QJM vol. 97 no. 9 © Association of Physicians 2004; all rights reserved.
Biologic |
Jaws
The auto-dislocating and deadly jaws of Carcharodon carcharias have killed, terrified and/or entertained many representatives of many species, from other elasmobranchs to Man. The specialized development of rather differently arranged jaws was an important step in mammalian development, marking an important step towards a predatory lifestyle and to hearing well in a less dense medium (air vs. water). But the development of the forebrain has an odd role in the whole business, and recent work in this area has, I know, been keeping many of you on the edge of your seats. A commentary may be helpful.
In jawed vertebrates (the gnathostomes), the lower jaw develops from the mandibular arch. In a previous article I commented on the necessary absence of ‘cephalic end’ Hox gene expression for development of the head and forebrain—it is necessary to avoid the imposition of a metameric (segmented) basic plan, so as to allow other things to happen. It is clear that this non-expression is also necessary for development of the jaws; in the lamprey (an early jawless vertebrate—an agnathan), a Hox gene is expressed in the mandibular arch. Later, the gill-arch-supporting cartilages of the agnathans became the jaws of the jawed fishes, their cartilages (neural-crest-derived) forming upper and lower bars that hinged in the middle. The upper portion of the cartilage supporting the second arch became the hyomandibular bone of the jawed fishes—it supports the skull and links the lower jaw to the cranium. That linkage was close to the otic capsule, and as dense material (bone) is a good sound conductor, probably helped emerging vertebrates to hear better through air then; they had just left the water. Thus the hinge and articulator was also a sound conductor.
At the beginning of the mammals (a Kipling-like term, but you know what I mean), the cranium became firmly attached to the rest of the skull, and the hyomandibular bone was no longer important in attaching the lower jaw; its secondary function became central and it formed the stapes. The major upper-jaw element, now the palatoquadrate, broke up. Part became the base of the skull and the sphenoid; the rest formed the incus and stapes. The malleus is the old articular bone of the reptile lower jaw.
Now in mammals, as the definitive jaws form, there is Hox gene expression. This occurs in a proximo-distal (nested) pattern along their long axis, showing that they are now modelled appendages (the Drosophila homologue of these particular genes, Dlx 1/2, 5/6 and 3/7, is called distalless and is involved in the controlling of the outgrowth of body appendages). In Dlx 5/6 double mutant mice, all of the jaw from the primary jaw joint (the joint between the malleus and incus of the mammalian middle ear) are missing, confirming the importance of the embryological watershed. So how did we end up with what we’ve got?
It was around 160 million years ago that the bones that formed the hinge attaching the jaws to the skull in mammalian ancestors moved back along the skull. In amphibians, reptiles and birds, the posterior part of the first embryonic arch forms the hinge between upper and lower jaw. But in mammals, this hinge has moved backwards, and the incus and stapes joined the inner ear around the time that the neocortex developed. It is thought that the expansion of the forebrain moved the rest of the cranium in such a way that the expanding arc between the maxilla and the inner ear pulled the ossicles backwards, away from the jaw. This was a further selection advantage for hearing (its hard to hear when you’re chewing if you’re a shrew-like primitive, nocturnal, insect-eating mammal).
This series of changes might be considered to show how minor movements over geological time gradually come to present selection advantages, and thus might be considered to be perfect support for gradualism rather than punctuated equilibrium in neo-Darwinism. I hope you will not see this as theoretical excess; it comes from a struggle with Steven Jay Gould's book on the Structure of Evolutionary Theory (I must advise you all to stick to ‘Bully for Brontosaurus’ and ‘Wonderful Life‘: he can be turgid).
But a more exciting piece of work shows how the various changes could also support a sudden change. In 2002, Anjem Chenn won the Eppendorf and ‘Science’ prize for his work on the control of brain size.1 The cerebral cortex has expanded relatively ‘suddenly’ in evolutionary terms, and the control of the process is not well understood. It is dependent on an increase in cell number giving rise to a profound morphological change; the 1000-fold increase in the size of the cortex between mouse and Man is only accompanied by a roughly two-fold increase in thickness.
Chenn has shown that a change in the proportion of cells undergoing symmetrical rather than asymmetrical division (that is, a change in the number of cells that divide to give two further precursor cells rather than a differentiated neuron and a sister that will remain in the dividing cell component) can alter brain size to a remarkable extent. He manipulated the expression of ß-catenin, a major component of adherens junctions between cells, and in embryos that expressed a form of the protein that was resistant to cellular degradation, he was able to double the size of the mouse cortex and make it convoluted, as in higher mammals. This was achieved without increasing cell cycle rate, decreasing cell death, or altering the paths of neuronal differentiation. It probably depends on intra-cellular cytoskeletal rearrangements—these are important in the early development of many embryological structures, including laterality.2
It is thus possible to argue that a single gene change might suddenly cause the developmental alterations that moved the jaws in the final development of the inner ear, a highly advantageous mammalian sensory detection system. This would provide data that support punctuated rather than gradual evolutionary change as the norm. Take your choice (or devise an experiment).
References
1. Chenn A. Eppendorf & Science Prize. Essays on science and society. Making a bigger brain by regulating cell cycle exit. Science 2002; 298:766–7.
2. Berry CL. Making a Pushmi-pullyu; the left or right handed model. Paed Devel Path 1999; 2:491–6.
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