What is DNA-centrism? Why is it wrong?

 

Question: is this music? Are the above symbols on a piece of paper music? What do you think?  My answer: of course not! It is encoded information. Only a specially trained person is able to read and translate that information into sounds with the help of specially designed devices. On their own, these ink stains are not music. 

Question: do the symbols on a piece of paper cause music? Are they the cause of music? My answer: of course not! The ink dots on a piece of paper are not the cause of the sounds we call music. Those symbols are dead and meaningless ink stains in themselves. One needs a person with specific knowledge of how to read and translate the symbols on paper. Furthermore, that person needs a special designed instrument. Do the hands cause the music? Or does the instrument cause the music? Or our ears? Or our brains? It is impossible to point to one cause. It is everything together. It is clear that here we have a chain of causal factors.

 

DNA centrism

"The basic principle is that if genes were abundantly available in the primordial pond, they could have randomly assembled to form various genomes, each capable of forming an organism." [1]

This is the most concise and extreme expression of DNA-centrism I know of. It is almost a definition of DNA-centrism in the context of the Origin of Life. The statement claims that life started with DNA. All you need is DNA and the organism will develop from it. On the other hand, in biology DNA-centrism means: DNA creates the organism. DNA is the cause of the organism. DNA controls every biological function in the organism. DNA-centrism in the context of Mendelian genetics is almost by definition gene-centrism because Mendelian genetics is not interested in the molecular details of how a gene affects the phenotype of the organism. For Mendelian genetics, the inner workings of an organism are a black box.

Now, let us ask the same questions about DNA as we did above about the musical notes on a piece of paper: does DNA cause an organism to develop, grow, breath and live? Of course not! Try it yourself: place a complete genome in a physiological saline solution in a Petri dish at 37°C and wait. Nothing will happen! But why? Because this is an unnatural environment? But if DNA has the power to create an organism, why does DNA do that? Apparently, DNA hasn't the power to create an organism. Apparently, the genome has to be in a cell and needs all the machinery to read and translate the information in the genome. Conclusion: it only seems that DNA is the cause of an organism because it is always in the right environment. We always assume the right environment.  

Compare this with the musical notes on paper: we are used to associating musical notes on paper with the sounds of music. Change a note (mutation) and the music changes (phenotype). But the musical notes on paper define, but do not create music. The right environment is required to create music [2]. We need a change of perspective to see this.

 Duck-Rabbit illusion (wikipedia)
Does DNA control the cell, or does the cell control DNA? 

We need a change of perspective because we have become the victims of the illusion that DNA itself controls everything. We forget that the cell controls the expression of genes. My eyes were opened at the moment that I realized that our DNA is a parasite in the same manner as a virus is a parasite. A virus is completely dependent on its host for its replication. A DNA genome is completely dependent on its host cell for its replication. DNA is replicated by the cell. DNA does not replicate itself. The cell delivers the resources for replication. The only difference with the virus is that 'our' DNA usually is for the benefit of the individual in which it is housed, whereas the virus DNA is detrimental to its host. But that does not give DNA special powers. In the Duck-Rabbit illustration above, the duck is DNA-centrism and the rabbit is cell-centrism. It is difficult to change perspective. It is even more difficult to see both perspectives at the same time. Since the birth of genetics, scientists always saw the duck (DNA controls the organism). Now it is time to see the rabbit. And when we have succeeded, we should try to see both. That takes some effort. But it is worth it because a scientific theory should not depend on one perspective. 

 

But what about genetic diseases?

Genetic disease seem to be a very strong argument against my position and for  DNA-centrism. What is the cause of Cystic Fibrosis? The answer: Cystic Fibrosisis is caused by a mutation in the CFTR gene. What is the cause of Huntington's Disease? Answer: HD is caused by a mutation in the Huntingtin gene. What is the cause of Duchenne Muscular Dystrophy? DMD is caused by a mutation of the dystrophin gene. What is the cause of Sickle cell disease? Sickle cell disease is caused by a mutation in the HBB gene. A clear case for DNA-centrism?

No. On closer inspection, it appears that genetic diseases are an argument against DNA-centrism. This is because all cells in our body have the same genome. If the fertilized egg (zygote) has a mutation, all cells in our body necessarily have that mutation. Yet, genetic diseases tend to affect specific organs in our body: blood, brain, muscles, heart, lungs, intestines, eyes, ears, etc. How could that be if all cells harbour exactly the same genome? Answer: it is the difference in expression of genes. Do genes express themselves? Of course not. Factors outside DNA trigger gene expression. Additionally, genetic diseases often start at different ages. For example, symptoms of Huntington's Disease typically appear in middle-aged people. How could that be? The genome doesn't change with age. Again: gene expression changes with age, not the gene itself. This is an argument against DNA-centrism because these examples show that DNA is passive, and factors outside DNA cause gene expression in specific organs at specific times. To understand this correctly, the whole cell should be in the centre ('cell-centric view of life'). 

Origin of Life 

The DNA-centric view of life spectacularly fails in the context of the Origin of Life. That's a hint that should make us think again. Life didn't and couldn't start with DNA. That is because DNA is a dead and meaningless molecule. It has no activity on its own. That is the famous vicious circle: the enzymes that transcribe and translate DNA must be present before those very enzymes can be produced.

Another powerful reason why DNA-centrism is wrong is that DNA is only one of the three components that constitute life:

Tibor Gánti model of life [3]

All living entities have three components:

1. chemical motor system: metabolism that produces the energy to run and maintain the organism
2. chemical boundary system: cell membrane that separates the inside from the outside of the cell
3. chemical information system: the hereditary material (DNA) 

Not one of the subsystems is dominant, all three determine the living organism. One subsystem is a chemical system and nothing more. 

This blog is an attempt to summarize my position, not a review of the literature. My position does not downplay the importance of DNA [4], I emphasize the passive role of DNA. This does not contradict any facts. However, my position appears non-mainstream due to sloppy language use in the scientific literature [5].

 

Acknowledgements

Susan checked my English. Thanks!

 

Notes

1. Periannan Senapathy (1994) 'Independent Birth of Organisms. A New Theory That Distinct Organisms Arose Independently From The Primordial Pond Showing That Evolutionary Theories Are Fundamentally Incorrect'. Introduction page 5.
2. Don't push the analogy with musical notation too far! Music is an event with a clear beginning and an end in time. It is produced by starting to read and translate the first note on paper, and to continue until the last note and stops there. Music or a book have a beginning and an end. This is not the way an organism is produced from a DNA genome. The genome has no beginning and end. There is no 'first' gene to start with in order to produce an organism. Secondly, the sheet music doesn't include instructions to build a musical instrument. On the other hand, there is a useful similarity here: musical notation on paper is a handy way to store and copy 'music'. Just like DNA.
3. Tibor Gánti (2003) The Principles of Life. (my review)
4. Philip Ball (2024) downgrades DNA to an extreme degree. For example, he relegates the 1962 Nobel Prize for DNA to a footnote. A blunder. (see my blogpost). In that blog post, I have already made many of the same points I make in this post.
5. For example: "Central to this are enhancers and promoters, DNA sequences that dictate the location, timing, and intensity of gene expression." in A tighter grip on gene expression, Science 3 Jul 2025. Note: "dictate", "timing". Especially, 'timing' is mysterious. How do DNA sequences dictate timing? I asked the author. No reply. I think this is a sloppy language caused by a DNA-centric view. [ 11-11-25 ]

Genes from random DNA? Is it really possible?

random DNA (source)

Can a random DNA sequence contain a gene by pure chance? If a 'gene' is defined as a sequence consisting of a number of bases that is divisible by three, starts with a START codon and ends with a STOP codon, then simple statistics show that genes can be found in random DNA. But, do random genes exist in reality?

ORF = Open Reading Frame.
ORF length distribution of random DNA in base pairs
found in random DNA of 50 million bases.
Vertical: number of ORFs with a specific length using a logarithmic scale
Horizontal axis: ORF length in base pairs [bp]
ORF: sequence of triplets between START (ATG) and STOP (TAA)
© Rolie Barth

Yes, short 'genes' can easily be found in random DNA by pure chance if the random sequence is long enough. The presence of START and STOP codons determines the length of the gene. START and STOP codons are triplets and consist of three bases (nucleotides). Everything between the START and STOP must consist of triplet codons. A STOP codon terminates the synthesis of each protein. The distance between a START and a STOP codon equals the length of a potential protein-coding gene. If that length is short, the corresponding protein will be too short to be useful. The START and STOP codons occur by chance in a random sequence. Therefore, the gene length is distributed according to statistical laws. The length of a gene is important. The statistics show that the maximum gene length found in a string of random DNA of 50 million bases is 354 base pairs = 118 triplet codons. See figure above. If transcribed and translated, those sequences would produce a protein of 118 amino acids in length. In the above simulation, most of the hypothetical genes are less than 150 base pairs or 50 amino acids in length. Proteins smaller than 50 amino acids are called peptides. A number of peptides are useful, but most functional proteins in animals and plants are much longer: on average 486 amino acids. 

In the above computer simulation, only one STOP codon is used for simplicity. That's why mainly peptides are found. If all 3 STOP codons are used in the simulation, ORFs are almost twice as short [2]. On the other hand, if a random sequence would have the length of the human genome, that is 3.5 billion base pairs or 60 times bigger than in the above simulation, than the maximum length of the hypothetical genes would be 470 bp. That is 1.35x longer [2]. 

In hindsight, it is not surprising that 'genes' can be found in random DNA. The beauty of the genetic code is that any 3-letter combination of A, T, C, G is a valid codon, including START and STOP codons. That means, that any such a sequence is potentially a protein-coding gene. The similarity between real and random genes is that they consist of a sequence of the same 4 letters A, T, C, G. On that level they cannot be discriminated. The differences lie elsewhere (see below). 

Interestingly, from the above computer simulation, several mathematical laws emerge. 

1. The first law: there is a maximum length of genes when a 'gene' is defined as a sequence between START and STOP, and it consists exclusively of triplets of bases (total length is divisible by 3). 
2. The second law is: the maximum length of a 'gene' depends on the length of the random sequence. The larger the random sequence, the larger the genes. 
3. The third law is:  gene length is bigger when only 1 STOP codon is used instead of standard 3 STOP codons (results not shown here). 

Mathematicians call the graph a Power Law. Please keep in mind that all this is purely mathematics. It depends on the underlying assumptions whether the results apply to living organisms. For now, it seems that genes of useful length could be found in random DNA with the length of the human genome (3.5 billion base pairs).

But does this sort of mathematics apply to the real world? Does random DNA exist in the real world? Yes, it could be. Our genome consists of 90% 'junk'. Junk DNA is not pure random DNA, it has an evolutionary history. It is subject to random mutation and decay. Therefore, it approaches random DNA. So, there are ample opportunities to find genes in junk DNA. Curious genome researchers have searched for functional random genes in real genomes. But first: how do you detect those random genes? How do you discriminate between 'normal' genes and 'random' genes? Again, both are a series of 4 letters in a sequence. Random sequence genes must be novel genes or de novo genes. They are also called orphan genes for obvious reasons. Since they are created from scratch, they do not have identical or similar genes in the genomes of closely related  species. Furthermore, the sequence of the putative gene must be present in non-coding DNA of closely related species in the same location on the chromosome. A researcher concluded:

"Although considered an extremely unlikely event, many genes emerge from previously noncoding genomic regions. (..) De novo genes arise from previously noncoding DNA, are short, and are expressed at low levels. (...) While most of the de novo genes are lost, a fraction of them becomes essential. [3]

Intriguingly, the ORFs of de novo genes are shorter than those of evolutionary old genes, but longer than expected by chance according to this researcher. We have seen in the above computer simulation that random genes tend to be smaller than real genes. Even more surprising, de novo genes can become essential.

In humans, at least three human protein-coding genes have emerged since the divergence with chimps some 7 million years ago. These loci are noncoding DNA in other primates (that is part of the definition of random genes). Other studies  estimate that 18 such cases are present in a genome of 24,000 protein-coding genes [4]. That's interesting, but the problem with this method is that the noncoding sequences could be the modified descendants of ancient genes or pseudo-genes. So, we cannot be 100% sure that they are truly random.

In 2013 genome researcher Sean R. Eddy proposed the Random Genome Project: 

"Suppose we put a few million bases of entirely random synthetic DNA into a human cell. (...). Will it be reproducibly transcribed into mRNA-like transcripts, reproducibly bound by DNA-binding proteins, and reproducibly wrapped around histones marked by specific chromatin modifications? I think yes." [1] 

Exactly this experiment has been done recently [5]. Investigators inserted a synthetic DNA sequence in yeast and in mouse cells. In yeast cells, the DNA was being read (transcriptional activity), but the mouse cells did nothing. The researchers concluded that regulatory DNA elements are required in order for the gene to be read. But reading a gene is only the first step. The product (mRNA) must be transported to the cytoplasm and translated by ribosomal machinery and transfer-RNA (tRNA) to a protein. Furthermore, the resulting protein must be able to fold in to a functional 3D form. A further requirement is that the new protein must fit into the existing network of biochemical reactions of the cell and the organism. Of course, it does matter whether the gene is active in every cell of the organism, or just in specific tissues or organs. Also, in what quantities it is produced. And whether it is produced in the embryo or in the adult, in males or in females. A lot of requirements indeed. No wonder that there aren't a lot of genes that originate from random DNA.

The discussion so far is about the origin of new genes from random DNA in real genomes of real organisms belonging to real species. But ultimately, the very first genes on Earth must have a random origin. How else could they originate? They have no ancestors. One genome researcher, Senapathy [6], did computer simulations like the simulations discussed here and has put forward a theory that long ago animals and plants originated in primordial ponds from random DNA genomes. For a few thousand reasons, genomes cannot be created from random DNA fragments ('genes'), and organisms cannot be created from random genomes. The ultimate reason is DNA- or genome centrism: the idea that a genome can create an organism. My next blog will be about 'DNA-centrism'.

 

Acknowledgements

Rolie Barth contributed the statistical analysis, corrected the draft and made suggestions for improvement. Susan checked my English. Thanks both!  

 

Notes

1. Sean R. Eddy (2013) The ENCODE project: Missteps overshadowing a success,   
2. Personal communication Rolie Barth, author of De kosmos en het leven - een Meesterwerk. (see also: korthof58.htm Note 507). Barth wrote two guest blogs: Circular causality, another secret of life – on the occasion of Philip Ball's How Life Works 25 March 2024. Rolie Barth replies to his critics: What have pufferfishes and plasmas in common? 28 March 2024.
3. Christian Schlötterer (2015) Genes from scratch—the evolutionary fate of de novo genes. 2015. Open Access.
4. David G Knowles, Aoife McLysaght  (2009) Recent de novo origin of human protein-coding genes.
5. Brendan R. Camellato, et al (2024)  Synthetic reversed sequences reveal default genomic states Open Access. Published: 06 March 2024. "The locus was designed by reversing but not complementing human HPRT1".
6. Periannan Senapathy (1994) 'Independent Birth of Organisms. A New Theory That Distinct Organisms Arose Independently From The Primordial Pond Showing That Evolutionary Theories Are Fundamentally Incorrect'. (review).

Op heterdaad betrapt midden in de nacht: Segrijn slakken eten kitlaag van de ramen (+updates)

De schilder die ons huis aan het schilderen was, merkte op dat de kitlaag van de ramen aangetast was. Eerlijk gezegd was het mij nog niet opgevallen. Het kwam door slakken zei hij. Hij raadde dubbelzijdig plakband aan. Maar ik vond het nogal bizar dat slakken een (giftige?) kunststof zouden eten. Er is toch voedsel genoeg in de tuin?

Ik wilde eerst weten of het hele verhaal klopte. Ik had nooit slakken op de kitrand gezien. Dat zou dan 's nachts moeten gebeuren? Er was maar één manier om het raadsel op te lossen: die slakken op heterdaad betrappen. Ik wilde 's nachts de Seissiger wildcamera opstellen. Toen ik in het donker de tuin in liep, hoorde ik gekraak onder mijn voeten. En ja hoor: ik trapte op een slak. LED-lampje er bij gehaald: het wemelde van de slakken op het pad. Gefotografeerd en ingevoerd in waarneming: bijna allemaal Segrijnslakken. Ze hebben een grotere schelp dan de bekende huisjesslakken en de schelp heeft allerlei patronen en is fraai gekleurd. De soort komt van oorsprong uit Zuid-Europa. Volgens waarneming.nl heeft de soort inmiddels de status 'algemeen' en 'inheems' en dus niet 'exoot'. Ze eten vooral tuinplanten en zouden zelf ook goed te consumeren zijn! Dat laatste was ik niet van plan.

Dit zijn de slakken die ik 's avonds tegen tienen aantrof op het tuinpad:

Segrijnslak 17 sep 21:36 FP5 ©GK

Segrijnslak 17 sep 21:37 FP5 ©GK

Segrijnslak 17 sep 21:38 FP5 ©GK

Segrijnslak 17 sep 21:39 FP5 ©GK

Zwartgerande tuinslak 17 sep 21:40 FP5 ©GK

Maar goed: 's avonds slakken op het tuinpad is nog geen bewijs dat ze ook van de kitlaag eten. Ik heb de wildcamera op timelapse gezet: iedere 5 min een opname. Op de sensor zetten werkt niet voor deze kleine en langzame dieren. En inderdaad, van 00:35 tot 03:30 u., was er een slak actief op de kitrand. Op heterdaad betrapt! Zo'n 3 uur op dezelfde plek!  

Seissiger wildcamera 19 sep 2025 00:30
Rode pijl: slak op de crime scene.
Groene pijlen: 2 aangetaste plekken.

Uit de opnames blijkt dat de slak naar een nieuwe plek is gekropen:

Seissiger wildcamera 19 sep 2025 00:35  
Op heterdaad betrapt. Rode pijl: slak.
Groene pijlen: 2 aangetaste plekken

 

Nadat hij zijn buikje vol gegeten had met de overheerlijke kit, verdween hij weer. De volgende ochtend was er een derde aantastingsplek te zien op de plek waar de slak bezig was geweest. Ik acht het voor 100% bewezen dat slakken de kit opeten. En voor 99% zeker dat het de Segrijnslak was. Omdat het donker was en de opnames in zwart-wit zijn, kan ik niet met 100% zeker concluderen dat het om deze soort gaat. Als je het 100% zeker wilt weten, zou je het DNA in de uitwerpselen moeten analyseren.  

De vraatsporen zijn vaak geribbeld en ongeveer 1 cm lang. Vaak vind je een langwerpig uitwerpsel in de buurt. Dat is een hint.  

Zo herken je de slak:
schade beeld in de kit met uitwerpsel

 

Segrijnslak in zijn natuurlijke milieu:

Segrijnslak op klimhortensia (SONY A6700 +macro)

detail van de kop

Gebeld met het schildersbedrijf. Ze stuurden vrij snel een glaszetter die de kitlaag begane grond verving door een ander product die de slakken niet zouden lusten. Ieder zijn vak. De kit is nu een week oud zonder schade.

Jika Sikaflex beglazingskit.

Update 7 Okt 25

Aan de voorkant van het huis was de kit nog niet vervangen en ik betrapte een 100% Segrijnslak op heterdaad op klaarlichte dag! 

100% Segrijnslak Cornu aspersum 7 Okt 2025 13:40u

Hij was op dat moment 'in rust', maar hij zat op een aangetaste plek op de kit. Het is nu 100% bewezen dat het Segrijnslakken de kit aantasten. Ik heb hem voorzichtig los gemaakt en in het bos gezet. Ik heb nog geen gewone huisjesslakken dit zien doen.

Segrijnslak (juveniel) 14 Okt 25. Zat op de oude kitlaag
's ochtends vroeg aangetroffen en meegenomen voor de foto.

Hij was actief aan het kruipen toen ik hem naar binnen haalde voor de foto. Bij wijze van experiment heb ik hem op de nieuwe slakken-bestendige kit gezet. Hij had geen belangstelling, hij kroop gewoon weg. Het kan zijn dat al zijn buikje vol had... 
 

Bronnen

Segrijnslak (wikipedia):  

• "De segrijnslak is een nachtdier." (klopt!). 
• "In Nederland en België is deze slakkensoort niet inheems, maar toch wijd verspreid". Waarneming.nl noemt de soort "algemeen, inheems".
• Exoot: "In andere werelddelen is de segrijnslak een succesvolle exoot, die na de introductie tot plagen kan leiden."
• "Segrijnslak als plaagdier": maar er staat niets over het eten van kit. Misschien kan hij bestanddelen van de kit (kalk?) gebruiken voor de opbouw van zijn huisje?
• Gastronomie: "De segrijnslak is zeer gewaardeerd als escargot."