How the Body Protects the Germline
Germline mutations – it could
have been much worse!
by Margaret Helder, PhD
In this age of high-tech medicine, we are all aware that each person carries a large burden of deleterious mutations which potentially can be passed on to one’s offspring. But, we now discover, that it could have been a lot worse!
Recently scientists have set out to investigate if there is a difference in mutation rates between the somatic cells (soma – normal body tissue) and the germline cells (involved in sexual production of offspring).1 In this article the scientists point out that “mutations in the germline can be transmitted to the next generation, making them the raw material of species evolution and the cause of hereditary diseases.”2 While mutations are supposed by many scientists to provide for evolution, in reality, mutations are a serious source of congenital diseases and population decline. The authors also declare from other studies, that 80% of inherited germline mutations come from the male (paternal) line.3
The scientists compared mutations within somatic tissue and germline cells. The comparisons were between the cell types of individual males. The authors found that the mutation burden within germ cells of the testis was 27-times lower than within cells lining the large intestine and all other somatic cell types.4 They further declared that the low germline mutation rate is “an intrinsic feature of the male germline compared with the soma.”5 Moore et al. further suggest that there must be superior mechanisms to maintain genomic integrity in the germline cells.6 They find this unexpected and mysterious since “We find that mechanisms underlying mutagenesis appear to be shared between the germline and the soma, suggesting that the germline has found ways to limit the mutagenesis caused by these processes.”7
How Do Cells Protect Against Germline Mutations?
In the above context, an article that appeared the previous week in Nature had described one such unique mechanism which protects the integrity of the germline DNA.8 The authors described proteins (called PIWI) which interact with special RNA sequences (piRNAs) to identify transposable elements (jumping genes) in the DNA and to permanently tie them up to silence their expression. This unique process in germline cells keeps jumping genes from moving around the DNA sequence and causing havoc in its expression. The authors conclude “We suggest that by shaping piRNA-target interactions, PIWIs can leverage the vast piRNA pool to restrict the escape of transposable elements from surveillance while minimizing off-targeting, and have thereby maintained metazoan [animal] germlines over the past 800 million years.”9
A Non-Darwinian Finding
Obviously the authors think that the PIWI-piRNA complex is highly important to the survival of all multicellular animals. The authors are perhaps too enthusiastic in positing animal existence and survival for 800 million years, since most specialists imagine that animals appeared in the Cambrian explosion dated more than 200 million years later. Be that as it may, it is evident that there is a conflict between evolution theory and reality. The ideal situation for evolution is the appearance in the germline of many mutations from which natural selection may select the best ones. Contrary to this idea is the need for organisms to protect their offspring from harmful mutations which can cause decline and extinction.
The question arises as to the source of special protection for germline cells. Evolutionary processes have no foresight to know that such protection is needed. Indeed, it is in the interests of the evolutionary process to favour more mutations, not fewer. But in the face of all those deleterious mutations, this would be the road to disaster for the population. The need for protection could only be foreseen by a personal supernatural agent. In this protection of the germline cells, we see the hand of God, the Creator.
1. Luiza Moore et al. The mutational landscape of human somatic and germline cells. Nature 597 #7876: 381-386.
2. p. 381.
3. p. 381.
4. p. 385.
5. p. 386. Emphasis mine.
6. p. 386.
7. p. 386. Emphasis mine.
8. Todd A. Anzelon et al. Structural basis for piRNA targeting. Nature 597 #7875: 285-289.
9. 288. Emphasis mine.
Margaret Helder completed her education with a Ph.D. in Botany from Western University in London, Ontario (Canada). She was hired as Assistant Professor in Biosciences at Brock University in St. Catharines, Ontario. Coming to Alberta in 1977, Dr Helder was an expert witness for the State of Arkansas, December 1981, during the creation/evolution ‘balanced treatment’ trial. She served as member of the editorial board of Occasional Papers of the Baraminology Study Group in 2001. She also lectured once or twice a year (upon invitation) in scheduled classes at University of Alberta (St. Joseph’s College) from 1998-2012. Her technical publications include articles in the Canadian Journal of Botany, chapter 19 in Recent Advances in Aquatic Mycology (E. B. Gareth Jones. Editor. 1976), and most recently she authored No Christian Silence on Science (2016) which promotes critical evaluation of scientific claims. She is married to John Helder and they have six adult children.