Some scientists believe that “homeotic” genes provide the answer to the specification of body plans and their development in an organism. In the late nineteenth century biologists noted that body parts of some animals sometimes grew to resemble other body parts. For example, in insects, an antenna might come to display the form of a leg (a condition called Antennapedia). Such forms were called homeotic. The prefix homeo means “like, or similar,” so a homeotic leg would be a body part that resembles a leg. In the twentieth century, the gene responsible for the mutation that causes Antennapedia in fruit flies was discovered and named antp. But the big question is not how a leg can grow in place of an antenna, but how such complex structures as legs and antennas came into existence in the first place—something not perfectly explained up to now by genetic researchers and developmental biologists.
Besides antp, there are other homeotic genes in the fruit fly, such as Pax-6, related to eye development. In 1995, Walter Gehring and his colleagues mutated Pax-6, causing eyes to grow on the antenna and legs of fruit flies. Pax-6 is similar in flies and mammals (humans included). Part of the gene (the DNA binding segment) is also found in worms and squids (Quiring et al. 1994). Researchers concluded that Pax-6 was “the master control gene for eye morphogenesis” and that it is universal in multicellular animals (Halder et al. 1995, p. 1792).
But Wells (1998, pp. 56–57) points out: “If the same gene can ‘determine’ structures as radically different as . . . an insect’s eyes and the eyes of humans and squids then that gene is not determining much of anything.” He adds: “Except for telling us how an embryo directs its cells into one of several built-in developmental pathways, homeotic genes tell us nothing about how biological structures are formed.”
In the case of the eye, evolutionists have to explain how this complicated biological structure arose not just once, but several times. Prominent evolutionists L. von Salvini-Palwen and Ernst Mayr (1977) say that “the earliest invertebrates, or at least those that gave rise to the more advanced phyletic lines, had no photoreceptors” and that “photoreceptors have originated independently in at least 40, but possibly up to 65 or more different phyletic lines.”
The Biological Complexity of Humans
The great complexity of the organs found in the human body defies evolutionary explanation. Darwinists have not explained in any detailed way how these organs could have arisen by random genetic variations and natural selection.
The eye
The human eye is one such organ of apparently irreducible complexity. The pupil allows light into the eye, and the lens focuses the light on the retina. The eye also has features to correct for interference between light waves of different frequencies. It is hard to see how the eye could function without all of its parts being present. Even Darwin understood that the eye and other complex structures posed a problem for his theory of evolution, which required that such structures arise over many generations, step by step. Darwin didn’t give a detailed account of how this happened, but pointed to different living creatures with different kinds of eyes—some just light sensitive spots, some simple depressions with simple lenses, and others more complex. He suggested that the human eye could have arisen in stages like this. He ignored the question of how the first light sensitive spot came into being. “How a nerve comes to be sensitive to light hardly concerns us more than how life itself originated” (Darwin 1872, p. 151; Behe 1996, pp. 16–18).
Darwin’s vague account of a light-sensitive spot gradually developing into the complex, cameralike human eye may have a certain superficial plausibility, but it does not constitute a scientific explanation of the eye’s origin. It is simply an invitation to imagine that evolution actually took place. If one wishes to turn imagination into science, one must take into account the structure of the eye on the biomolecular level.
Devlin (1992, pp. 938–954) gives a fairly detailed biochemical description of the human vision process. Biochemist Michael Behe (1996, pp. 18–21) summarizes Devlin’s explanation like this: “When light first strikes the retina a photon interacts with a molecule called 11-cis-retinal, which rearranges within picoseconds to trans-retinal. . . . The change in the shape of the retinal molecule forces a change in the shape of the protein, rhodopsin, to which the retinal is tightly bound. . . . Now called metarhodopsin II, the protein sticks to another protein, called transducin. Before bumping into metarhodopsin II, transducin had tightly bound a small molecule called GDP. But when transducin interacts with metarhodopsin II, the GDP falls off, and a molecule called GTP binds to transducin. . . . GTP-transducin-metarhodopsin II now binds to a protein called phosphodiesterase, located in the inner membrane of the cell. When attached to metarhodopsin II and its entourage, the phosphodiesterase acquires the chemical ability to ‘cut’ a molecule called cGMP . . . Initially there are a lot of cGMP molecules in the cell, but the phosphodiesterase lowers its concentration, just as a pulled plug lowers the water level in a bathtub. Another membrane protein that binds cGMP is called an ion channel. It acts as a gateway that regulates the number of sodium ions in the cell, while a separate protein actively pumps them out again. The dual action of the ion channel and pump keeps the level of sodium ions in the cell within a narrow range. When the amount of cGMP is reduced because of cleavage by the phosphodiesterase, the ion channel closes, causing the cellular concentration of positively charged sodium ions to be reduced. This causes an imbalance of charge across the cell membrane that, finally, causes a current to be tranmitted down the optic nerve to the brain. The result, when interpreted by the brain, is vision.”
Another equally complex set of reactions restores the original chemical elements that started the process, like 11-cis-retinal, cGMP, and sodium ions (Behe 1996, p. 21). And this is just part of the biochemistry underlying the process of vision. Behe (1996, p. 22) stated: “Ultimately . . . this is the level of explanation for which biological science must aim. In order to truly understand a function, one must understand in detail every relevant step in the process. The relevant steps in biological processes occur ultimately at the molecular level, so a satisfactory explanation of a biological phenomenon—such as sight, digestion, or immunity—must include its molecular explanation.” Evolutionists have not produced such an explanation.
The vesicular transport System
The lysosome is a compartment within the cell that disposes of damaged proteins. There are enzymes within the lysosome that dismantle the proteins. These enzymes are manufactured in ribosomes, compartments found inside another cellular compartment called the endoplasmic reticulum. As the enzymes are being manufactured in the ribosomes, they are tagged with special amino acid sequences that allow them to pass through the walls of the ribosomes into the endoplasmic reticulum. From there, they are tagged with other amino acid sequences that allow them to pass out of the endoplasmic reticulum. The enzymes make their way to the lysosome, where they bind to the surface of the lysosome. Then yet another set of signal tags allow them to enter the lysosome, where they can do their work (Behe 1998, pp. 181–182; Alberts et al. 1994, pp. 551–650). This transportation network is called the vesicular transport system.