Meiotic recombination—designed for inducing genomic change
Creationary biologists have recognized that the diversity seen within created kinds today cannot be adequately explained by the shuffling of pre-existing gene versions (alleles) and accidental errors that accumulate within the genome.1 Within the context of creation, the development of genetic diversity has been a means by which God has enabled his creatures to adapt to the many different environmental niches they occupy today (Genesis 1:22; 8:17; Isaiah 45:18). Further, it has played an important role in adding variety, beauty, and productivity in various domesticated plants and animals.2
There is certainly no logical reason to believe that unguided chance processes can bring about a functional genome.3 Neither is there sound reason to believe that accidental changes to the genome are a productive source of useful genetic diversity. Logically, therefore, the genome must contain biological information that allows it to induce variation from within.4 One mechanism involved in this is meiotic recombination.5 Continued scientific research is elucidating some amazing details of this process.
Meiosis is a special type of cell division necessary for the formation of gametes (eggs or sperm) so sexual reproduction can take place. In most plants and animals, chromosomes come in pairs (homologs, one derived from each parent), but gametes only carry one of each homolog. Early in meiosis, each chromosome must be drawn to its homolog and stably pair. Then each homolog will be pulled in the opposite direction so that the two cells that form during the division will have exactly one of each homolog.
Meiotic recombination is no accident
God designed meiosis in a way that naturally tends to increase diversity. In order for the chromosomes to stably pair, recombination occurs between the homologs. The process is initiated by an enzyme which cuts the DNA on one homolog, forming a double-stranded break. Then each side of the break is resected in one direction. This leaves two tails, which are important in repairing the break (figure 1).
There are several pathways by which the break can be repaired. The best known resolution of the break is called crossing over. For this to occur, both of the tails must invade the homolog to form a double Holliday junction (dHJ). DNA synthesis occurs extending these tails. Then, depending on which enzymes are used to cut this structure apart, the distal ends of the chromosomes are swapped.
This swapping between homologs is important in helping to shuffle alleles, which allows for new combinations that may be advantageous. The method of DNA repair described above is known as double-stranded break repair (DSBR). It does not always result in crossing over. A different enzyme can be used to cut the dHJ at a different location and gene conversion will result instead. In gene conversion, a segment from one homolog is copied onto the other. A second pathway for resolving double-stranded breaks is called synthesis-dependent strand annealing (SDSA). In this circumstance only one tail invades the intact homolog and gene conversion is the result.6
Meiotic recombination is mutagenic
Technically, swapping portions of a chromosome and gene conversion are mutations when they alter the nucleotide sequence. Other mutations can also occur during the repair of double-stranded breaks. It appears to be more common with gene conversion. One study in yeast revealed a mutation rate 1,000 times higher during gene conversion than the normal spontaneous mutation rate for that locus. Most mutations were base pair substitutions. About 40% of the mutations were attributable to some form of template switching. In yeast strains with a proofreading defect in a DNA polymerase, template switch mutations were absent.7 This suggests that template switching is a complex, enzyme-driven process.
There is a bias to where meiotic recombination occurs. In a study of Drosophila, crossing over tended to occur in specific hot spots, but these were not influenced by whether or not it was a genic region. Gene conversion had a more uniform distribution, was more common among genic sequences, and was seen where crossing over was rare or absent. The authors emphasized the importance of having information on rates of recombination to include in population genetics models.8 Studies in plants indicate that a variety of genetic and epigenetic factors influence the frequency of crossing over.9
There are several other pathways by which double-stranded breaks can be repaired. One of the most interesting and mutagenic is break-induced replication (BIR). It has been shown to produce complex rearrangements including copy number variation (CNV) and non-reciprocal translocations. These often involve multiple rounds of template switching. Specific endonucleases are necessary for proper BIR; an absence of these endonucleases has been shown to significantly reduce template switching.10
Significance of mutations
At times mutations are explained as the result of accidents which introduce errors into the DNA sequence. The concept of non-directed change is foundational in the standard evolutionary model. Logically, accidental changes in a complex system should be consistently harmful to some degree. Creationists have pointed this out in emphasizing the implausibility of accidents in accounting for the complexity of life.
However, when diversity is examined within a creation model, it is evident that significant diversity has arisen since the time of the Flood. In contrast to the notion that all mutations are harmful, the observed diversity does not appear to be typically harmful, and much is considered to be healthy. It has been pointed out that this useful diversity is not logically the result of accidents, but some designed mechanism(s) must be producing it.1
Several specific examples are worth noting. In a gene influencing coat colour, a pattern of in-frame indel (insertion or deletion) mutations was noted across several unrelated kinds. These generally result in a black coat colour. Statistically, only one in three indels should be in-frame. It does not appear that natural selection can explain this bias toward in-frame indels, and so a designed mechanism was suggested as its source.11
Resistance to organophosporous insecticides has been studied in sheep blowflies. There is a particular gene where specific mutations can confer resistance to one organophosphate or another. Resistance to one of these insecticides (malathion) was identified in pinned specimens that pre-dated the first use of that insecticide; therefore, selection would be a reasonable explanation for how it spread in the fly population. Resistance to a second insecticide (diazinon) appears to have arisen by mutation since the insecticide was introduced. This rapid appearance of resistance is quite impressive (though disheartening for those trying to get rid of this pest). In addition to this, flies have emerged that are resistant to both insecticides as a result of gene duplication (a form of CNV). It appears that such gene duplications have arisen at least three separate times in these flies, and always involve the resistant alleles.12
The point here is that the mutagenic nature of meiosis appears to provide a plausible mechanism for inducing this type of variation within a creationary timeframe. The requirement of specific enzymes and non-random pattern of change in meiotic recombination suggests it could play a significant role in producing the observed useful genetic diversity.
Gene conversion, a designed mechanism which can result in fixation of alleles
Gene conversion can lead to a transmission distortion, a deviation from the expected ratio of alleles in the gametes. Studies in mice revealed an example of this due to a preferential induction of double-stranded breaks on one homolog, which yielded an over-transmission of the allele from the other. Given the distortion, population simulations predicted that the favoured allele would be fixed in the population in less than 1,200 generations.6
Transmission distortion is extremely significant. Most models attempting to explain the changes in allele frequency of a population assume that a heterozygous parent would have an equal chance of passing either of the alleles on to the offspring. The fixation of alleles within a population is generally attributed to natural selection, although genetic drift is also recognized as a possibility. These are naturalistic explanations that fit well within the ‘anti-designer’ presuppositions of the evolutionary model.
Despite the appeal of scenarios crediting natural selection, they may have little semblance to reality if designed mechanisms are involved in changing allele frequencies. One example in animals would be migration. Perhaps animals move to where they are most comfortable because God gave them the wisdom to do so, thus enabling them to survive and reproduce. This comfort factor may be related to having a genotype compatible with (adapted to) that environment. So essentially, animals with adaptive alleles stay, and the others leave. This is rather the reverse of natural selection (where the environment ‘selects’ the animals), as it is the animal making a conscious choice.
Transmission distortion due to gene conversion, as described above in mice, may also prove to be an important mechanism for fixation of adaptive alleles in populations. If this turns out to be the case, it is a serious problem for evolutionists. It would be another major blow to the view that naturalistic processes adequately explain the origin of new species. Instead, designed mechanisms would be important for both the generation of diversity and fixing adaptive alleles within a population. If designed processes are necessary for adaptive changes even within created kinds, it points again to an awesome Creator!
One thing is clear; the evolutionary based inference that mutations (any change in the DNA sequence) are always accidents or copying errors is false. Changes in DNA sequence can arise for a number of reasons. One reason is that meiotic recombination, an essential step in reproduction for many plants and animals, is designed to induce genetic changes. This is highlighted by the fact that enzymes are necessary for this complex processes, including enzymes which induce the double-stranded breaks and facilitate template switching. Since this is the case, I fully expect that better understanding meiotic recombination will be one piece in the puzzle to better understanding how diversity has risen so quickly within created kinds since the time of the Flood.
- Lightner, J.K., Karyotypic and allelic diversity within the canid baramin (Canidae), J. Creation 23(1):94–98, 2009. Return to text.
- Lightner, J.K., The effect of mutations down on the Farm, Answers in Depth 5(1), 2010, www.answersingenesis.org/articles/aid/v5/n1/effect-of-mutations-down-on-farm, accessed 27 December 2012. Return to text.
- Such reasoning only ‘makes sense’ if one is grossly ignorant of the complexity of the genome and/or refusing to consider the possibility of a creator; Romans 1:16–22. Return to text.
- Terborg, P., The design of life: part 3 an introduction to variation-inducing genetic elements, J. Creation 23(1):99–106, 2009. Return to text.
- Ashcraft, C.W., Genetic variability by design, J. Creation (formerly TJ) 18(2):98–104, 2004. Return to text.
- Cole, F., Keeney, S. and Jasin, M., Preaching about the converted: how meiotic gene conversion influences genomic diversity, Annals of the New York Academy of Sciences 1267:95–102, 2012. Return to text.
- Malkova, A. and Haber, J.E., Mutations arise during repair of chromosome breaks, Annual Review of Genetics 46:455–473, 2012. Return to text.
- Comeron, J.M., Ratnappan, R. and Bailin, S., The many landscapes of recombination in Drosophila melanogaster, PLoS Genetics 8(10):e1002905, 2012. Return to text.
- Henderson, I.R., Control of meiotic recombination frequency in plant genomes, Current Opinion in Plant Biology 15:556–561, 2012. Return to text.
- Pardo, B. and Aguilera, A., Complex chromosomal rearrangements mediated by breakinduced replication involve structure-selective endonucleases, PLoS Genetics 8(9):e1002979, 2012. Return to text.
- Lightner, J.K., Genetics of coat color I: The melanocortin 1 receptor (MC1R), Answers Research J. 1:109–116, 2008. Return to text.
- Lightner, J.K., Pattern of change over time: organophosphorous resistance in the Australian sheep blowfly, Lucilia cuprina, J. Creation 22(1):81–84, 2008. Return to text.
I am guessing here, but can some of these results be summarized as "Main stream evolution predicts there are random mutations of which natural selection selects the good mutations; but this Creationist Model predicts that there are also good mutations purposefully induced by a cell division algorithm".
Now it is not clear if the inducing algorithm is a non-decision making algorithm or a decision making one. An example of the former would be if the genome contained segments of compressed genetic data of which some can be randomly selected to be decompressed to form new alleles, thus making a predetermined change. An example of latter is if the cell determines whether a mutation is good or bad in systematic way, and only allows it if it is good; much like our immune system works out which foreign bodies are bad rather than this knowledge being preprogrammed into it.
There may be more than one variation inducing program in operation, but that in essence sums up the difference between neo-Darwinism and creation on the genome. As to what types of algorithms there may be, there may be examples of both, and may even be variation-inducing programs we have not yet thought of. We are still discovering whole coding conventions in the genome; it's not a stretch to think that there are a myriad classes of variation inducing programs that operate in the genome.
This information means that we creationists will have to be careful declaring that "mutations are almost always harmful/information-destroying". On the other hand, what a wonderful confirmation of God's creative power and ingenuity. It once more undercuts evolutionary arguments for the "origin of species" by chance alone, rather than by design.
We are talking about mutations that are regulated by the genome itself, right? So if the genome is inducing changes on itself and if we logically assume that it is not doing it randomly, are these changes actually existing genetic traits stored in the genome that are just being released by the genome's data compression/decompression mechanisms?
Are these changes being induced by external factors or just to encrease variation in a "just in case" manner?
Apart from changing the base pairs, are these changes maybe also the result of new combinations of exons?
Perhaps compression/decompression occurs in the genome; however, data compression involves storing the same information in a smaller space. In biology traits are usual thought of as being from different alleles (versions of a gene). A mutation (change in the DNA sequence) can result in a new allele of a gene. In reality it gets more complex than that. Sometimes a particular allele will have a noticeable effect on a trait (e.g. coat color), other times traits are influenced by multiple interacting alleles (e.g. height in humans). Due to the complex networks involved it is probably not a matter of "pulling out stored traits" but adjusting whole networks. The networks are impressive not only because they work well, but because they were designed to allow for some adjustment.
In the creation model potentially useful mutations could be in response to the environment or they could be from mechanisms deigned to increase variability as a hedge against potential future adverse conditions. I suspect both occur. It is possible that new combinations of exons may be produced, but I cannot think of an example off hand.
I wonder if any research has been done on external factors affecting Meiotic recombination. Like would sustained heat or cold temperatures cause greater mutations (or more hardy genes that are resistant to heat or cold arise) during the process. Does the mother and father's physical health or mental health directly correlate to the frequency of mutations during meiotic recombination? (I am not a scientist and I may be way off base in my questioning. Please don't laugh...)
Actually those are very good questions and I have wondered about that type of thing myself. There are times where stressful conditions are associated with an increase in mutations, though there is debate over whether it is a generalized increase or a response directed at resolving the stress. Age can affect mutations as well. There is really much we still do not know. While evolutionists, having a naturalistic model, have heavily promoted the idea all mutations are just chance errors, it appears research is making this view more untenable. I will be very interested in seeing what future research reveals involving these questions.
For clarity your saying that these mutations are good? I was under the impression from other articles on your website that mutations were going in the wrong direction. (Loss of function)
Does that argument not hold water anymore? Thanks
We are saying that these mutations can be good, but like everything in biology, it isn't 100% effective. This process may work somewhat like an algorithm; they work within a defined set of parameters for a specific purpose; they can't just go changing anything at all. The genome is likely full of such algorithm-like programs that enable it to respond to various environmental challenges, such as in our immune system. The big difference here is that this sort of 'algorithmic adaptation' is occurring in reproductive cells, not somatic cells, and so can be passed on to the next generation. For more information, please see The limits of Neo-Darwinism, Can mutations create new information?, and Basics of biblical biology.
Can someone please write a layman's version of this article with lots of pictures? :)
I struggled through all the uncommon words to find more than 2 sentences in a row that made sense. It sounds very interesting and a good antidote against the freak occurrences required by evolution - but only if I could grasp some of it.
This article is from our peer-reviewed publication Journal of Creation. Part of what we do as an information ministry is provide a forum for creationist research and debate in our peer-reviewed publication Journal of Creation. We feature articles from the Journal regularly on the website (most Fridays) to give the research a wider hearing. We appreciate that not everyone will be able to understand all those articles (I'm part of the editorial team for the Journal, and there are still a number of articles I struggle to understand!). This is why we commonly mark the link to these articles from front page with "Creation in-depth", as we did with this article, and also why we usually only showcase one per week on our front page. However, we pray that they, like our more layman-friendly articles, will be a useful resource available for all.
But let me offer a summary of this article. 'Meiosis' is a special type of cell division sequence that produces the reproductive cells—sperm and eggs. In that process, cells end up with half of the genome of a normal body cell (e.g. the human genome consists of 46 chromosomes (a chromosome is a distinct package of DNA—our genome has 2 copies of each type of chromosome), but human sperm and egg cells have 23 chromosomes) which allows a sperm and an egg cell to combine to form a new organism (sperm (23) + egg (23) = new human (46)). During meiosis, some genetic material gets swapped between chromosomes, and can even produce genetic changes—a process called 'meiotic recombination'. The system was designed to make such changes to create greater variation and preserve adaptive genetic changes. As such, these sorts of 'mutations' are generally not bad changes—it's more like putting weather chains on your car tyres for new conditions (see Basics of biblical biology for more information). In other words, not all genetic changes are harmful mutations because God designed genomes to be adaptable to different conditions.