Opening a probability

Evolution is opening a probabilistic survival opportunity.

The essence of evolution is not competition, selection or adaptation. It is not an improvement, nor is it getting better in efficiency.

The essence of evolution is opening a probabilistic survival opportunity in an uninhabitable space. This looks adaptation in hindsight. However, this is completely independent of competition or selection. Accidental changes are accidentally suited to survival in previously uninhabitable environments. The original population does not need to go there because they have enough resources to continue in their own habitat. The uninhabitable space is not needed for their continuity.

This is not getting better (i.e. improvement) or being efficient in the original context of their own habitat. The changes can be unnecessary or even disadvantageous in their original habitat. However, they are essential for survival in the previously uninhabitable space. When this occurs, a new species emerges with a new niche. No one cares because the place was uninhabitable until then.

The survival of living organisms is determined by the interplay between intrinsic properties and extrinsic environmental conditions. There are two types of environmental conditions. One is uniform, ubiquitous conditions, such as water for marine organisms, oxygen for land organisms, climates and temperatures. No one can avoid. And as long as they are in the area, they are relatively uniform and ubiquitous. The other is opportunistic encounter conditions, such as food, mates and predators. This can be measured as the frequency and density of opportunities. The first uniform, ubiquitous condition dictates the second encounter condition.

The frequency and density of encounter opportunities determine the carrying capacity of an open local area. The number of individuals in a species and the frequency and density of opportunities form an equilibrium. 

Individual survival is opportunistic, depending on where and when one exists at a given moment. What one encounters and the order of one’s encounters are unpredictable. Local bias may arise from uneven opportunity density.  

A species is a group of individual organisms that share a stable and consistent range of phenotypic variation. This common variation is stable and consistent, providing enough opportunities for sufficient numbers of survivors for the species continuity in its local environments. 

At speciation, a new species emerges with a new common variation. The new common variation opens a new probabilistic survival opportunity in the previously uninhabited place. For the original species, the place is uninhabitable because it is too toxic, too hot/cold, too dry/wet, has no food, is too full of predators, etc.  The real reason for the uninhabitable has remained unknown until it is overcome by a new species. The emergence of a new species will make sense retrospectively as a new common variation overcomes the place’s previous uninhabitable conditions. 

Some may say that this is natural selection as the environment selects survivors. However, the terminology ‘natural selection’, as indicated by Darwin and neo-Darwinism, is different. It says that the environment provides competition. Survivors are selected based on heritable intrinsic properties in competition. Over generations, through population adaptation, a species will adapt better to its environment than it did before.

Aiming to live in an uninhabitable place is not a competition, but just unnecessary. There is a place where the species can live. The uninhabitable is outside of it and not even given a faint consideration. However, something changes intrinsically and accidentally. Then, the changes permit survival in the previously uninhabitable. Retrospectively, the process makes sense. Prospectively, unimaginable and crazy. Imagine if something changes in humans, allowing them to live in water or space without equipment. Or we gain the ability of hibernation. None needs to live in the current human societies, but is allowed to survive outside of them.

Then the question is: how could this happen? Is it possible to happen?

One strategy is working together with others. It would be impossible by oneself, but working together with others might be. Symbiosis, symbiogenesis, multicellularity, and social activities are examples. As long as staying inside the original habitat, living alone is possible. However, a collaboration with others with different expertise may take them outside the inhabitant. The previously uninhabited place can be inhabited.  Multicellularity and social activities are on the same line. As long as staying the original habitat, they are not required. However, multicellularity and social activities may enable survival in a previously uninhabited place, even though some individual properties must be compromised.  Through working together, enough opportunities are created for a sufficient number of survivors to continue in a new environment.

Can a slow, gradual accumulation of random mutations do this? Unlikely.

If an uninhabitant is caused by one parameter, this could be overcome by the dominant effect of one gene change. For example, bacterial resistance to antibiotics. However, uninhabitability often arises from a combination of uniform, ubiquitous conditions and opportunistic encounter conditions. One gene change would be insufficient to generate enough opportunities for a sufficient number of survivors.

The differences between two species are not defined by one gene or one phenotypic trait. Each species is primarily defined by anatomical and morphological properties, and the differences between two closely related species are often subtle, consistent properties. They are not defined by a single gene but by multiple genes and their interactions.

As I mentioned above, a species is a group of individual organisms that share a stable and consistent range of phenotypic variation. The common variation. Two species are different in their common variations.

How does a new species create a new common variation from the original common variation? I believe that the founder effect and chromosomal rearrangement.

The founder effect is a powerful filtering effect on population variation. It is often called a bottleneck. This filtering effect does not need to be linked to any phenotypic change. Imagine five colours of marble beads in a bottle, like white, black, red, blue and green. There are 100 beads in 5 colours in a bottle. Only one bead can pass through the bottleneck in a single flip. Flipping five times does not guarantee recovering all five colours, even if their numbers are even. Most likely, fewer than five colours. There is a chance that all five beads are in one colour, by chance.  

This is different from competition, selection and adaptation.

Chromosome rearrangement is not a rare event but occurs occasionally and can cause human diseases, including congenital anomalies and cancer.  It can be a deletion, an inversion and a translocation, which is a combination of an insertion and a deletion.

One simple chromosomal event affects multiple junctional DNA sequences. A deletion disrupts two junctions and creates one new junction. An inversion disrupts two junctions and creates two new junctions. A translocation disrupts three junctions and creates three new junctions.

If a junction is in a gene sequence, it likely disrupts the gene function. Theoretically, a single chromosomal event can affect multiple genes. In addition, it has been recognized that for a gene to function properly in our body, its expression must be regulated properly, in addition to its gene sequence. The surrounding DNA sequences of each gene play important roles in its regulation of gene expression.

Gene regulation can be conducted from proximal and distal DNA sequences called enhancers. It is important to recognize that a DNA polymer is not a straight solid stick. It is a string that curls and twists. Not fixed, but the patterns of curling and twisting have some reproducibility based on the DNA sequence.  The patterns of curling and twisting change the proximity of two DNA sequences in the 3D space. The 3D patterns of the DNA sequences within a chromosome contribute to gene expression regulation.   

Chromosome recombination could alter this 3D pattern. A curled or twisted area might be moved as a structural block. Or a new curl or twist might be created. A simple chromosomal event can generate three to six junctional events. This could result in no change in gene expression or multiple changes in gene expression.

Even if there is no change in gene expression, chromosomal recombination is problematic in a reproductive process called meiosis. During meiosis, two homologous chromosomes must align with each other. This leads to chromosomal crossover and the swapping of chromosomal regions between them (meiotic recombination).

Dependent on the size and degree of chromosomal recombination, this process gets compromised. Deletion, inversion or translocation could prevent the process of alignment, crossover or meiotic recombination. Failure of meiotic recombination results in sterility or subfertility. Interestingly, meiotic recombination is more sensitive in males than in females. The same chromosome recombination can cause male sterility, but female normal fertility or subfertility.   

Gene/chromosomal change is always personal and private. It occurs at a single gene locus on a single chromosome in a single cell of a single organism. No exception. The change could be linked to dominant or recessive phenotypic traits. There are two types of cells in multicellular organisms, somatic and germ cells. To observe phenotypic traits in an organism, the change must occur in a somatic cell. To expect the change to be inherited by offspring, it must occur in a germ cell.

Let’s imagine a gene/chromosomal change occurs on a single chromosome in a single cell. The cell becomes heterozygous, one original WT chromosome and one altered chromosome. Let’s assume this change has a recessive phenotypic trait. So, heterozygous cells have no phenotype.

However, heterozygous cells in the germ lineage may have problems with meiotic recombination. If the problem is too severe, this first individual will be sterile. The end of the story. On the other hand, if the problem is not too severe, this individual will be subfertile. The number of sperm or oocytes that it can produce could be 5%, 20% or 80% of normal individuals. Although the number is fewer, the first individual could still produce offspring (the founder 1, F1).

Among those F1 offspring, half will be heterozygous individuals. Heterozygous individuals have no phenotype for the recessive trait, but they are still subfertile due to meiotic problems.

If two F1 heterozygous individuals mate, since both could have fertility problems, the number of F2 offspring could be even fewer. However, 25% of F2 offspring will be homozygous for the altered chromosome.

The homozygous F2 offspring should exhibit the recessive phenotypic traits for the first time after the gene/chromosomal event. Interestingly, the reproductive problem caused by meiosis-related incompatibility disappears in homozygous individuals.

Homozygous individuals differ phenotypically from the original population due to recessive traits. They have no reproductive problems, unlike heterozygous individuals.

Does this new population that is homozygous for the altered chromosome survive as a new species? Yes, if they are different from the original. This doesn’t mean competitively better. Simply different. If the interests of the new population are different from those of the original, the original population does not care. If they survive and continue as a new species, it makes sense retrospectively. But this is always in hindsight. Smaller and lighter are beneficial in some contexts. Abnormality or weakness in one context could be a necessity and a strength in other contexts.

I hope readers recognize that a strong bottleneck effect occurs when this process works. Not only the altered chromosome, but also other chromosomes with variations will be fixed. Many phenotypic traits, not associated with the altered chromosome, are also fixed due to the tight bottleneck. Subtle, stable, consistent differences between two species emerge.

A species is a group of individuals exhibiting a stable and consistent range of phenotypic variations. The foundation of a species is a range of stable and consistent common variations. The variations can swing locally and seasonally, but the range is stable and consistent. This range guarantees enough opportunities for a sufficient number of survivors as a species in its local environment.

Individual survival is opportunistic, depending on where and when one exists at a given moment. The range of common variations has been working to survive in its environment; therefore, a species exists.

A species must be a highly stable entity, permitting robustness and plasticity in an individual through a complex network with many detours for compensatory and adaptive responses to internal and external insults.

Opening a new possibility is not necessary for the existing species, because their existence is already built on it. However, it happens because of errors. Errors, luck in accessible uninhabitable and the ratchet-like property in meiosis. They must be the foundation for the diversity in the natural world. No one knows what is good or bad. Better cannot be predicted. Everything is retrospective. In hindsight, something new always starts from errors and wrongness.