No naturally occurring protocells have been observed in the wild

If even one of these 39 complex protein machines is missing or defective, cell division (reproduction) of the bacteria is impossible.

Question: How was the first imaginary cell able to develop all these protein machines during its short life?

Bacterial binary fission is a complex and highly coordinated process that involves at least 39 various protein machines and assistant proteins. Below is a comprehensive list of the necessary proteins categorized based on their roles in the different stages of bacterial cell replication:

1. Initiation of Chromosome Replication

• DnaA: Initiator protein that binds to the origin of replication (oriC) and unwinds DNA.
• DnaB (Helicase): Unwinds the DNA double helix.
• DnaC: Helicase loader protein that assists DnaB.
• DnaG (Primase): Synthesizes RNA primers necessary for DNA polymerase to start DNA synthesis.

2. DNA Replication Machinery (Replisome)

• DNA Polymerase III Holoenzyme: The main enzyme complex responsible for DNA synthesis.
  • α (alpha) subunit: Polymerase activity.
  • ε (epsilon) subunit: Proofreading activity.
  • θ (theta) subunit: Stabilizes the ε subunit.
• β (beta) clamp: Sliding clamp that holds DNA polymerase III onto the DNA.
• Clamp loader complex: Loads the β clamp onto the DNA.
• Single-Strand Binding Proteins (SSB): Stabilize single-stranded DNA.
• DNA Gyrase (Topoisomerase II): Relieves supercoiling ahead of the replication fork
• DNA Topoisomerase IV: Decatenates interlinked daughter chromosomes.

3. Elongation and Proofreading

• DNA Polymerase I: Replaces RNA primers with DNA.
• DNA Ligase: Seals nicks in the DNA backbone, joining Okazaki fragments on the lagging strand.

4. Termination of Replication

• Tus Protein: Binds to ter (termination) sites on the chromosome to halt the replication fork.

5. Chromosome Segregation

• MukBEF Complex: Condenses and organizes the chromosome.
• ParAB System: Segregates chromosomes into daughter cells.
• FtsK: DNA translocase involved in chromosome segregation and cell division coordination.

6. Division Site Selection

• MinCDE System: Ensures the division septum forms at the cell center.
  • MinC: Inhibits FtsZ polymerization.
  • MinD: ATPase that recruits MinC to the membrane.
  • MinE: Regulates MinD activity and localization.

7. Septum Formation (Z-ring Assembly)

• FtsZ: Tubulin-like protein that forms the Z-ring at the future division site.
• FtsA: Actin-like protein that connects FtsZ to the membrane.
• ZipA: Anchors FtsZ to the cytoplasmic membrane.
• ZapA, ZapB, ZapC, ZapD: Accessory proteins that stabilize the Z-ring.

8. Constriction and Cell Division

• FtsK: DNA translocase involved in coordinating septation with chromosome segregation.
• NOTE: This is a very complex protein machine. It has 1329 amino acids.
• FtsQ: Scaffold protein that recruits other division proteins.
• FtsL, FtsB: Part of the divisome complex, involved in stabilizing the constriction machinery.
• FtsW: Lipid II flippase involved in peptidoglycan synthesis.
• FtsI (PBP3): Penicillin-binding protein involved in septal peptidoglycan synthesis.
• FtsN: Activates peptidoglycan synthesis and finalizes septum formation.

9. Cell Wall Synthesis and Remodeling

• Penicillin-Binding Proteins (PBPs): Involved in peptidoglycan synthesis and remodeling.
• Autolysins: Enzymes that remodel peptidoglycan to allow cell separation.

10. Membrane Remodeling

• Amidases: Enzymes that separate daughter cells by hydrolyzing peptidoglycan cross-links.
• Phospholipid Synthases and Transferases: Involved in membrane synthesis and remodeling.

This categorization highlights the key proteins involved in bacterial binary fission and their roles in different stages of the process. The absence or malfunction of any of these proteins can significantly impair or prevent successful bacterial cell division. Every protein needs an extremely accurate design with atomic precision as scientists have noted. Conclusions: It is impossible for the complex protein machines necessary for cell division to have evolved step by step because cell division cannot succeed until all the necessary protein machines are precisely in place and functional. No naturally occurring protocells have been observed in the wild. Evolution never happened.

Adaptation of organisms accelerates genetic decay

Food type changes epigenomes

We have been taught that Darwin's finches have undergone random mutations, leading some birds to develop thick and strong beaks while others have developed thin and delicate beaks. The size and shape of the beak, in turn, have driven different species of finches to different types of food. This is how natural selection works, according to Charles Darwin.

In the bright light of modern science, this is absolutely wrong! Random mutations and selection are definitely not the reason why some finches have thick beaks and others have delicate ones. No! According to modern science, the size and shape of finches' beaks are the result of epigenetic regulation influenced by the diet the birds consume. If a finch starts eating seeds, its offspring will develop thick and strong beaks. If a finch eats insects, its offspring will have more delicate beaks. This is how epigenetic regulation works. It is based on the modification of existing information.

Scientific studies confirm these observations:

https://phys.org/news/2017-08-epigenetics-darwin-finches-rapid-environmental.html#nRlv

"These species of finch have distinct diets which could explain the differences in methylation patterns as diet is known to influence epigenetics."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6320837/

"Nutrition is one of the strongest modifiable factors, which plays a direct role in DNA methylation pathways. Large numbers of studies have investigated the effects of nutrition on DNA methylation pathways, but relatively few have focused on the biochemical mechanisms. Understanding the biological mechanisms is essential for clarifying how nutrients function in epigenetics."

There are other factors affecting the epigenomes of organisms such as stress, climate, toxicants, pheromones, etc. Organisms have specific receptors by which they are able to receive and transmit signals from the environment to the cells.

Changing methylation patterns lead to genetic errors

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9624357/

"CpG sites mutate 10-50 times faster than any other genomic motif. This mutability is attributable to DNA methylation: a methylated cytosine is an order of magnitude more likely to mutate than an unmethylated cytosine. Obviously, not every CpG site mutation is a direct result of methylation and some mutations will occur by chance at unmodified CpG sites. However, this fraction will be extremely small, as the mutation rate of methylated cytosines is nearly 20,000 times that of unmethylated cytosines. In addition to somatic cells, CpG mutations are also expected to occur in the germline, which will influence how such mutations are inherited."

“Of more than 50,000 genetic changes currently known to be associated with disease in humans, 32,000 of those are caused by the simple swap of one base pair for another.” – David Liu

https://www.zmescience.com/medicine/genetic/crispr-rna-gene-editing-0432432/

Nearly half of human pathogenic point mutations are caused by methylated-cytosine-to-thymine mutations.

CpG island and cytosine methylation result in decrease in GC content

The strong tendency of CpG islands and individual cytosine bases to mutate to thymine when methylated leads to a GC-AT imbalance in the cell. The cell must balance the GC-AT ratio during reproduction through a process known as meiotic recombination, where the cell rearranges DNA to achieve a sufficiently high GC content for essential functions. This process inevitably results in the loss of information. A high AT content also causes chromosomal damage and breakages, forcing the cell to rearrange DNA and fuse chromosomes together, which reduces their overall number.

Summary:

• Organisms adapt to changing conditions thanks to built-in mechanisms that modify existing information.
• Darwin was wrong.
• Random mutations and selection never lead to any evolution.
• The mutation rate of methylated cytosines is nearly 20,000 times that of unmethylated cytosines.
• Adaptation results in changing methylation patterns. This increases the possibility for more cytosine-to-thymine mutations to occur.
• The cell tries to balance the GC-AT ratio by rearranging DNA.
• DNA is passive information.
• In this process, information is lost.
• Loss of information and DNA rearrangement can be observed as so-called speciation.
• Genetic entropy is a biological fact. Evolution never happened. The theory of evolution is the most serious heresy of our time.