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Human evolution: how random process fulfils divine purpose.

Some people deny that speciation and macroevolution have occurred, and that new genetic functionality can arise from the randomness of mutational mechanism. The genome sequences of many mammalian species are now available for comparison, and have provided a wealth of data that can address these issues. The aim of this article is to show that humans and other mammals share distinctive genomic features that have arisen from singular mutational events. These shared features provide compelling evidence that (1) the human species is descended from ancestors shared with other mammals, so establishing the truth of speciation (our own) and of macroevolution, and (2) new genes have been generated by mutational events that are recognized to occur randomly. This article reflects on how the randomness of natural process achieves God's creative purposes. We can see this pattern in the way God constrains the randomness of history (or indeed of our own lives) into his purposed end.


The opposition of some Christians to evolutionary biology is frequently featured in the media. Positions taken by many in this debate seem to be so polarized as to preclude resolution. But there is an irony to this controversy. Even as some Christians deny that new species can evolve, that macroevolution has taken place, and that complexity can develop through natural genetic processes, the genomic revolution of this century has established the truth of all three evolutionary concepts.

This article is written from the perspective that Scripture possesses the very authority of God. (1) This includes the early chapters of Genesis. Indeed attentiveness to the structure of Genesis 1 has led Old Testament scholars to the conclusion that this text uses rich symbolism to instruct the reader that the incomparably majestic Creator of the universe is the God of Israel, so repudiating all other conceptions of deity. Genesis 1 is arranged in a stylized form. It presents no chronological sequence and implies no mechanism. It describes a transformation from the waters of chaos to the establishment of rest. It reveals to us a God of power, wisdom, purpose, and goodness--a God of order who makes science possible. (2)

Thus one of the key themes of Genesis 1 is that God the Creator transforms chaos into order. This theme is then echoed repeatedly, and in many forms, throughout Scripture. God creatively transformed the chaos of slavery in Egypt into nationhood. Under his creative authority, the turmoil of history led "in the fullness of time" to the climax of the Incarnation. He transformed the Crucifixion into the glory of the Resurrection. He transforms the human state of sin, estrangement, and death into justification, reconciliation, and life. (3)

This theme is compatible with the evolutionary pattern revealed by the post-2001 revolution in comparative genomics. The randomness of genetic process has been shown to underlie the current form of the human genome. Genetic mechanism in all its happenstance has produced the genetic basis of humanness. Genetics describes the process, ordained and upheld by God, to make the creature that expresses God's "image and likeness" (Gen. 1:26-28). That God uses the randomness inherent in the natural world to achieve his purposes should be no surprise to people who believe that he is transforming the chaos of history into the new creation. (4)

The following sections describe how our genome shares particular, uniquely arising innovations with the genomes of a range of other species. Shared genetic markers establish the fact that we and other creatures share common ancestry, and delineate the route of our evolutionary development. This approach reveals how familiar mutational processes have constructed new genes and generated novel genetic functionality.

New Genes from Recycled Spare Parts

In female Eutherian (placental) mammals, one copy of the X chromosome in every cell is inactivated, due to the activity of the Xist gene. The Xist gene is found only in Eutherians, and in no other vertebrates. Part of the Eutherian Xist gene arose from segments of DNA left over from a pre-existing gene (Lnx3) found in lower vertebrates (Figure 1). Fragments of the Lnx3 gene were converted into Xist gene sequences through mutational events that include the insertion of bases. Such insertion mutations typically destroy the protein-coding function of genes, but in the case of the Xist gene (which does not encode a protein), contributed to its formation (Figure 2). (5)


This example illustrates how novel genes may arise by mutational mechanisms that are familiar to geneticists. In the brief segment of genetic sequence shown in Figure 2, the original gene (represented by the chicken Lnx3 gene) has undergone three separate insertion mutations (arrows). These mutations added one base (at two sites) and two bases (at one site) to the original sequence, and are found at the identical positions in all the Eutherian species for which sequences have been obtained. It is highly unlikely that the same insertion mutations would have occurred independently in multiple species. It is vastly more probable that each mutation represents a unique event, and that all the species that now possess the inserted bases received them by inheritance. This means that all Eutherians are descendants of the one individual in which each mutation occurred. And a gene that is integral to our status as Eutherian mammals was formed by the stepwise accumulation of mutations in a lineage of common ancestors.


New Genes from Duplications

Five percent of the human genome consists of large segments of DNA that have been duplicated from elsewhere in the genome. Such segmental duplications are a familiar feature of genomes, and generate multiple copies of the genes that lie within them. (8) If such duplications provide a survival advantage to the organisms that possess them, they will persist through the effects of natural selection. These duplications have increased the number of copies of some genes over the last few thousand years of human history. For example, human populations that derive much of their food from plant starch (agriculturalists such as the Japanese) have more copies of the salivary amylase gene in their genomes than populations that do not depend on dietary starch (pastoralists and fishermen such as the Siberian Yakut). (9)

Segmental duplications arise randomly. They often arise in cancers, and drive cancer development. If multiple cells in a tumor share the same duplication, they are recognized as descendants of the one progenitor cell in which the duplication arose. (10) Similarly, if two species share such a duplication, it may be accepted that they are descendants of the one progenitor in which the singular originating event occurred. Genome comparisons have shown that two-thirds of the segmental duplications in our genome are shared with chimps. (11)

If mutations accumulate in each of a pair of duplicated genes, the proteins they encode may acquire different activities. The end result of reiterated duplications will be families of genes of diverse function.

Genes for visual pigment proteins called opsins are required for color vision. New World Monkeys (NWMs) have two opsin genes; apes and Old World Monkeys (OWMs) have three. The third gene appeared when an ancestral opsin gene (and part of a nearby gene of unknown function, TEX28) on the X chromosome was duplicated to form the tandem arrangement: red opsin-truncated TEX28-green opsin-TEX28 (Figure 3). Comparison of the uninterrupted sequence to the left of the present red opsin gene, and of the interrupted sequence to the left of the present green opsin gene identifies the exact position of one of the two breakpoints that occurred during the duplication. This breakpoint is common to apes and OWMs, and demonstrates that the duplication arose in a unique event, and that it that has been inherited by all the species that now possess it. This finding indicates that trichromatic vision arose in a random DNA duplication event. Subsequent mutations conferred distinct spectral properties on the pair of opsin proteins. (13)


The human leukocyte antigen (HLA) gene complex is critical to the functioning of our immune system. The HLA Class I region is 1,800,000 bases long, and was generated by several rounds of segmental duplications. Many of the genes and surrounding genetic markers (inserted transposable elements; see later) are arranged in multiple repeated units, which are shared by multiple primate species. (14) Gene families arising by similar processes of DNA duplication have been documented in a large number of cases.

New Genes from Transposable Elements

Half of the DNA in our genome has been contributed by jumping genes or transposable elements. These are discrete segments of DNA that reside in the genomes of fungi, plants, and animals. They are units of genetic material that possess the ability to propagate themselves haphazardly within genomes. They insert new copies of themselves into chromosomal DNA at loosely preferred sites, chosen largely at random from the vast number of potential sites distributed throughout the genome. The insertion process is marked by a particular signature: the inserted transposable element is flanked by short duplications of target site DNA. Such target site duplications arise from the mechanism by which transposable elements propagate. They can be classified into two main groups called DNA transposons and retrotransposons. (15)

One in every ten people may have a new insert in their germ-line DNA arising from the activity of these agents. (16) Because transposable elements invade new sites at random, they insert into and disrupt existing genes at an appreciable frequency. These agents are insertional mutagens, and their current activity is responsible for a significant burden of human genetic disease. (17) They are relevant to our understanding of human evolution for two reasons.

Firstly, the probability that two transposable elements of the same class would insert independently into the same site in the DNA of two individuals is negligible. Thus, if two (or more) individuals share the same parasitic insert in their DNA, it may be concluded that they are descendants of the one individual in which that unique insertion event occurred. Such instances exemplify the well-established concept of founder mutations. (18) Analogously, if two (or more) distinct species share the same parasitic insert in their DNA, it may be concluded that they are descendants of the one individual in which that unique insertion event occurred. (19) Genomic science has shown that >99% of the millions of genetic parasites inserted in the human genome (20) are shared with chimpanzees, (21) and the great majority are shared with macaques, an OWM. (22) Such findings establish that humans, chimps, and (more remotely) macaques share common ancestors.

Secondly, transposable elements are individualistic genetic parasites. The transposable elements scattered throughout our genomes have traditionally been dismissed as "junk." However, it is now established that at least some of this DNA has been co-opted to provide essential genetic functionality. (23) The activities of these insertional mutagens are random with respect to the functioning of the host organism, but they have contributed to the development of complexity.

DNA Transposons

DNA transposons are short segments of self-propagating DNA that reside in the genomes of many organisms. Their origins are lost in remote history. They possess an enzyme called a transposase which enables them to cut-and-paste themselves into new sites in the genome. They appear to increase in number by co-ordinating their activities with episodes of cellular DNA synthesis. There are nearly 400,000 individual DNA transposons inserted into our genome, of which essentially all are shared with apes and OWMs. (24)

Many of the DNA transposons scattered throughout our genome have acquired genetic functionality since the time they inserted into the primate germ-line. Some now function as genes that generate RNA molecules involved in widespread and important regulatory functions. (25)

Other DNA transposons have contributed to the information content of genes that make proteins. A DNA transposon of the Hsmar1 class inserted itself into a pre-existing gene (known as the SET gene) in an ancestor of apes and monkeys. This insertion event converted the SET gene into the novel SETMAR gene. This hybrid gene now makes a protein that may function in DNA repair processes, or in the regulation of genome activity (Figure 4). The portion of the SETMAR protein that was donated by the transposon retains many of the enzymatic functions performed by the original transposon-coded protein. (27)



Retrotransposons are parasitic residents of the genome that copy-and-paste themselves into new sites of genomic DNA via an RNA intermediate (Figure 5):

parent DNA insert [right arrow] RNA copies [right arrow] daughter DNA inserts

The LTR retrotransposons constitute one class of these agents. They are related to the retroviruses that cause human disease. Indeed our DNA contains many segments of retroviral DNA, known as endogenous retroviruses, which originally invaded the genome as infectious agents. We have inherited at least 300,000 LTR retrotransposons and endogenous retroviruses in our DNA. Nearly all of them are shared with chimps, and most with macaques. Most of them are genetic fossils that are degenerating into the genetic background, but some have assumed vital genetic functions. (28)

A few endogenous retroviruses have, against all odds, retained one of their genes in a form that can direct the production of an active protein. A gene that has excited particular interest is the envelope gene. (29) One of the endogenous retroviruses that retains an active envelope gene is the unique ERVWE1 insert that became resident in primate DNA in an ape-OWM ancestor (Figure 6). (30) The ERVWE1 insert directs the production of an active envelope protein that is made in a specific population of cells in the placenta, and that appears to be necessary for placental and fetal development. (31) A gene added to primate DNA as part of the viral infection apparatus has been transmogrified into a gene that is essential for our life-cycle.



It appears that endogenous retroviruses repeatedly have donated genetic information that has contributed to the form and function of the placenta. The PEG10 gene arose from a retrovirus-like agent that inserted into mammalian DNA in an ancestor of marsupials and Eutherians. It is also implicated in the formation of the placenta. (33) Mammalian development has been promoted through the exploitation of genetic material contributed by potentially pathogenic insertional mutagens.

Many other classes of retrotransposons in our DNA have contributed raw material that has led to the development of genetic novelty. Alu elements are found only in primates. There are at least 1.1 million of these inserts in our DNA. Nearly all of these inserts are shared with chimps (>99.9%) and most with macaques (90%). Alu elements have provided raw material from which new genes have been constructed. (34) They have inserted themselves into pre-existing genes, thereby generating alternative forms of those genes. (35) For example, an insert in the survivin gene, which controls life-and-death decisions in cells, entered the primate germ-line in an ancestor of the apes (Figure 7).

Mammalian-wide interspersed repeat (MIR) elements are very ancient and widely distributed in the DNA of all mammals. Essentially all of the 300,000 MIR elements present in our DNA are shared with chimps and macaques. Some genes (including the ZNF639 and POMC genes) contain MIR inserts that have been found in all mammals tested including the egg-laying platypus. (36) Numerous other families of very ancient transposable elements have contributed functional units to our genome and each insert common to mammals establishes that the mammals are monophyletic (descended from a single common ancestor). (37)


Via Enzymatic Machinery of Retrotransposons

During the normal activities of cells, genes are copied into RNA, which performs housekeeping or regulatory functions, or directs the synthesis of proteins. RNA is normally short-lived, but sometimes, an RNA molecule becomes entangled in the enzymatic machinery of retrotransposons, and a DNA copy gets inserted back into chromosomal DNA. Our DNA contains thousands of copies of such randomly copied-and-pasted genes. Most have lost the capacity to make proteins, and are called pseudogenes. (39)

parent gene in DNA [right arrow] RNA copy [right arrow] daughter pseudogene in DNA

Despite the haphazard nature of this process, some of these copied-and-pasted inserts retain the capacity to direct the production of proteins. These additions to our gene complement are called retrogenes.

Our genome possesses a family of novel genes that arose following the insertion of a DNA segment from one gene (encoding a protein called [beta]-actin) into another gene (called the POTE gene). This novel hybrid gene subsequently spawned a family of POTE-actin genes. The presence of a unique [beta]-actin insertion site (with its tell-tale target site duplications) establishes that one original insertion event was followed by a series of gene duplication events. The outcome of this series of mutational events is that our genome possesses seven genes that contain the insertion (Figure 8). POTE-actin genes are found in apes and OWMs. This insertion mutation involving actin gene sequences is an unambiguous marker indicating that a novel gene family, and the complexity of function entailed in the interactions of its members, developed from a random event that occurred in an ancestor of apes and OWMs. (40)


The PIPSL gene (also an interesting hybrid gene) was inserted into the DNA of a great ape ancestor, and the GLUD2 gene in an ape ancestor. (42) Retrogenes have accumulated in the DNA of our ancestors at a steady rate through primate history. (43) The process of transposable element-mediated gene generation has been in operation as far back in time as we are able to see. The YY2 and REX1 genes arose early in the development of placental mammals, (44) and other copied-and-pasted genes shared widely with other mammals are being identified all the time. (45)

These copying-and-pasting events have generated a host of retrogenes from which small RNA molecules are made. These RNA molecules perform a range of housekeeping jobs pertaining to genome function, and act as master regulators of genome activity. Most are shared with chimps; and some with creatures as distantly related as mice. (46) We are at least partially what our parasitic transposable elements have made us.

Genome Data and the Christian Worldview

An outline of the evolutionary development of the human species is depicted in Figure 9. This evolutionary tree has been established by many approaches. The comparative genomic approaches have provided compelling corroboration of the evolutionary relationships depicted. They have resolved long-standing controversies regarding some branch points. They have shown how genes have arisen at particular times through natural processes. Many similar events have been mapped to every point, and together have established the pattern of evolutionary branching.

This discussion has been limited to events in mammalian evolution because it is only in the timescale of mammalian evolution that the unambiguous genetic markers of our evolutionary history have survived. Transposable elements provide tantalizing molecular evidence for human-avian common ancestry, (47) without reporting (for example) any surviving shared transposable elements flanked by target site duplications. However, there is no reason to doubt the reality of earlier evolutionary transitions (inferred through other means) just because they occurred so long ago that unambiguous genetic markers establishing common descent have been eroded beyond recognition. How should Christians respond to such data, which are a small selection of what is available? (48)

An authentically biblical worldview requires that we view the world through critically realist eyes. Our mind-set must be critical in the sense that the data of experience must consistently challenge and correct our understanding of reality. It must be realist in the sense of recognizing that we face a world of which there is an objective truth, even though we will never fully grasp it. This mind-set governs Christian approaches to both the natural world (49) and to Scripture. (50) Transposable elements that disrupt genomes today possess genetic information that is highly similar to that in transposable elements that we share with other mammalian species. We must accept that they all arose through the same elaborate biochemical mechanisms. Genes present in our DNA really arose when transposons acquired coding capacity in simian ancestors. Christians have defended critical realism in other historical situations. The earth really revolves around the sun (contra the Aristotelians, who claimed that Galileo's heliocentric model merely saved the appearances as an interpretive device). (51) Christ really suffered (contra the docetists, who claimed he only appeared to do so).

If we are God's creation, then our DNA sequence is an authoritative text that God has written. It is the Primal Testament that describes how God in faithfulness has created, via the randomness of genetic happenstance, the creature that bears his image and that he intends to glorify. Francis Collins has stated that shared transposable elements have implications for common ancestry that are "virtually inescapable." (52) We must listen attentively to this text, and respond appropriately.


Creation and Evolution: Agency and Process

It follows that the theological assertion that God is our Creator may not be seen as an alternative to the evolutionary mechanism of human origins. This "either-or" position represents a false dichotomy. Creation refers to personal agency (the intentionality and action of God), (53) which may be described in terms such as goodness, love, and grace. (54) Evolution refers to material process. God creates. Transposable elements and genomes evolve. Indeed, transposons and genomes evolve in the world that God has chosen to create. Creation refers to God's continuous covenantal relationship with the entirety of creation--past, present, and future. (55) Evolution, with its physical components (bases, transposons) and its processes (duplications, insertions), describes only relationships within creation.

For Christians, the life, death, and resurrection of Christ constitute the necessary and sufficient basis of faith in the self-revealing God. From this foundation, all presuppositions that inform our interpretation of the world are necessarily theistic. Thus, all scientific descriptions of physical phenomena (such as the molecular mechanisms which gave rise to genes), since they are describable in physical terms, can and must be included within a Christian perspective of reality as creation. We dare not exclude any biological process--including evolutionary ones--from the creative work of God.

Neither is the agency of God an alternative to natural law. MacKay stated that "the laws of nature we discover are not alternatives to divine activity, but only our codification of that activity in its normal manifestations." (56) Similarly, Van Till stated:
 Natural laws are held to be statements describing
 the patterned behavior that matter and material systems
 exhibit as a consequence of divine governance.
 Natural laws are not prescriptive laws of nature for
 its own behavior but descriptive representations of
 the laws of God for nature, which is his creation. (57)

And to Polkinghorne, "Everything in the world--its form and its substance, the nature of law and the nature of matter--is contingent upon his will alone." (58)

Physical laws that describe the behavior of DNA and the way it mutates (no matter how probabilistic their operation may be) are laws that reflect God's faithful dealings with his creation. The lawful processes of segmental duplication and of retrotransposon insertion, responsible for the generation of new genes in now-extinct ancestors, are open to experimental analysis, are starkly molecular in nature, and are inalienably part of that physical reality that we recognize as creation. Thus any claims that "evolution is religion" cannot refer to evolution as description of biological history, but only to the metaphysical (atheistic) denial of God as its Author.

Creation and Random Process

This article has described how random mutations (insertions and deletions of bases, large duplications, and the actions of retroviruses and transposable elements) have arisen during primate history. In the timescale of a human life, they are commonly encountered as disease-causing mutations. (59) But over the timescales of mammalian history, these same events have helped to generate the human genome and humanity. The preponderant harmful mutations have not survived.

The roles of random mutagenic events in the evolutionary development of genes and their regulatory networks present no new issues to Christian theology. Genetic randomization processes are integral to sexual reproduction, and so reflect the creative work of God in the generation of every human being. It is axiomatic that sex exists to shuffle genetic material, partly through random assortment of chromosomes into gametes. The biological origin of each one of us is the outcome of the probabilistic segregation of chromosomes: given that humans possess two sets of chromosomes, each of which has twenty-three members, there are [2.sup.23] (8.4 million) possible ways of assorting them when gametes are formed. And to compound the degree of randomization, elaborate mechanisms exist to shuffle material between chromosome pairs. (60) To the Christian it is also axiomatic that each one of us is a created being (Ps. 139). Scientifically, we are the product of random genetic process. Theologically, we are the outcome of loving divine purpose. Molecular randomness (in scientific terms) and createdness (in theological terms) inevitably go hand-in-hand.

The operation of random (probabilistic) processes in gene and species formation cannot be an alternative to divine creativity, but is an aspect of divine creativity. Indeed, because of their evident role in contributing to the formation of new genes, such random processes (chance) in the context of the directing effects of selection (necessity) lead to predictable results. This lawful interaction between chance and necessity demonstrates the potentiality inherent in matter. The combination of randomness and determinism, chance and necessity, was God's way of generating life--including humanity. (61) The potentiality of the interaction between chance and necessity is a pointer to the rationality and purpose of God, analogous to the powerful problem-solving capacities of genetic algorithms, computer programs that select optimum solutions from a range that is randomly generated. (62)

Our genome has developed by incorporating novel features provided by random mutagenic events (of which over three million are recognizable as the insertions of transposable elements alone). These genetic processes are part of the divine creative strategy by which the creature that would bear God's image has come to be.

Divine Purpose and Creaturely Freedom

Is it legitimate to suggest that in the random events that transform evolving genomes, God's directing hand acts covertly and immediately to achieve his purposes? (63) Theological justification for this has been suggested by recourse to Prov. 16:33: "The lot is cast into the lap, but the decision is wholly from the Lord." (64) By this reasoning, God determines mutations, and so directs evolution.

But Kidner disallows this interpretation. He states: "The Old Testament use of the word lot is not about God's control of all random occurrences, but about his settling of matters properly referred to him." (65) In addition, the postulate that God controls phenomena that are to us random is problematic because the random events that have added novelty to our genome (over the long term) are identical to those that disrupt genomes and cause genetic disease (over the short term). There are good theological reasons for denying that God is the immediate cause of genetic mutations, because if he were, he would be the immediate cause of genetic diseases such as cancer. God is not the author of disease and suffering. Rather he is the implacable foe of disease and suffering. The healing works of Jesus and the cost of Calvary are the guarantee that he is committed ultimately to destroying not only evil but also disease (Isa. 53:4; Rev. 21:4). (66)

God sustains the lawfulness of the world, but is not the direct cause of each event. Thomas Aquinas spoke of God as the first cause. The universe and everything in it depends directly upon him. But a secondary level of causation exists. This is the interlocking and interdependent cause-and-effect network that constitutes the operation of the physical universe. McGrath has stated:
 Events within the created order can exist in complex causal
 relationships, without in any way denying their ultimate dependency
 upon God as final cause ... This classic approach laid the
 conceptual foundations for the development of the natural sciences
 in the later middle ages. (67)

Israel's concept of creation entailed that the universe is subject to a single code of law that has been established for all time. God has devolved a self-sufficient mode of operation upon creation (it is autonomous), but this freedom exists only in relation to God who conferred it on creation (it is relative). Nature possesses relative autonomy. (68)

It seems that God has conferred the gift of freedom upon his created world, and upon the molecular processes that mold our genomes. (69) God does not determine DNA rearrangements (duplications, transposon insertions), but they are part of the network of autonomous secondary causation. Evolutionary transformations thus manifest the features of authentic history. The lawful behavior of the world sustained by God has provided channels by which our genome has freely evolved into what it is now. (70)

It is a paradox that the God of love has ordained a way of generating humankind that entails the possibility of disease and suffering. "If God allows sin and suffering, he remains answerable for them." (71) God is implacably opposed to pathogens and cancers, and is committed to destroying evil in all its manifestations. The resolution to this paradox is found in the mystery of God Incarnate, bearing the evil of the natural world as well as the totality of our sin. Calvary is the proof that God will eliminate evil from creation. The "Eschatological Doctrine of Providence" stems from the Resurrection and describes the hope that God will transform creation and remove all suffering from it. (72)

Creaturely Freedom in History

Genes describe biological (evolutionary or natural) history. (73) Biological history is analogous to human or biblical history. In each, God achieves his purposes with creatures that are endowed with freedom (the relative autonomy to act through secondary causes). The freedom of evolutionary process thus presents no new problems for Christians.

God is the sufficient condition for the existence of the world: he alone is the source of all reality. But God limits himself to being the necessary condition for every occurrence in the world: he does not determine everything that happens. If God did not grant such freedom, "neither the relative autonomy of natural processes in the world which we express in the probabilistic statements of natural laws nor human freedom would be possible." (74)

Polkinghorne draws an analogy between the freedom God gives to creation (seen in the randomness of natural process, and which may result in natural evil) and free will exercised by people (which results in moral evil). The "free-process" defense argues that a free world with the capacity for disease and disaster is superior to a wholly deterministic one. The "free-will" concept argues that a world in which people have the capacity to act in evil ways is better than a world of automata. (75)

God does not determine the way in which people will live. He gives people free choice--which is often used in selfish, evil, and irrational (arbitrary) ways that are opposed to his holy nature. And yet in the context of God's faithfulness, history progresses through this chaotic matrix (randomness) toward the glory that God has purposed. Biblical history provides many examples of how arbitrary human evil, exercised in freedom and contrary to the nature and will of God, has contributed to the fulfilment of God's goals.

Pharaoh acted freely in defiance of God but the biblical interpreters saw his arbitrary evil choices as contributing to the achievement of God's purposes (Rom. 9:17). The Assyrians in all their sadistic ruthlessness were (unwittingly) the "rod" of God's anger (Isa. 10:5), the "bees" God summoned to effect his purposes (Isa. 7:18). The ruthless Nebuchadnezzar was God's "servant" (Jer. 25:9; 27:6; 43:10). Cyrus, acting out of political expediency, was God's "messiah" in allowing the exiles to return (Isa. 45:1). Those who collaborated to murder Christ, acting in opposition to the nature of God, were unwittingly bringing the purpose of history to its fulfilment (Acts 2:23, 36; 3:13-15, 18). The messy "randomness" of history is incorporated by God to achieve his ends. These ends are the ongoing creation of the nation of Israel (Isa. 43:1, 15; 44:2); a reformed Israel after the Exile (Isa. 4:5; 41:17-20); a new, redeemed humanity (2 Cor. 5:17; Eph. 2:10, 15); and the eschatological Kingdom of God (Isa. 65:17; 66:22; 2 Pet. 3:13; Rev. 21:1).

The insights of the Princeton theologian B. B. Warfield are pertinent in trying to understand how God achieves his ends through secondary causes (whether random genetic mutations or arbitrary human agents). Warfield was supportive of evolution as a theory operating under the control of providence. Indeed, natural laws were the expression of divine supervision. (76) This must be true of natural laws which are probabilistic, such as those that describe mutational events.

Warfield emphasized that "evolution could be given a teleological reading, that mechanical explanations in nature were thoroughly consistent with his Calvinistic conception of divine creation" (1889). Moreover, teleology was inseparable from a complete system of natural causation: "Every teleological system implies a complete 'causo-mechanical' explanation as its instrument" (1908). (77)

Warfield integrated God's purpose with evolution's freedom using the concept of concursus. In the same way as Scripture is at once wholly the outcome of the will of God and the action of humans, so evolution is entirely the work of God and also of the operation of natural causes.

God is not known by Aristotelian "proofs," whether these come from the schools of Thomas Aquinas, William Paley, or the Intelligent Design movement. (78) He is known only by his self-revelation through history, and climactically in Christ. Christians reflecting on the randomness of genetic history as revealed by comparative genomics may marvel that we are here, and so worship God for bringing humanity into being via genetic randomness. Biological evolution, just like the progressive unfolding of God's purposes in the messiness of history, is testimony to the sovereign wisdom and authority by which God brings a freely operating world to fulfilment, and so transforms randomness into glory.

There is of course mystery in this. The achievement of God's purposes in the light of genetic or human freedom is a paradox to which we must hold. The actions of God in history are not obvious to the casual observer. Butterfield wrote that we cannot find the hand of God in secular history unless we have first gained assurance of God's involvement by personal experience. (79) It is Christ who makes sense of Israel's tumultuous past. Once we have recognized how God's blessing for the world arose from Israel's tragic history, we may perceive with worship that he has created humanity by the random evolutionary route attested by our genome.

The vision of God's sovereign action revealed in biological and human history is a comfort to each of us as individuals. For in the chaos of our lives--the "randomness" of accident, sickness, irrational and selfish choices--the God in whom we have placed our trust is faithfully at work to bring those lives to the ends which he has purposed. The God who created the human species through the turbulent genetic history recorded in its genome can be trusted to bring us, through the happenstance of our lives, to completion in his presence.


(1) N. T. Wright, Scripture and the Authority of God (London: SPCK, 2005).

(2) H. Blocher, In the Beginning: The Opening Chapters of Genesis (Downers Grove: InterVarsity Press, 1984); V. P. Hamilton, The Book of Genesis Chapters 1-17 (Grand Rapids: Eerdmans, 1990); D. Kidner, Genesis: An Introduction and Commentary (London: The Tyndale Press, 1967); E. Lucas, Genesis Today (London: Scripture Union, 1989); M. W. Poole and G. J. Wenham, Creation or Evolution: A False Antithesis? (Oxford: Latimer House, 1987); W. S. Towner, Genesis (Louisville: Westminster John Knox Press, 2001); L. A. Turner, Genesis (Sheffield: Sheffield Academic Press, 2000); B. K. Waltke and C. J. Fredricks, Genesis: A Commentary (Grand Rapids: Zondervan, 2001); G. J. Wenham, Word Biblical Commentary Genesis 1-15 (Nashville: Thomas Nelson Publishers, 1987); G. J. Wenham, Exploring the Old Testament Vol. 1: The Pentateuch (London: SPCK, 2003).

(3) A. Konig, New and Greater Things: Re-evaluating the Biblical Message on Creation (Pretoria: UNISA, 1988), 135-6.

(4) R. Colling, Random Designer (Bourbonnais: Browning Press, 2004).

(5) L. Duret,C. Chureau, S. Samain et al., "The Xist RNAGene Evolved in Eutherians by Pseudogenization of a Protein-Coding Gene," Science 312 (2006): 1653-5; Z. C. Yen, I. M. Meyer, S. Karalic, and C. J. Brown, "A Cross-Species Comparison of X-Chromosome Inactivation in Eutheria," Genomics 90 (2007): 453-63.

(6) Ibid.

(7) Ibid.

(8) B. Conrad and S. E. Antonarakis, "Gene Duplication: A Drive for Phenotypic Diversity and Cause of Human Disease," Annual Review of Genomics and Human Genetics 8 (2007): 17-35.

(9) G. H. Perry, N. J. Dominy, K.G. Claw et al., "Diet and the Evolution of Human Amylase Gene Copy Number Variation," Nature Genetics 39 (2007): 1256-60; E. Patin and L. Quintana-Murci, "Demeter's Legacy: Rapid Changes to our Genome Imposed by Diet," Trends in Ecology and Evolution 23 (2008): 56-9.

(10) N. Vogt, S.-H. Lefevre, F. Apoiu et al., "Molecular Structure of Double-Minute Chromosomes Bearing Amplified Copies of the Epidermal Growth Factor Receptor Gene in Gliomas," Proceedings of the National Academy of Sciences of the USA 101 (2004): 11368-73.

(11) Z. Cheng, M. Ventura, X. She et al., "A Genome-Wide Comparison of Recent Chimpanzee and Human Segmental Duplications," Nature 437 (2005): 88-93.

(12) K. S. Dulai, M. von Dornum, J. D. Mollon, and D. M. Hunt, "The Evolution of Trichromatic Color Vision by Opsin Gene Duplication in New World and Old World Primates," Genome Research 9 (1999): 629-38. Patas monkey and chimp sequences upstream of the breakpoint were inferred from the PCR primer sequences used to amplify the breakpoint; H. Ueyama, R. Torii, S. Tanabe et al., "An Insertion/Deletion TEX28 Polymorphism and Its Application to Analysis of Red/Green Visual Pigment Arrays," Journal of Human Genetics 49 (2004): 548-57.

(13) Ibid.

(14) T. Shiina, G. Tamiya, A. Oka et al., "Molecular Dynamics of MHC Genesis Unraveled by Sequence Analysis of the 1,796,938-bp HLA Class 1 Region," Proceedings of the National Academy of Sciences of the USA 96 (1999): 13282-7; T. Anzai, N. Shiina, N. Kimura et al., "Comparative Sequencing of Human and Chimpanzee MHC Class I Regions Unveils Insertions/Deletions as the Major Path to Genomic Divergence," Proceedings of the National Academy of Sciences of the USA 100 (2003): 7708-13; K. Fukami-Kobayashi, T. Shiina, T. Anzai et al., "Genomic Evolution of MHC Class I Region in Primates," Proceedings of the National Academy of Sciences of the USA 102 (2005): 9230-4; J. K. Kulski, T. Anzai, and H. Inoko, "ERVK9, Transposons and the Evolution of MHC Class I Duplicons within the Alpha-Block of the Human and Chimpanzee," Cytogenetic and Genome Research 110 (2005): 181-92.

(15) V. V. Kapitonov, A. Pavlicek, J. Jurka, "Anthology of Human Repetitive DNA," Encyclopedia of Molecular Cell Biology and Molecular Medicine 1, ed. R. A. Meyers (Weinheim: Wiley-VCH Verlag and Co. , 2004), 251-305; J. Jerka, V.V. Kapitonov, O. Kohany, and M. V. Jurka, "Repetitive Sequences in Complex Genomes: Structure and Evolution," Annual Review of Genomics and Human Genetics 8 (2007): 241-59.

(16) R. Cordaux,D. J. Hedges, S. W. Herke, and M. A. Batzer, "Estimating the Retrotransposition Rate of Human Alu Elements," Gene 373 (2006): 134-7.

(17) J.-M. Chen, P. D. Stenson, D. N. Cooper, and C. Ferec, "A Systematic Study of LINE-1 Endonuclease-Dependent Retrotranspositional Events Causing Human Genetic Disease," Human Genetics 117 (2005): 411-27; J.-M. Chen, C. Ferec, and D. N. Cooper, "LINE-1 Endonuclease-Dependent Retrotranspositional Events Causing Human Genetic Disease: Mutation Detection Bias and Multiple Mechanisms of Target Gene Disruption," Journal of Biomedicine and Biotechnology (2006): 1 (Article ID 56182); P. A. Callinan and M. A. Batzer, "Retrotransposable Elements and Human Disease," Genome Dynamics 1 (2006): 104-15; D. V. Babushok and H. H. Kazazian, "Progress in Understanding the Biology of the Human Mutagen LINE-1," Human Mutation 28 (2007): 527-39.

(18) M. Watanabe, K. Kobayashi, F. Jin et al., "Founder SVA Retrotransposal Insertion in Fukuyama-type Congenital Muscular Dystrophy and Its Origin in Japanese and Northeast Asian Populations," American Journal of Medical Genetics Part A 138 (2005): 344-8; C. Bouchet, S. Vuillaumier-Barrot, M. Gonzales et al., "Detection of an Alu Insertion in the POMT1 Gene from Three French Walker Warburg Syndrome Families," Molecular Genetics and Metabolism 90 (2006): 93-6; S. Makino, R. Kaji, S. Ando et al., "Reduced Neuron-Specific Expression of the TAF1 Gene Is Associated with X-Linked Dystonia-Parkinsonism," American Journal of Human Genetics 80 (2007): 293-406.

(19) D. A. Ray, J. Xing, A.-H. Salem, and M. A. Batzer, "SINEs of a Nearly Perfect Character," Systematic Biology 55 (2006): 928-35.

(20) International Human Genome Sequencing Consortium, "Initial Sequencing and Analysis of the Human Genome," Nature 409 (2001): 860-921; "Finishing the Euchromatic Sequence of the Human Genome," Nature 431 (2004): 931-45.

(21) The Chimpanzee Sequencing and Analysis Consortium, "Initial Sequence of the Chimpanzee Genome and Comparison with the Human Genome," Nature 437 (2005): 69-87.

(22) Rhesus Macaque Genome Sequencing and Analysis Consortium, "Evolutionary and Biomedical Insights from the Rhesus Macaque Genome," Science 316 (2007): 222-3; K. Han, M. K. Konkel, J. Xing et al., "Mobile DNA in Old World Monkeys: A Glimpse through the Rhesus Macaque Genome," Science 316 (2007): 238-40.

(23) J.-N. Volff, "Turning Junk into Gold: Domestication of Transposable Elements and the Creation of New Genes in Eukaryotes," BioEssays 28 (2006): 913-22; A. R. Muotri, M. C. N. Marchetto, N. G. Coufal, and F. H. Gage, "The Necessary Junk: New Functions for Transposable Elements," Human Molecular Genetics 16 (2007): R159-R167; M. Wu, L. Li, and Z. Sun, "Transposable Element Fragments in Protein-Coding Regions and Their Contributions to Human Functional Proteins," Gene 401 (2007): 165-71.

(24) J. K. Pace II and C. Feschotte, "The Evolutionary History of Human DNA Transposons: Evidence for Intense Activity in the Primate Lineage," Genome Research 17 (2007): 422-32.

(25) J. Piriyapongasa and I. K. Jordan, "A Family of Human MicroRNA Genes from Miniature Inverted-Repeat Transposable Elements," PLoS ONE (February 2007): e203.

(26) R. Cordaux, S. Udit, M. A. Batzer, and C. Feschotte, "Birth of a Chimeric Primate Gene by Capture of the Transposase Gene from a Mobile Element," Proceedings of the National Academy of Sciences of the USA 103 (2006): 8101-6; D. Liu, J. Bischerour, A. Siddique et al., "The Human SETMAR Protein Preserves Most of the Activities of the Ancestral Hsmar1 Transposase," Molecular and Cellular Biology 27 (2007): 1125-32.

(27) Ibid.

(28) L. N. van de Lagemaat, J.-R. Landry, D. L. Mager et al., "Transposable Elements in Mammals Promote Regulatory Variation and Diversification of Genes with Specialised Functions," Trends in Genetics 19 (2003): 530-6.

(29) N. de Parseval and T. Heidmann, "Human Endogenous Retroviruses: From Infectious Elements to Human Genes," Cytogenetic and Genome Research 110 (2005): 318-32.

(30) F. Mallet, O. Bouton, S.Prudhommeet al., "The Endogenous Locus ERVWE1 Is a Bona Fide Gene Involved in Hominoid Placental Physiology," Proceedings of the National Academy of Sciences of the USA 101 (2004): 1731-6; B. Bonnaud, O. Bouton, G. Oriol et al., "Evidence of Selection on the Domesticated ERVWE1 env Retroviral Element Involved in Placentation," Molecular Biology and Evolution 21 (2004): 1895-901; S. Prudhomme, G. Oriol, and F. Mallet, "A Retroviral Promoter and a Cellular Enhancer Define a Bipartite Element Which Controls env ERVWE1 Placental Expression," Journal of Virology 78 (2004): 12157-68; M. Caceres, NISC Comparative Sequencing Program, and J. W. Thomas, "The Gene of Retroviral Origin Syncytin 1 Is Specific to Hominoids and Is Inactive in Old World Monkeys," Journal of Heredity 97 (2006): 100-6; B. Bonnaud, J. Beliaeff, O. Bouton et al., "Natural History of the ERVWE1 Endogenous Retroviral Locus," Retrovirology 2 (2005): 57; A. Muir, A. M. L. Lever, and A. Moffett, "Human Endogenous Retrovirus-W Envelope (syncytin) Is Expressed in Both Villous and Extravillous Trophoblast Populations," Journal of General Virology 87 (2006): 2067-71.

(31) M. Langbein, R. Strick, P. L. Strissel et al., "Impaired Cytotrophoblast Cell--Cell Fusion Is Associated with Reduced Syncytin and Increased Apoptosis in Patients with Placental Dysfunction," Molecular Reproduction and Development 75 (2008): 175-83; K. A. Dunlap,M. Palmarini,M. Varela et al., "Endogenous Retroviruses Regulate Periimplantation Placental Growth and Differentiation," Proceedings of the National Academy of Sciences of the USA 103 (2006): 14390-5.

(32) Bonnaud, Beliaeff, Bouton et al., "Natural History of the ERVWE1 Endogenous Retroviral Locus."

(33) S. Suzuki, R. Ono, T. Narita et al., "Retrotransposon Silencing by DNA Methylation Can Drive Mammalian Genomic Imprinting," PLoS Genetics 3 (2007): 531-7.

(34) V. Y. Kuryshev, B. V. Skryabin, J. Kremerskothen et al., "Birth of a Gene: Locus of Neuronal BC200 snmRNA in Three Prosimians and Human BC200 Pseudogenes as Archives of Change in the Anthropoidea Lineage," Journal of Molecular Biology 309 (2001): 1049-66; T. Khanam, T. S. Rozhdestvensky, N. Bundman et al., "Two Primate-Specific Small Non-protein-Coding RNAs in Transgenic Mice: Neuronal Expression, Subcellular Localization and Binding Partners," Nucleic Acids Research 35 (2007): 529-39; A. Courseaux and J.-L. Nahon, "Birth of Two Chimeric Genes in the Hominidae Lineage," Science 291 (2001): 1293-97.

(35) S. S. Singer, D. N. Mannel, T. Hehlgans et al., "From 'Junk' to Gene: Curriculum vitae of a Primate Receptor Isoform Gene," Journal of Molecular Biology 341 (2004): 883-6; M. Krull, J. Brosius, and J. Schmitz, "Alu-SINE Exonization: En Route to Protein- Coding Function," Molecular Biology and Evolution 22 (2005): 1702-11; G. Mola, V. Vela, M. I. Fernandez-Figueras et al., "Exonization of Alu-Generated Splice Variants in the Survivin Gene of Human and Non-human Primates," Journal of Molecular Biology 366 (2007): 1055-63.

(36) M. Krull, M. Petrusma, W. Makalowski et al., "Functional Persistence of Exonised Mammalian-Wide Interspersed Repeat Elements," Genome 17 (2007): 1139-45; A. M. Santangelo, F. S. J. de Souza, L. F. Franchini et al., "Ancient Exaptation of a CORE-SINE Retroposon into a Highly Conserved Mammalian Neuronal Enhancer of the Proopiomelanocortin Gene," PLoS Genetics 3 (2007): e166.

(37) G. Bejerano, C. B. Lowe, N. Ahituv et al., "A Distal Enhancer and an Ultraconserved Exon Are Derived from a Novel Retroposon," Nature 441 (2006): 87-90; M. Kamal, X. Xie, and E. Lander, "A Large Family of Ancient Repeat Elements in the Human Genome Is Under Strong Selection," Proceedings of the National Academy of Sciences of the USA 103 (2006): 2740-5; C. B. Lowe, G. Bejerano, and D. Haussler, "Thousands of Mobile Element Fragments Undergo Strong Purifying Selection near Developmental Genes," Proceedings of the National Academy of Sciences of the USA 104 (2007): 8005-10; A. J. Gentles, M. J. Wakefield, O. Kohany et al., "Evolutionary Dynamics of Ttransposable Elements in the Short-tailed Opossum Monodelphia domestica," Genome Research 17 (2007): 992-1004.

(38) Mola, Vela, Fernandez-Figueras et al., "Exonization of Alu- Generated Splice Variants in the Survivin Gene of Human and Nonhuman Primates."

(39) D. Zheng and M. B. Gerstein, "The Ambiguous Boundary between Genes and Pseudogenes: The Dead Rise Up, Or Do They?" Trends in Genetics 23 (2007): 219-24; D. Zheng, A. Frankish, R. Baertsch et al., "Pseudogenes in the ENCODE Regions: Consensus Annotation, Analysis of Transcription, and Evolution," Genome Research 17 (2007): 839-51.

(40) Y. Lee, T. Ise, D. Ha et al., "Evolution and Expression of Chimeric POTE-Actin Genes in the Human Genome," Proceedings of the National Academy of Sciences of the USA 103 (2006): 17885-90.

(41) Ibid.

(42) D. V. Babushok,K. Ohshima, E.M. Ostertag et al., "A Novel Testis-binding Protein Gene Arose by Exon Shuffling in Hominoids," Genome 17 (2007): 1129-38; F. Burki and H. Kaessmann, "Birth and Adaptive Evolution of a Hominoid Gene That Supports High Neurotransmitter Flux," Nature Genetics 36 (2004): 1061-3. Note that the African apes include humans, chimps, bonobos, and gorillas; the great apes include, in addition, the orangutan; and the apes include, in addition, the gibbons and siamangs.

(43) A. C. Marques, I. Dupanloup,N. Vinckenbosch et al., "Emergence of YoungHumanGenes after a Burst of Retroposition in Primates," PLoS Biology 3 (2005): 1970-9; N. Vinckenbosch, I. Dupanloup, and H. Kaessmann, "Evolutionary Fate of Retrotransposed Gene Copies in the Human Genome," Proceedings of the National Academy of Sciences of the USA 103 (2006): 3220-5.

(44) C. Luo, X. Lu, L. Stubbs, and J. Kim, "Rapid Evolution of a Recently Retroposed Transcription Factor YY2 in Mammalian Genomes," Genomics 87 (2006): 348-55; J. D. Kim, C. Faulk, and J. Kim, "Retroposition and Evolution of the DNA-binding Motifs of YY1, YY2, and REX1," Nucleic Acids Research 35 (2007): 3442-52.

(45) H. Sakai, K. O. Koyanagi, Y. Imanishi et al., "Frequent Emergence and Functional Resurrection of Processed Pseudogenes in the Human and Mouse Genomes," Gene 389 (2007): 196-203; A. J. Wood, R. G. Roberts, D.Monk et al., "A Screen for Retrotransposed Imprinted Genes Reveals an Association between X Chromosome Homology and Maternal Germ-Line Methylation," PLoS Genetics 3 (2007): 0192-203. A table of seventy-four potentially active retrogenes is available on the journal website under "Supporting Information."

(46) J. Perreault, J.-F. Noel, F. Briere et al., "Retropseudogenes Derived from the Human Ro/SS-A Autoantigen-Associated hY RNAs," Nucleic Acids Research 33 (2005): 2032-41; J. Schmitz, G. Churakov, H. Zischler, and J. Brosius, "A Novel Class of Mammalian-Specific Tailless Retropseudogenes," Genome Research 14 (2004) 1911-5; M. J. Weber, "Mammalian Small Nucleolar RNAs Are Mobile Genetic Elements," PLoS Genetics 2 (2006): e205; Y. Luo and S. Li, "Genome-Wide Analyses of Retrogenes Derived from the Human Box H/ACA snoRNAs," Nucleic Acids Research 35 (2007): 559-71; E. J. Devor, "Primate MicroRNAs miR-220 and miR-492 Lie within Processed Pseudogenes," Journal of Heredity 97 (2006): 186-90.

(47) Bejerano, Lowe, Ahituv et al., "A Distal Enhancer and an Ultra-conserved Exon Are Derived from a Novel Retroposon"; Kamal, Xie, and Lander, "A Large Family of Ancient Repeat Elements in the Human Genome Is Under Strong Selection"; Lowe, Bejerano, and Haussler, "Thousands of Mobile Element Fragments Undergo Strong Purifying Selection near Developmental Genes"; Gentles, Wakefield, Kohany et al., "Evolutionary Dynamics of Ttransposable Elements in the Short-tailed Opossum Monodelphia domestica."

(48) This discussion has paid little attention to how mutational events have provided regulatory content to our genomes. For example, inserted transposable elements have contributed many short sequences that act as binding sites for proteins that activate genes. See P. Polak and E. Domany, "Alu Elements Contain Many Binding Sites for Transcription Factors and May Play a Role in Regulation of Developmental Processes," BMC Genomics 7 (2006): 133; T. Wang, C. B. Lowe, R. G. Sellers et al., "Species-Specific Endogenous Retroviruses Shape the Transcriptional Network of the Human Tumor Suppressor Protein p53," Proceedings of the National Academy of Sciences of the USA 104 (2007): 18613-8; D. Laperriere, T. T. Wang, J. H. White, and S. Mader, "Widespread Alu Repeat-Driven Expansion of Consensus DR2 Retinoic Acid Response Elements During Primate Evolution," BMC Genomics 8 (2007): 23; A. B. Conley,W. J. Miller, and I. K. Jordan, "Human Cis Natural Antisense Transcripts Initiated by Transposable Elements," Trends in Genetics 24 (2008): 53-6. Given that transposable elements have contributed profoundly towards the unique biology of the human species, a study of their effects might be expected to point to the way by which irreducible complexity evolves.

(49) J. Polkinghorne, One World: The Interaction of Science and Theology (London: SPCK, 1986), 22-3.

(50) N. T. Wright, The New Testament and the People of God (Minneapolis: Fortress, 1992), 35-7.

(51) O. Gingerich, God's Universe (Cambridge, MA: Belknap Press, 2006): 91-2.

(52) F. S. Collins, The Language of God (New York: Free Press, 2006), 136-8.

(53) D. C. Spanner, Biblical Creation and the Theory of Evolution (Exeter: Paternoster, 1987), chap. 4.

(54) A. Konig, New and Greater Things, 132-3.

(55) H. J. Van Till, The Fourth Day (Grand Rapids: Eerdmans, 1986), 226-7; 246-7.

(56) D. M. MacKay, The Clockwork Image (London: InterVarsity Press, 1974), 60.

(57) Van Till, The Fourth Day, 256.

(58) J. Polkinghorne, Science and Christian Belief (London: SPCK, 1994), 76-7.

(59) Chen, Stenson, Cooper, and Ferec, "A Systematic Study of LINE-1 Endonuclease-Dependent Retrotranspositional Events Causing Human Genetic Disease"; Chen, Ferec, and Cooper, "LINE-1 Endonuclease-Dependent Retrotranspositional Events Causing HumanGenetic Disease"; Callinan and Batzer, "Retrotransposable Elements and Human Disease"; Babushok and Kazazian, "Progress in Understanding the Biology of the Human Mutagen LINE-1."

(60) W. P. Pawlowski and W. Z. Cande, "Coordinating the Events of the Meiotic Prophase," Trends in Cell Biology 15 (2005): 674-81; R. U. Vallente, E. Y. Cheng, and T. J. Hassold, "The Synaptonemal Complex and Meiotic Recombination in Humans: New Approaches to Old Questions," Chromosoma 115 (2006): 241-9.

(61) A. Peacocke, God and the New Biology (London and Melbourne: J. M. Dent and Sons, 1986), 62-5; J. Polkinghorne, Science and Creation (London: SPCK, 1989), 47 f.; J. Wright, Designer Universe (Crowborough: Monarch, 1994), 42, 61-83.

(62) H. Rolston III, Genes, Genesis and God: Values and Their Origins in Natural and Human History (Cambridge: Cambridge University Press, 1999), 34 f.

(63) Gingerich, God's Universe, 100-1; Rolston, Genes, Genesis and God, 367-70.

(64) MacKay, Clockwork Image, 49; Spanner, Biblical Creation, 48-9.

(65) D. Kidner, Proverbs: An Introduction and Commentary (London: Tyndale, 1964), 84; as, for example, when the land was allotted, Josh. 14:1, 2.

(66) A. Konig, E. van Niekerk, and D. F. Olivier, Doctrine of Creation (Pretoria: University of South Africa, 1986), chap. 29.

(67) A. McGrath, Science and Religion: An Introduction (Oxford: Blackwell, 2005), 104-5.

(68) C. B. Kaiser,"The Early Christian Belief in Creation: Background for the Origins and Assessment of Modern Western Science," Horizons of Biblical Theology 9, no. 2 (1987): 1-30, esp. pp. 3-4; C. B. Kaiser, Creation and the History of Science (Grand Rapids: Eerdmans, 1991), 15 f.

(69) Polkinghorne, Science and Creation, 63.

(70) Rolston, Genes, Genesis and God, 370. The world is not a watch; there is no watchmaker. God acts in grace as a covenant partner, not a technician.

(71) Konig, van Niekerk, and Olivier, Doctrine of Creation, 327.

(72) Konig, van Niekerk, and Olivier, Doctrine of Creation.

(73) Rolston, Genes, Genesis and God, chap.1, esp. pp. 50-3.

(74) C. Schwobel, God: Action and Revelation (Kampen: Pharos, 1992), 31.

(75) J. Polkinghorne, Reason and Reality (London: SPCK, 1991), 84; J. Polkinghorne, Science and Christian Belief (London: SPCK, 1994), 83-5.

(76) D. N. Livingstone, Darwin's Forgotten Defenders (Grand Rapids: Eerdmans, 1987), 116-7.

(77) D. N. Livingstone and M. A. Noll, "B. B. Warfield (1851-1921): A Biblical Inerrantist as Evolutionist," Isis 91 (2000): 283-304.

(78) A. Konig, Here I am: A Believer's Reflection on God (Grand Rapids: Eerdmans, 1982), esp. chap. 3.

(79) H. Butterfield, Christianity and History (London and Glasgow: Fontana, 1957), 140-1.

Graeme Finlay has worked as a cell biologist in the Auckland Cancer Society Research Centre for twenty-five years. Since 2000, he has been Senior Lecturer in scientific pathology in the Department of Molecular Medicine and Pathology, University of Auckland. His reading and teaching of cancer genetics led to an interest in comparative primate genetics. He has sought to increase awareness of the evidence for human evolution, and the compatibility of these findings with Christian theology. He delivered the termly lecture in science and religion on "Human Genetics and the Image of God," in the Faraday Institute, University of Cambridge, November 2006.
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Date:Jun 1, 2008
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