Thus, it is necessary that hundreds of millions of sperm cells are released in order to have a reasonable chance of the egg cell being fertilized.
Seminal fluid also provides essential nutrients to support the survival and motility of the sperm. These include fructose — which serves as a source of energy for the sperm, fueling the mitochondrial production of ATP — as well as other sugars, amino acids, and enzymes. If the seminal fluid did not contain fructose, to power the mitochondria, this would have drastic implications for sperm cell motility and viability.
The seminal fluid is also alkaline. This is important because the vagina has an acidic pH, produced by the normal flora (bacterial populations) of the vagina. This environment would be unfavorable to sperm cells. But the alkalinity of the seminal fluid helps to neutralize the vagina’s acidic pH, assisting the survival of the sperm.
Following ejaculation, the seminal fluid initially coagulates to form a gel-like consistency. This coagulation helps to keep the semen in the vagina and cervix, preventing it from immediately leaking out and thereby greatly increasing the odds of a successful fertilization. This occurs upon exposure to the air or the alkaline environment of the female reproductive tract, activating clotting factors present in the seminal fluid, including tissue transglutaminase. The transglutaminase converts semenogelin (a major protein in seminal fluid secreted by the seminal vesicles) into a sticky protein called fibrin. Fibrin forms a network-like structure that entraps sperm and other components of the semen.
If the semen remained in this state, the sperm would be permanently immobile and unable to fertilize the egg. Over time, however, the coagulated semen liquefies due to enzymes present in the fluid that slowly break down the fibrin network, allowing the sperm to move more freely. Anamthathmakula and Winuthayanon note that “The liquefaction process is crucial for the sperm to gain their motility and successful transport to the fertilization site in Fallopian tubes (or oviducts in animals). Hyperviscous semen or failure in liquefaction is one of the causes of male infertility.”1 In fact, targeting these serine proteases has been suggested as a target for novel non-hormonal contraceptives.2From an evolutionary perspective, it is difficult to envision a scenario where semen coagulation evolved, without simultaneously having a mechanism for liquefaction. This is a prime example of a non-adaptive intermediate that is prohibitive to evolution by natural selection.
Sperm Capacitation
In order for a sperm cell to fertilize an egg, it has to undergo capacitation. This takes place in the female reproductive tract. The process of capacitation involves a series of biochemical and physiological changes that prepare the sperm for successful interaction with the egg and is crucial in order for the sperm cell to acquire the ability to fertilize.
When sperm are initially ejaculated, they possess certain molecules and proteins on their surface that inhibit their ability to fertilize an egg. During capacitation, these surface molecules, such as cholesterol and glycoproteins, are removed or modified, allowing the sperm to become more receptive to the egg. As capacitation progresses, the motility pattern of sperm also changes. They undergo hyperactivation, which is characterized by increased amplitude and asymmetrical beating of the tail. Hyperactivated sperm exhibit vigorous movements, which help them to navigate through the female reproductive tract and reach the egg. Capacitation also involves changes in the composition and fluidity of the sperm cell membrane. These changes allow the sperm to better interact with the egg’s zona pellucida. The acrosome becomes primed for the acrosome reaction, which releases these enzymes to allow penetration of the egg membrane.
Capacitation is associated with an increase in calcium ion influx into the sperm. Calcium plays a crucial role in various intracellular signaling processes that are necessary for sperm function and fertilization. For a much more detailed treatment of what is known about the mechanisms of sperm capacitation, there are good reviews of this subject, to which I direct readers.3,4
Conclusion
In summary, various features of the head, middle piece, and flagellum, together with the properties of the seminal fluid, are critical to the sperm cell’s function of reaching and fertilizing an egg. If any one of these parts is not present or fails to function properly, the sperm cell is rendered completely impotent, and reproduction cannot occur. The phenomenon of human reproduction points to a cause with foresight — one that can visualize a foreordained outcome and bring together everything needed to realize that end goal. There is no cause in the universe that is known to have such a capacity of foresight other than intelligent design.
Notes
Anamthathmakula P, Winuthayanon W. Mechanism of semen liquefaction and its potential for a novel non-hormonal contraception†. Biol Reprod. 2020 Aug 4;103(2):411-426.
Ibid.
Puga Molina LC, Luque GM, Balestrini PA, MarÃn-Briggiler CI, Romarowski A, Buffone MG. Molecular Basis of Human Sperm Capacitation. Front Cell Dev Biol. 2018 Jul 27;6:72.
Stival C, Puga Molina Ldel C, Paudel B, Buffone MG, Visconti PE, Krapf D. Sperm Capacitation and Acrosome Reaction in Mammalian Sperm. Adv Anat Embryol Cell Biol. 2016;220:93-106.
Caiaphas : the Watchtower Society's Commentary.
Caiaphas:
Joseph Caiaphas was the high priest during Jesus’ earthly ministry. (Lu 3:2) He was the son-in-law of High Priest Annas (Joh 18:13; see ANNAS) and was appointed to office by the predecessor of Pontius Pilate, Valerius Gratus, about the year 18 C.E., although some say as late as the year 26 C.E. He held the office until about the year 36 C.E., longer than any of his immediate predecessors, this being due to his skillful diplomacy and cooperation with Roman rule. He and Pilate were reportedly good friends. Caiaphas was a Sadducee.—Ac 5:17.
A ringleader in the plot to do away with Jesus, Caiaphas prophesied, though not of his own originality, that Jesus would shortly die for the nation, and to that end he gave his wholehearted support. (Joh 11:49-53; 18:12-14) At Jesus’ trial before the Sanhedrin, Caiaphas ripped his garments and said: “He has blasphemed!” (Mt 26:65) When Jesus was before Pilate, Caiaphas was undoubtedly there crying: “Impale him! Impale him!” (Joh 19:6, 11); he was there asking for the release of Barabbas instead of Jesus (Mt 27:20, 21; Mr 15:11); he was there shouting: “We have no king but Caesar” (Joh 19:15); he was also there protesting the sign over Jesus’ head: “The King of the Jews” (Joh 19:21).
The death of Jesus did not mark the end of Caiaphas’ role as a chief persecutor of infant Christianity. The apostles were next haled before this religious ruler; they were sternly commanded to stop their preaching, were threatened, and were even flogged, but to no avail. “Every day in the temple and from house to house they continued without letup,” Caiaphas notwithstanding. (Ac 4:5-7; 5:17, 18, 21, 27, 28, 40, 42) The blood of righteous Stephen was soon added to Jesus’ bloodstains on the skirts of Caiaphas, who also armed Saul of Tarsus with letters of introduction so the murderous campaign could be extended to Damascus. (Ac 7:1, 54-60; 9:1, 2) However, not long thereafter Vitellius, a Roman official, removed Caiaphas from office.
File under "Well said" XCV
"What gets us into trouble is not what we don't know. It's what we know for sure that just ain't so."
Mark Twain
On empiricism and Darwinism
The Naked Ape: An Open Letter to BioLogos on the Genetic Evidence
Dennis Venema, professor of biology at Trinity Western University, has written a series of articles that have been noted by evolutionists for their clarity and persuasiveness. So as a collector of evidences and reasons why evolution is a fact, I was interested to see Venema’s articles. What does the professor have to say to help confirm what Samuel Wilberforce rhetorically called “a somewhat startling conclusion”?
One of Venema’s basic points is that the genomes of different species are what we would expect if they evolved. Allied species have similar genomes, and genetic features fall into evolution’s common descent pattern:
If indeed speciation events produced Species A – D from a common ancestral population, we would expect their genomes to exhibit certain features when compared to each other. First and foremost, their overall genome sequence and structure should be highly similar to each other – they should be versions of the same book, with chapters and paragraphs of shared text in the same order. Secondly, the differences between them would be expected to fall into a pattern.
Does the evidence confirm these evolutionary expectations? Venema answers with an emphatic “yes.”
Here Venema is appealing to the empirical evidence. He is comparing the evidence to the theory of evolution, and finding that the evidence confirms evolution’s predictions. This means the theory can be empirically evaluated. And if evolution can be genuinely evaluated empirically, then it is, at least theoretically, possible for evolution to fail. If the evidence can confirm evolution, then it also can disconfirm evolution.
This is important because focusing the attention on the evidence means the non scientific arguments go away and science is allowed to speak. What does it say? Here I will take the opposing view, for it seems that what the science shows is that Venema’s claim, that the genetic evidence confirms evolutionary predictions, is inaccurate.
This is not to say that evolutionary explanations cannot be offered. As philosophers well understand, another sub hypothesis is always possible. Such hypotheses raise more profound questions of parsimony, likelihood and so forth. But it seems that such philosophical questions ought to be addressed after there is a consensus on what the empirical evidence has to say. The goal here is to move toward that consensus. Venema, and evolutionists in general, make a straightforward claim about the evidence. We ought to be able to dispassionately evaluate that claim.
Of course I realize that reaching consensus is not as simple as reading an article. There will be differing interpretations by fair-minded critics. And the topic of origins is certainly not always dispassionate. If you argue against evolution you will be disparaged. My response to such attacks has and always will be to forgive.
One final preliminary is simply to point out that it is a challenge just to do justice to this story. A thorough treatment could easily require an entire volume. But a few, typical, examples will have to suffice. They can provide readers with an approximate understanding how the evidence bears on Venema’s claim.
What does the evidence say?
For starters, phylogenetic incongruence is rampant in evolutionary studies. Genetic sequence data do not fall into the expected evolutionary pattern. Conflicts exist at all levels of the evolutionary tree and throughout both morphological and molecular traits. This paper reports on incongruent gene trees in bats. That is one example of many.
MicroRNAs are short RNA molecules that regulate gene expression, for example, by binding to messenger RNA molecules which otherwise would code for a protein at a ribosome. Increasingly MicroRNAs are understood to be lineage-specific, appearing in a few species, or even in just a single species, and are nowhere else to be found. In fact one evolutionist, who has studied thousands of microRNA genes, explained that he has not found “a single example that would support the traditional [evolutionary] tree.” It is, another evolutionist admitted, “a very serious incongruence.”
Trichodesmium or “sea sawdust,” a genus of oceanic bacteria described by Captain Cook in the eighteenth century and so prolific it can be seen from space, has a unique, lineage-specific genome. Less than two-thirds of the genome of this crucial ammonium-producing bacteria codes for proteins. No other such bacteria has such a low value, and conversely such a large percentage of the genome that is non coding. This lineage-specific genome, as one report explains, “defies common evolutionary dogma.”
It is not unusual for similar species to have significant differences in their genome. These results have surprised evolutionists and there does not seem to be any let up as new genomes are deciphered.
The mouse and rat genomes are far more different than expected. Before the rat genome was determined, evolutionists predicted it would be highly similar to the mouse genome. As one paper explained:
Before the launch of the Rat Genome Sequencing Project (RGSP), there was much debate about the overall value of the rat genome sequence and its contribution to the utility of the rat as a model organism. The debate was fuelled by the naive belief that the rat and mouse were so similar morphologically and evolutionarily that the rat sequence would be redundant.
The prediction that the mouse and rat genomes would be highly similar made sense according to evolution. But it was dramatically wrong.
One phylogenetic Study attempted to compute the evolutionary tree relating a couple dozen yeast species using 1,070 genes. The tree that uses all 1,070 genes is called the concatenation tree. They then repeated the computation 1,070 times, for each gene taken individually. Not only did none of the 1,070 trees match the concatenation tree, they also failed to show even a single match between themselves. In other words, out of the 1,071 trees, there were zero matches. It was “a bit shocking” for evolutionists, as one explained: “We are trying to figure out the phylogenetic relationships of 1.8 million species and can’t even sort out 20 yeast.”
What is interesting is how this false prediction was accommodated. The evolutionists tried to fix the problem with all kinds of strategies. They removed parts of genes from the analysis, they removed a few genes that might have been outliers, they removed a few of the yeast species, they restricted the analysis to certain genes that agreed on parts of the evolutionary tree, they restricted the analysis to only those genes thought to be slowly evolving, and they tried restricting the gene comparisons to only certain parts of the gene.
These various strategies each have their own rationale. That rationale may be dubious, but at least there is some underlying reasoning. Yet none of these strategies worked. In fact they sometimes exacerbated the incongruence problem. What the evolutionists finally had to do, simply put, was to select the subset of the genes that gave the right evolutionary answer. They described those genes as having “strong phylogenetic signal.”
And how do we know that these genes have strong phylogenetic signal. Because they gave the right answer. This raises the general problem of prefiltering of data. Prefiltering is often thought of merely as cleaning up the data. But prefiltering is more than that, for built-in to the prefiltering steps is the theory of evolution. Prefiltering massages the data to favor the theory. The data are, as philosophers explain, theory-laden.
But even prefiltering cannot always help the theory. For even cleansed data routinely lead to evolutionary trees that are incongruent (the opposite of consilience). As one Study explained, the problem is so confusing that results “can lead to high confidence in incorrect hypotheses.” As one paper Explained, data are routinely filtered in order to satisfy stringent criteria so as to eliminate the possibility of incongruence. And although evolutionists thought that more data would solve their problems, the opposite has occurred. With the ever increasing volumes of data (particularly molecular data), incongruence between trees “has become pervasive.”
What is needed now is less data. Specifically, less contradictory data. As one evolutionist Explained, “if you take just the strongly supported genes, then you recover the correct tree.” And what are “strongly supported” genes? Those would be genes that cooperate with the theory. So now in addition to prefiltering we have postfiltering.
Another issue are the striking similarities in otherwise distant species. This so-called convergence is rampant in biology and it takes on several forms.
Consider a Paper from the Royal Society on “The mystery of extreme non-coding conservation” that has been found across many genomes. As the paper explains, there is currently “no known mechanism or function that would account for this level of conservation at the observed evolutionary distances.” Here is how the paper summarizes these findings of extreme sequence conservation:
despite 10 years of research, there has been virtually no progress towards answering the question of the origin of these patterns of extreme conservation. A number of hypotheses have been proposed, but most rely on modes of DNA : protein interactions that have never been observed and seem dubious at best. As a consequence, not only do we still lack a plausible mechanism for the conservation of CNEs—we lack even plausible speculations.
And these repeated designs, in otherwise different species, are rampant in biology. It is not merely a rare occurrence which perhaps evolution could explain as an outlier. That the species do not fall into an evolutionary tree pattern is well established by science.
Furthermore, these repeated designs do not merely occur twice, in two distant species. They often occur repeatedly in a variety of otherwise distant species. So now the evolutionist must not only believe that there are many of these repeating design events, but that in most cases, they repeat multiple times, in disparate species.
Evolutionists have labeled this evidence as recurrent evolution. As a recent paper Explains:
The recent explosion of genome sequences from all major phylogenetic groups has unveiled an unexpected wealth of cases of recurrent evolution of strikingly similar genomic features in different lineages.
In addition, many instances of a third more puzzling phylogenetic pattern have been observed: traits whose distribution is “scattered” across the evolutionary tree, indicating repeated independent evolution of similar genomic features in different lineages.
If the pattern fits the evolutionary tree, then it is explained as common evolutionary history. If not, then it is explained as common evolutionary forces.
With all of this contradictory evidence, even evolutionists have realized in recent years that the traditional evolutionary tree model is failing. As one evolutionist Explained , “The tree of life is being politely buried.”
There are many more fascinating examples of biological patterns that are not consistent with the expected evolutionary pattern. These are not anomalies or rare exceptions. Here we have focused on the genetic level since that was the theme of Venema’s article. It seems that the species and their genomes do not fall into a consistent evolutionary pattern as evolutionists such as Venema claim. This does not mean evolutionists cannot explain any of this. They have a wide spectrum of mechanisms to draw upon, of varying levels of speculation and likelihood. These explanatory mechanisms greatly increase the theory’s complexity. They raise questions of realism, and whether the theory is following the data, or the data is following the theory. But such questions are for another day.
The point here is that evolutionist’s claims that the genomic data broadly and consistently fall into the evolutionary pattern and expectations do not seem to reflect the empirical data. This is the first step in moving the discourse forward. We need to reach consensus on what the evidence reveals.
Next time I will continue with an examination of the next evidences Venema presents.
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