Ernst Haeckel (1834-1919), the main propagandist for evolution in Germany, was one of the first scientists to propose a model for the development of multicellular organisms from unicellular ancestors. He proposed that the embryological development of animals today reflects the past development in terms of its evolution. This concept is termed the biogenetic law, which states the following:

Ontogeny [development of the individual] is a concise and compressed recapitulation of phylogeny [the ancestral sequence]...The organic individual repeats during the rapid and short course of its individual development, the most important of the form changes which its ancestors traversed during the long and slow course of their palaeontological evolution according to the laws of heredity and adaptation.ⁱ

Haeckel proposed that organisms go through a series of stages during their ontogeny that resemble the adult forms of phylogenetic ancestors, but as the facts do not always fit the proposal, Von Baer's suggestion that young stages resemble young ancestral stages enjoys wider acceptance.

Haeckel's theory is largely discredited today on various morphological grounds, but it is also not tenable in terms of genetics. Evolution is based on genetic change through mutations over time. Recapitulation requires both retention of the ancestral features and change. Just because homologies appear to exist (homology refers to the similarity of biological features in different species or groups because of their descent from a common ancestor) does not mean that structures are indeed homologous. As Michael Denton points out, homologous organs and structures may develop by radically different embryogenic routes, and "the evolutionary basis of homology is perhaps even more severely damaged by the discovery that apparently homologous structures are specified by quite different genes in different species."ⁱⁱ 

Ernst Haeckel also proposed a mechanism whereby unicellular organisms may have evolved to form multicellular, and eventually multi-layered organisms. This theory is known as the Gastraea Hypothesis. Today, the Planula Hypothesis, a variant of the Gastraea Hypothesis, is more popular, but the problems remain the same as for the Gastraea Hypothesis of Ernst Haeckel.

Using the embryology of metazoa as a model, Haeckel proposed that multicellular organisms evolved from hypothetical unicellular organisms which he called Cytaea. Eventually these cells remained attached after cell division and a multicellular organism which he termed Moraea evolved. The Moraea gave rise to a jelly-filled hollow ball of cells, called Blastaea which developed an indentation on one side and thus gave rise to the Depaea. Through completion of the indentation, the Depaea gave rise to the Gastraea.

The Gastraea then underwent further differentiation. A third layer of cells developed between the original germ layers. It is proposed that this layer, the mesoderm, arose through cellular migration from the outer ectoderm and inner endoderm, thus giving rise to triploblastic organisms (animals with three layers) which would then also have evolved bilateral symmetry after becoming bottom dwellers. Associated with the change in structure there would also have occurred cellular differentiation and specialization, thus giving rise to complex organisms where cells became arranged into organ systems.

For most of these proposed ancestral forms, analogous living forms are presented as evidence for the viability of such organisms. The Cytaea could have resembled living protozoa of the Class Mastigophora, the Moraea represents colonial protozoa such as Pandorina, the Blastaea in turn can be compared to colonial protozoa such as Volvox. The evolution of subsequent stages would have required some complex changes, and it is proposed that the modes of feeding and locomotion of the ancestral types would have affected further differentiation. The bottom dwelling triploblastic animals that developed bilateral symmetry could be compared to present day flatworms.

On the basis of morphology, this theory seems to provide a reasonable pictures of how events may have proceeded during the evolution of multicellular organisms, but at the genetic level, there are serious obstacles. In order to survive as living cells, the early ancestral cells needed a genotype (complement of genes) capable of producing all the relevant proteins required to fulfil their physiological and structural needs. These early cells would have had genes coding for all the essential enzymes required to maintain the physiological processes and genes coding for all the necessary proteins involved in the structure or morphology of the cells. Previously, we discussed the problems that would have precluded the evolution of such a cell, but for the sake of this argument, we will assume that such a cell did in fact arise. Furthermore, it is not too difficult to imagine that a situation could have arisen where cells remained stuck together after cell division, thus resulting in multicellular colonies with the cells embedded in a common matrix. Problems arise, however, when the evolution of cell differentiation and eventual specialization are considered. If the colony arose through cell division, then each of the original colonial cells would have had the same genetic composition, coding for the simplest of cells.

The evolution of specialized cells requires that the different cells also evolve different morphologies and specialized structures dictated by their function. New and diverse morphological and physiological features had to develop as the organisms became more and more complex. The simple colonies would thus eventually consist of more than one cell type. In order to ensure continuity, the genetic changes would have to be transferable to subsequence, generations which in turn requires a far more complex gene arrangement than existed in the unicellular organism. All the variants would have to be located in each cell, with the possibility for selective activation of one or the other batteries of genes.

Assuming that the new genes somehow did evolve, and the organism was endowed with different sets of genes governing the different morphological expressions, there would then be an even greater obstacle to overcome, namely selection. The genes of cells in particular situations would have one set of genes activated and cells in another situation would have the alternative genes activated. As a comparison, in organisms living today, nerve cells have a set of genes activated which distinguish them morphologically and physiologically from liver cells, which have a different part of the genome activated, although both possess the full gene complement.

This differential activation of either the one battery of genes or the other requires a complex system of controlling genes, which would all have to come about by chance, but natural selection can only operate at the level of the phenotype. The chances of all the new genes and controlling genes coming into existence by chance are extremely remote. The probability of just one function gene arising by random chance process is less than one in the number of particles in the entire universe. In fact, it is more probable for an explosion in a woodpile to construct a functional house by chance than it is for just one such new gene to come about by random chance processes. Moreover, one would have to postulate the same scenario thousands of times as cell differentiation increased. This requires a great deal of faith.

The complexity of the genetic requirements for just two different cell types to coexist within an organism is awesome, as can be illustrated by the following example.

If we look at the relationship between a muscle cell and a nerve cell, then it is obvious that there is a great deal of morphological and functional difference between the two. This requires different gene complements to be activated in the two cell types.

Of course, these two cell types would have to cooperate with each other in the living organism in order to be of any value to the organism. Also remember that at the level of the genotype, the processes occur by chance and natural selection can only come into play once the phenotype has been produced. We are not dealing with just a simple genetic variance to achieve these goals, but a hose of new genes is required to allow just these two cell types to coexist, let alone the thousands of cell types present in complex multicellular organisms.

For just these two cells, the following genes are required at minimum:

1. Promoter genes enabling the selective activation of either the one or the other. In nerve cells, only those genes which are required for nerve cells will be activated. In muscle cells only those required by muscle cells will be activated.

2. Genes, or DNA sequences, which are sensitive to the environmental cues.
3. Genes which will govern the cooperation between the two cell types. This is a very complex arrangement. The two cells would have to link up morphologically in order for the one to activate the other, and there would have to be receptors that enable transfer of information from one to the other.

    

Where did all these genes come from? The first simple organism required more of these genes which make cooperation between different cells possible. As natural selection does not operate at the level of the genotype, and cannot create anything anyways (only sort out that which is already there), these genes had to come about by either chance or design. Considering the complexity of the system, design seems to be the only option. Haeckel's Gastraea theory is based on a simple morphological sequence, which looks good on paper, but is untenable.

Genotype Phenotype

Let us briefly discuss the various ways in which variation is increased today:

1. Built in variation in the gene pool.

For most character traits present in organisms, more than one allele exists. The different genes must have come about by chance alone, because we are dealing with genotype. The genotype of an organism includes both latent and patent genes. Only genes that have been activated are expressed in the phenotype. A new gene must first be expressed before natural selection comes into play.

As far as alleles are concerned, expression is governed by a complex system of dominance versus recessiveness. Furthermore, the frequency of genetic expression can also alter the phenotype. For example, the gene coding for growth hormone can influence the size of the organism. Variation in size does thus not necessarily require new genes, just differential expression of the same genes. An example of built-in variation in the gene pool can be seen in the various breeds of dogs. As to how the genes responsible for the variation came in to existence, chance or design are the only options given, since we are dealing with genotype.

By selecting from the built-in natural variation of the gene pool, various breeds of dogs and domestic cattle were produced. Great changes in physiology and morphology are involved, and evolution is here certainly excluded. Differences in dogs are greater than the differences in genera of the family Canidae.ⁱⁱⁱ 

From a creationist perspective, the vast initial gene pool makes possible a vast range of adaptive morphologies and physiologies. This general gene pool is called "kind" in the Bible. Adaptive radiation as observed by evolutionists is thus nothing other than the end product of sorting the gene pool by extraneous factors, such as differences in climate and habitat. Gene patterns suited to the environment are selected and change is rapid. Genetic expression is also influenced, so as to bring about differences in structural expression by the genes in terms of size. Differential hormonal modulation in response to "Zeitgebers" (an environmental stimulus that initiates a hormonal process) can alter the time and magnitude of response, effectively producing reproductively isolated communities which would be regarded as different species by evolutionists, but are in effect merely extremes of genetic expression within an existing gene pool. The vast numbers of latent genes would then be accounted for.

Evolutionists recognize that changes in genotype frequencies do occur to produce changes in gene distribution as predicted by the Hardy-Weinberg law. They, however, explain most changes as resulting from chance mutations, and this is not tenable.

Even evolutionists admit that preadaptation must have played a major role in enabling organisms to survive environmental changes. Preadaptation, however, requires preexisting genes capable of responding to environmental stimuli—precisely what creationists claim. Where did these fully expressional genes come from? Once again, chance or design are the only options.

2. Variation is increased by reproductive exchange.

This statement is more than a mouthful in terms of its genetic implications. Through sexual reproduction, genetic material is exchanged. This induces genetic recombination. The significance of this is obvious; the exchange of material increases the variation. This holds particular advantages to populations and is considered by evolutionists to be an innovation that greatly enhances the evolutionary process.

We know what sexual reproduction achieves; it increases the variation. However, increased variation in the genotype is of no value until it is expressed in the phenotype. The new varieties must be expressed in the offspring before natural selection can feast on this increased variation. The process that brings about the variation (sexual reproduction) is not subject to selection, only the result thereof (the increased variation in the offspring) is subject to selection.

Again, we are faced with the awesome question, how did sexual reproduction arise? If the process was not subject to selection, then only two options remain: chance or design. It requires a great deal of faith to believe in the chance development of sexual reproduction. At the genetic level, sexual reproduction is extremely complex and scientists have investigated these processes with a sense of wonder.

The exchange of gametes (sex cells) requires a modified form of cell division which is the process of meiosis. During meiosis, the number of chromosomes is halved, resulting in the gametes having half the chromosomes. Sexual fusion of two gametes then restores the diploid number of chromosomes. Variation in the genome is greatly increased by two processes occurring during meiosis: independent assortment and crossing over. Both these processes are extremely complex, but in themselves are not subject to selection. They rearrange the genetic material, resulting in new combinations of the material. As this reshuffling occurs at the level of the genotype, it is not subject to natural selection until the new combinations have been expressed in the phenotype. 

i) Independent Assortment

Independent assortment is achieved when chromosomes line up in homologous pairs and move independently to the one pole or the other. The process is governed by complex enzyme systems which in turn must also have come about by chance. The possible variation that can be achieved by independent assortment depends on the number of chromosomes present. In humans, there are 46 chromosomes, which would arrange themselves in 23 homologous pairs. The variations that can be achieved are thus: 223 x 223 = 80 trillion. (23 pairs of chromosomes of which each chromosome could move in either of two directions.)

ii) Crossing Over

Crossing over is an awe-inspiring process. When homologous chromosomes are lined up during meiosis, they can, in a very precise way, exchange genetic material. There are five steps in achieving this:

a) Enzymes open the double helix of DNA in the aligned chromosomes to permit intermolecular base pairing.

b) One strand of each helix is cut at equivalent positions.

c) The enzyme ligase joins them to form a half chromatid chiasma (because only one strand of each chromatid cross over), resulting in a cross-shaped molecule.

d) The cross-shaped molecule is cut in half by an enzyme, leaving a break in one strand of each recombinant.

e) The break is sealed by ligase.

The process has to be extremely precise. If even one nucleotide is transferred incorrectly, the genetic message becomes useless. A typical textbook description for the process will illustrate this complexity:

A normal crossover is really a miraculous process. Somehow the genetic material from one parental chromosome and the genetic material from the other parental chromosome are cut up and pasted together during each meiosis, and this is done with complete reciprocity. In other words, neither chromosome gains or loses any genes in the process. In fact, it is probably correct to say that neither chromosome gains or loses even one nucleotide in the exchange. How is this remarkable precision attained?...However, the process is complex (especially in eukaryotes) and the genes controlling it must be many.^iv  

It might be safely said that the crossing over process is more complex than anything man has ever designed. However, it would have had to come into existence by chance if the evolutionary paradigm is accepted. Chance or design are the options at this level, and chance requires more faith than most could muster.

3) Transposable elements increase the variation.

Transposable elements are sometimes called "jumping genes." They consist of segments of DNA that can move from one position on a chromosome to another. In 1951, Nobel prize-winning Dr. Barbara McClintock proposed that genes are not fixed on chromosomes, but that they can move around on the chromosome. At first her findings were discarded because they contradicted the genetic concept of the day. Today, her discovery of what she calls transposable elements has an established place in science. Through transposable elements, we know that R factors can transmit antibiotic resistance and increased variation. The genes move because they are part of a small circular auxiliary genome called a plasmid, which enters and leaves the main genome at a specific place where there is a nucleotide sequence that is also present on the plasmid. Other genes move within small fragments of the genome called transposons. Together, transposons and plasmids produce genetic recombinations.

Integration at a new position also transfers the gene to that new position. The repositioning may be random, but occurs at sequence-specific insertion points which means that the process is orderly. The splicing and repositioning is carried out by enzyme systems and involves the transfer of complete information.

4) Variation is increased by the recombination of chromosomes.

Changes in chromosomal structure have been cited as important contributing factors in providing variation, and as a mechanism for speciation. Changes in chromosomes can include changes in chromosome number, arm number, translocation, deletions, duplications, inversions, or even radical reorganization of the genome.

It is important to note that none of these create any new material, they just rearrange or duplicate the existing material.

All mechanisms that produce variation rely on existing genetic material. None of them were subject to selection, and each of them had to come about by chance or design. 

The faith required to believe that any one of these mechanisms, let alone all of them, came about by chance is extraordinary. If design is the option chosen, then obviously variation of organisms is a hallmark of tCreation. God did not then create immutable, unchangeable species, but rather an enormous capacity for change.

The question is no longer whether chance can take place or not, but rather how much change and where are the limits. Also how rapidly can the change take place and what does it entail? The modern classification system is largely based on resemblance's of species on the morphological level, and current biochemical approaches often contradict the morphological approach. Recent examples are inconsistencies between molecular and morphological data in the classification of mice; contradictions in molecular and morphological phylogenies of rodents, rabbits, and primates; and even conflicting classifications in whales.^v,vi,vii 

Present-day mechanisms that prevent most species from crossbreeding are cited to have evolved over long periods of time to maintain the integrity of a species. There are, however, many ways in which these could develop rapidly by reshuffling the existing genome. The flexibility of the genome allows for very rapid change that has nothing to do with evolution, but rather with the built-in capacity for variation.

The Biblical concept of a "kind" must also be redefined as a consequence of the above data. A "kind" can obviously not be equated with a species, but rather with that of a higher taxonomic level such as the generic level and in some cases even the family level. In terms of Darwin's finches, Darwin was thus right when he postulated a common ancestry. The mechanism of change was, however, neither micro-evolution nor macro-evolution, but merely differential activation and reshuffling of the existing genome. No new material was added to the genome, as the capacity to produce variation was more than ample.

If the Creation model is correct, how did all the modern life forms attain their present status so rapidly after the deluge, and how did they disperse themselves over the planet?

i M.W. Strickberger, Evolution (Jones and Bartlett Publishers International, 1996).

ii Michael Denton, Evolution: A Theory in Crisis (London: The Hutchinson Publishing Group, 1985).

iii R.K. Wayne, "Cranial morphology of domestic and wild canids: the influence of development on morphological change," Evolution 40 (1986): 243-261.

iv D. Suzuki et al., An Introduction to Genetic Analysis (San Franscisco: W.H. Freeman and Company).

v P.C. Chevret et al., "Molecular evidence that the spiny mouse (Acomys) is more closely related to gerbils (Gerbillinae) than to true mice (Murinae)," Proceedings of the National Academy of Sciences 90 (1993):3433-3436.

vi D. Graur, "Molecular phylogeny and the higher classification of eutherian mammals" Trends in Ecology and Evolution 8 (1993):141-147. 

vii M.C. Milinkovitch, et al., "Revised phylogeny of whales suggested by mitochondrial ribosomal DNA sequences," Nature 361 (1993):346-348.

Updated January 2009.