Should creationists fear the walking spider, knee-deep in evolution?
Spiders and other arachnids have knees—though no kneecaps. Their knees, like ours, connect longer leg parts, but spider knees can move much more freely.
What good are knees to a spider? After all, other arthropods—insects, lobsters, centipedes, and so forth—get along without them. All have segmented legs, but only arachnids—the subgroup that includes spiders, scorpions, and mites—have knees. The arachnid knee, or patella, is short and bell-shaped. Interspersed between longer segments, the knee increases overall limb flexibility. The arachnid knee makes it possible for the leg below it to move independently in almost any direction.
While trying to learn why some spiders have longer legs than others, scientists from Germany’s University of Göttingen were surprised to discover that spiders have not one but two dachshund genes. The dachshund gene was named after the stumpy-legged wiener dog bred to poke its long body into badger holes. The dachshund (dac) gene was originally discovered in fruit flies, which have only one, and dac-mutant flies have short, malformed legs.1 The spider’s dachshund genes don’t affect the length of its legs, but one of them, it turns out, gives the spider its knees!
The two spider versions of the dachshund gene are called dac1 and dac2. The dac1 gene is expressed in multiple leg segments throughout the spider embryo’s development. The dac2 gene, however, is most keenly expressed in the embryo’s knees, and it is there that its loss is dramatically manifested.2 The scientists discovered that dac2 is essential to knee formation and to the spider’s survival.
Ironically, although it was named for the short-legged dachshund historically bred to hunt burrowing animals, neither the dachshund (dac) gene originally found in fruit flies nor the vertebrate dachshund (dach) gene3 is responsible for this dog’s short legs. Dachshunds do have short legs, however, because of a real copying mutation. This mutation duplicated the gene FGF4 (fibroblast growth factor) and reinserted it at a different place in the dog genome. This gene duplication causes bone growth plates to harden prematurely. The resulting dwarfism, a desirable trait enabling mutant dogs to pursue a badger into its burrow, was maintained in the dachshund by selective breeding. This copying mutation did not add information to the genome but, by preventing normal growth, produced a characteristic phenotypic effect. Of course, this mutation should in no way be considered an example of upward evolution. Not only did the duplication mutation fail to increase the genetic information in the dog genome, but it was maintained in the genome through selective breeding rather than random chance processes, and the dogs—though they are mutant mutts—are and will remain dogs.
When scientists deactivate the dac2 gene, the knee develops not as a short, freely mobile, bell-shaped segment, but rather as a malformed bump fused to the segment below it. The resulting stiff-legged spider nymphs cannot walk properly. They are readily cannibalized by their normal siblings.5 The survivors die during the second stage of their molting process, unable to extricate their fused knobby-kneed legs from their outgrown exoskeletons.
The evolutionary researchers consider dac2 a duplicate of dac1. They believe an ancient ancestor took a major evolutionary step toward becoming a spider by putting an accidentally duplicated copy of its dachshund gene to work growing knees.
The researchers are convinced that their deformed spiders represent the anatomy of a knee-less pre-spider. They write, “Removing dac2 function experimentally restores the segment composition of the arthropod leg before the origin of dac2 in the arachnid lineage.”6 Leaping to the conclusion that a duplicated dachshund gene must have acquired a brand new function critical to spider evolution, they add, “In this way, we are able to provide a link between the origin and neofunctionalisation of dac2 and the evolution of a morphological novelty in the arachnid appendage.”7
The authors of the study, published in Molecular Biology and Evolution, make a poor choice of words in calling dac2 a “duplicate gene.” Their terminology and their presumption that dac2 arose through random mutation followed by acquisition of a new function result not from scientific observations but from the authors’ evolutionary worldview.
Dachshund genes are identified on the basis of sequence similarities to genes in mice and fruit flies.8 Spider dachshund genes are much more like the fruit fly’s. But the two versions of the dachshund gene in spiders are far from identical. The dac2 gene contains a sequence that codes for a chain of 30 amino acids not found in dac1. Furthermore, the so-called duplicate dac2 ends earlier than dac1. Given these dissimilarities and the fact that spider knees do not form without dac2 and that their knees are not just enhancements but are necessary for survival, the evidence suggests that dac2 was part of the spider’s original design. It would be better to reserve the word duplicate for cases in which a copying mutation is clearly evident.
Multiple copies of genes—with or without variations—may result from random mutations or be a designed feature of an organism. If functional, they may enhance an existing function. This has been seen in Salmonella bacteria that more efficiently manufacture the amino acid tryptophan if they have duplicate copies of the necessary gene. (See “New Function through Gene Duplication” to learn more.) Duplicates also may affect the expression of existing genes. This is seen in E. coli bacteria that are better able to utilize citrate as a fuel if a duplicate copy of the gene governing citrate transport is located close enough to its regulatory region to keep the gene switched on. (Learn more about this in “De-Regulation of an Existing Trait.”)
Duplicate genes may alter the properties of proteins in a way that ultimately serves other purposes for the organism. This seems to be the case with snake venom. Toxic components of some snake venoms are associated with duplications of the genes that produce nontoxic substances used elsewhere in the body. (You can read more about this in “Evolution of Snake Venom: A New Use for Old Genes?” and “Mamba Venom Derives from Gene Duplication.”)
Evolutionists believe gene duplication is a mechanism by which increasingly complex organisms evolved.
Evolutionists believe gene duplication is a mechanism by which increasingly complex organisms evolved. They believe that multiple versions or copies of a gene—even if they vary—must be the result of copying mutations. And they believe that the use of those genes for different purposes is evidence of neofunctionalization in the gene’s primordial past. Neofunctionalization is the process by which a duplicated gene supposedly acquired a new function in the evolutionary past. “Species constantly adapt and evolve by inventing new body features,” says team leader Nikola-Michael Prpic. “Our work shows how a gene can be duplicated and then used during evolution to invent a new morphological feature.”9
But have the researchers shown that dac2 invented a new anatomical feature in a knee-less ancestor? No. They’ve only shown that spiders have two dachshund genes, that one of them (dac2) is necessary for embryonic knee formation, and that spiders don’t survive without knees.
Neither duplicate genes nor similar genes are proof that they and their functions came to exist through random evolutionary processes. Duplicate copies of a gene, when they do occur, contain the same information, just as a hundred copies of a book contain no more information than one. Even if the hundred books are used in different ways—some to prop open doors, some to decorate coffee tables, some to smack intrusive spiders, and some to educate children—the information in the hundred books is the same as the information contained in just one.
Furthermore, the scientists have not discovered how the information for producing spider knees came to exist in the first place. Neither have they observed neofunctionalization. As we’ve already pointed out, dac2, though similar to dac1, has substantial structural differences. In fact, even their claim that dac2 has a function completely different from dac1 is quite a stretch!
Here’s why. The dachshund genes in fruit flies and in vertebrates make transcription factors that help regulate expression of other genes during embryonic development.10 Thus dachshund genes have essentially the same regulatory function—a regulatory one—but produce different results depending on where and when they are expressed in the embryo. Rather than claiming dac2 evolved a new function—something that has never been observed—it would be more accurate to say that in spiders this regulatory gene is strongly expressed in the knee and controls correct development there, just as dac1 controls correct development of the leg overall.
The deformity produced by the deactivation of dac2 is not a picture of the spider’s evolutionary past. It is only observational proof of the gene’s essential role in the present. Scientists can learn about how the gene governs spider knee development in the present. They cannot observe how spiders hypothetically evolved in the past.
Observable embryologic development is not a reliable roadmap to an unobservable evolutionary past.
Evolutionists look for clues to explain the origin of signature traits like spider knees in their embryologic development. Embryonic development, because it lays out the steps that actually work in real time to form a single animal, helps evolutionists come up with a plausible sequence of changes that would be required if evolution of one kind of animal into a more complex one could occur. However, observable embryologic development is not a reliable roadmap to an unobservable evolutionary past.
Two functional versions of a gene do not demonstrate that the organism possessing them evolved through gene duplication with neofunctionalization. The alternative explanation is that two similar genes, dac1 and dac2, were designed to ensure formation of functional legs with knees in spiders. Of course this is not acceptable to evolutionists who presuppose that random naturalistic processes of molecules-to-man evolution are the source of all life.
Furthermore, the genetic underpinning of knees in other arachnids varies. Mites have knees but only one known dachshund gene, whereas scorpions have knees and have three dachshund genes, all much shorter than those in spiders. Each was designed with knees and the genes to form them. To try to connect the evolutionary dots between different kinds of animals through genetic similarities is a purely imaginary pursuit.
We know how the spider got its knees. God designed spiders with knees. It is delightful to see scientists unravel the genetic mechanism He designed in order to equip all spiders with them. God even commented on the lowly spider’s resulting dexterity in His Word:
The spider skillfully grasps with its hands,
And it is in kings’ palaces. (Proverbs 30:28)
So the next time you see a spider nimbly scuttling about in your palace or garden, perhaps meticulously manipulating its web or the things caught in it, consider how its tiny bell-shaped knees, a gift from its Creator, our common designer and a master engineer, have for 6,000 years equipped spiders for their unique lifestyle.
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