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Abstract: The “Intelligent Design” movement has upheld the blood clotting mechanism as a striking example of an irreducibly complex system, suggesting that it could not have evolved through the gradual process of natural selection. However, the arguments in favour for Darwinian evolution, which is greatly supported by the continuous growth of scientific evidence, strongly suggests a different outlook - in that, a series of gene duplications is now acknowledged to be responsible for the manifestation of this multipart system - which therefore dismisses the need for any direct supernatural interference.
The study of evolution, including other areas of biology, has been abruptly augmented by the sudden upsurge and rapid diffusion of molecular knowledge - knowledge with a generality, depth, precision, and satisfying simplicity almost unique in the biological sciences.
The most fundamental process in evolution is the change in frequency of individual genes and the emergence of novel types by mutation and duplication. For many years, evolutionists could only base their inferences about these processes on observation of phenotypes, inferences that have usually been meandering and tentative. However, the growing succession of techniques in molecular genetics is increasingly shifting the scene as the structure and activity of genetic material is being revealed by direct assays of genotypes. Furthermore, the old limitation of classical genetics - the failure to execute breeding experiments between incompatible species - has been removed. Gene comparisons between chimpanzees and humans, between vertebrates and invertebrates, between animals and plants, and even between eukaryotes and prokaryotes are now regularly carried out; thanks to a molecular methodology that bypasses Mendelian analysis.
The study of molecular evolution has its roots in two different fields of thought: population genetics and molecular biology. Population genetics and intra-species evolution involves many mathematical speculations and thus provides the theoretical foundation for the study of evolutionary processes. However, despite its empirical contribution, it is a frequent criticism that experimental study has not been closely tied to the theory. Nevertheless, the progress of molecular biology has introduced, in increasing detail, new information on molecular mechanisms for producing genetic variation, and has thus provided the empirical data, which has accelerated the advancement of evolutionary studies.
Haldane was the first to recognise the evolutionary significance of gene duplication in 1932 and Muller, later in 1935, suggested that a redundant duplicate of a gene may acquire various mutations, which ultimately emerges as a new gene with different functions. However, it was only when biochemical and molecular biology techniques had advanced significantly, that many examples of duplicate genes were discovered. Protein sequencing methods was an important tool for the study of evolution, which had developed in the 1950s. Moreover, it was in the late 1950s, that the α and β chains of haemoglobin were recognised to have been derived from gene duplication. The evidence for the frequent occurrence of gene duplication in evolution was further supported when isozyme, DNA-RNA hybridisation, and cytogenic studies added additional evidence.,
Unfortunately, however, the theory of evolution does not receive the entire stimulus it deserves, due to a strong opposition in the face of it all. Intelligent Design (ID), an idea not so different from traditional creationism, dismisses the theory of evolution offhand as superfluous and highly improbable. However dissimilar the creationist advocacy may appear on superficial scrutiny, in the grand scheme of things, it has always remained the same. The main argument put forward is that of statistics - an organ, such as an eye, or a biochemical pathway, such as the Krebs cycle, is too improbable to have come about by mere chance; therefore it must have been designed. One of the main reasons for this rejection may be because a modern understanding of the molecular basis of evolution tends to eliminate the notion of “purpose” altogether, which may imply to some that religiosity is therefore worthless and life in general is meaningless. However, Darwinian evolution does not inevitably suggest a nihilistic, or atheistic, worldview - in fact, many prominent biologists, such as geneticist Francis Collins, director of the Human Genome Project, have shown that the existence of God is very plausible indeed. Although this philosophical question is of deep fascination, our aim in this discussion is not to show whether God exists or not, rather, it is to show that Darwinian evolution is currently the best explanation of the development of biological complexity.
If Darwinism cannot give a satisfying explanation of the interconnected complexity of biochemistry, then it is certainly ill-fated. Can Darwinism, then, explain the development of complex biochemical mechanisms, such as blood coagulation? This is a question of fundamental importance, and will therefore be explored in what follows.
The Process of Blood Coagulation
It is obviously very essential for any animal, with a closed circulatory system, to have a way in which blood clotting can occur. It turns out, however, that the blood clotting system in human beings is almost identical to the systems in other mammals, and nearly all vertebrates.
At the core of it all, the blood coagulation cascade (Figure 1) consists primarily of proteins that serve as enzymes or cofactors, which function to hasten thrombin formation and localize it at the site of injury. These proteins are listed in Table 1. The key feature of blood coagulation is that inactive coagulation factors are present in blood and that they are activated in a stepwise fashion. The proenzymes (Factors VII, XI, IX, X, XII, and prothrombin) are serine proteases that successively activate each other down the cascade by cleavage. This sequential activation provides rapid acceleration and amplification of the response. Thrombin converts fibrinogen into fibrin and therefore forms the clot. Fibrinogen consists of two pairs of three non-identical polypeptide chains (α, β and γ) joined by disulphide bonds. The subunit structure is usually denoted as (AαBβγ)2. The presence of many negative charges in the A and B portions of the alpha and beta chains prevents aggregation of fibrinogen. However, when these are removed by the action of protease thrombin, the fibrin molecules formed can aggregate, become insoluble and form a clot of weak tensile strength as they surround the platelet plug. Stabilisation of the clot occurs through formation of bonds between lysine and glutamine residues in alpha and gamma chains in adjacent fibrin molecules. These reactions are catalysed by the active form of factor XIII (XIIIa), which is a fibrin transamidase.
However, the above scheme would cause clotting to occur whenever fibrinogen, thrombin and factor XIII were present and this would be disastrous. Since fibrinogen is always present in normal individuals, then the enzymes must not be active under normal conditions. They exist as proenzymes (zymogens) which must be modified to become active when a clot is required to plug up a damaged vessel. Thrombin is generated in the process of coagulation from its precursor in plasma, prothrmbin