S1C3: Information & Evolution

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a) Structure and function

During the first and second chapters we built up our understanding of the nature of molecules and macromolecules, how they come to be, and the nature and variables involved in chemical reactions. We are now entering the domain of biology but there is still a long way before we can understand the nature of life, organisms and how they can sustain and replicate themselves. The first overarching comment I would like to make is that there exists millions of different macromolecules, which should come as no surprise given how many chemical elements exist and the total number of atoms that can comprise a macromolecule. Hence, in a perfectly random world, even accounting for the ease of creation of some particular intramolecular bonds versus others, we would have a wide array of macromolecules floating around, as they probably did in the hypothesized “primordial soup” from which life emerged close to 4 billion years ago. So, from there, how did we and other species come to be? Surely it is not purely coincidental self-assembly, the odds are more than vanishingly small and it would not explain how life can be sustained. In fact, there is a lot that would not be explained, such as the inheritance of traits or the facts that species have pretty much the same macromolecular make up and that over 96% of our body weight come from only four chemical elements: oxygen (~65%), carbon, hydrogen, and nitrogen – whereas the mass of the earth is dominated by iron, oxygen, silicon and magnesium, that of the atmosphere is 99% oxygen plus nitrogen, and the universe is more than 97% hydrogen and helium.

To help us understand how nature created order out of randomness and, ultimately living organisms, we need to introduce and think about the notions of “function” and “information”. The idea of function could be described as the fulfilling of a specific role. We will describe some of those key roles and explain how they are achieved in the next chapter, continuing on our progressive build up in chemical and organisational complexity, but before doing so we must understand nature’s great escape out of randomness. This journey starts with a simple query: what are the implications of some chemical compounds being capable of fulfilling specific functions?

At this stage, I need to introduce the notion of comparative advantage. If a chemical compound X has a function F and a chemical compound Y has no function then there are two possible scenarios: either F is useful or it is not. Useful should be understood as increasing the chance, directly or indirectly, of X not being destroyed or being replicated – something I will expand on in the next section. If F is not useful then X offers no comparative advantage versus Y, meaning there is no reason to choose one over the other based on their outcome. Conversely, if F is useful then X has a higher chance of surviving or being replicated.

However, you may think, does this really matter if ultimately the useful property F was a product of luck? Even if it provides an advantage, it is not like nature will notice and actively seek to reproduce this property. In other words, the edge it provides is not sustainable. This is undeniable, nonetheless the existence of a set of instructions allowing for the consistent replication of F does provide a way around the issue. In its technical sense, this is what we call information: a particular sequencing with a specific effect or interpretation. The concept of information runs very deep in nature, it is what brings order out of chaos, that which counters entropy, the gradual decline into disorder predicted by thermodynamics. However, information on its own is not sufficient, it has to be selected for, bit by bit, so that it can grow incrementally. This is where function and competitive advantage come in, those are the selective criteria, the pathfinders.

There is still a missing piece though. How is this information instantiated and how is it retained over time and, when it comes to organisms, transmitted across generations? Enter the genes.

b) Genes

There is no strict agreed-upon definition of the gene in the scientific community, or perhaps it would be fairer to say that it carries two meanings. The first one centres on the medium of storage and describes genes as sequences of macromolecules and the second one on linking specific nucleotide sequences with traits that can be passed on by an organism to its offspring, a characteristic termed “heredity”. Oversimplifying somewhat, these definitions focus on substance and function, respectively.

At the chemical level, a set of molecules (a nucleobase, a five-carbon sugar called deoxyribose, and a phosphate) combine to form one of five nucleotides. These units called monomers are then joined together in a chain through covalent bonds to form a very (very) long polymer called a DNA strand – DNA stands for deoxyribonucleic acid. Out of the five potential nucleotides, four of them are used in DNA: guanine, adenine, cytosine, and thymine; those are generally represented by their initials G, A, C, T, respectively. A sequence of three nucleotides forms a codon – not a separate type of macromolecule per se, rather one can think about them as the letters used in the genetic alphabet. Doing the maths, there are 64 different codons (4x4x4) and 61 of them are used to encode for amino acids while the remaining three are used as stop signals, as an analogy to the morse code used for telegrams.

Interestingly, but not coincidentally, the four nucleotides can form two base pairings through hydrogen bonds: A with T and C with G. So, quite naturally, one DNA strands will be matched with another strand to form a continuous series of base pairs. These 2 strands coil to form the famous double helix of DNA. This seems redundant though, why have two strands that essentially contain the same information since, if we know the content of one side, we can deduce the content of the other? Well, it turns out to be the point since, in addition to providing a sturdier physical structure, having a second strand allows for information to be encoded with higher fidelity. If one strand somehow gets damaged, it can be repaired by leveraging the nucleotide sequence of the complementary one.

Is accurate retention of information really such an important consideration though? There is no debate it is, and the fact that such a concept as the double helix developed and has been maintained throughout the animal and plant kingdoms is in itself a strong empirical evidence to support this statement. The fundamental reason why high fidelity in genetic information storage is crucial lies in the fact that the sequencing of nucleotides provide all instructions required for an organism to grow and sustain itself and in particular the template to create proteins with specific functions. More on this in the next section.

Back to our base pair sequencing, in humans there are about 3 billion pairs of DNA and even in a bacteria there can be more than a million of them whilst the number drops to a few thousands for viruses. Altogether, this forms what is called a genome and, in the case of humans, the double-helix strands are packaged into 23 pairs of chromosomes. Why have multiple chromosomes? Probably because having only one would be unwieldy and not volume-efficient.

Why have pairs? We will look into this shortly.

Why 23 pairs? There probably is no particular reason for this other than the number works well for the human genome. Our cousins the apes have 24 pairs (looks like two chromosomes fused at some stage during the evolution of the human species), elephants have 28 pairs, oaks have 12 pairs and so have tulips.

c) Gene expression and phenotype

Having covered the need for information and its storage modalities, we can now turn our sights toward the manner in which this information is used and how this discussion fits in the progression from the molecules of chemistry up to the complex living systems of biology.

Recall the earlier comment about the encoding of instructions in the form of DNA as being necessary to create protein. At a high level, this involves a two-step process: translation then transcription. During the initial step, the double strand of DNA is temporarily separated at a specific location where coding instructions for the desired biomolecule are situated and a messenger RNA (mRNA) polymer strand is created. RNA stands for ribonucleic acid and is very similar to DNA except one of the four nucleotides it is made of differs: uracil (U) is substituted for thymine (T) so the hydrogen bonds occur between A and U instead of A and T. Think of the 2 DNA strands D1 and D2 being unzipped in one location with a RNA strand R1 being produced by matching its nucleotide sequence with that of R2 using the system of complementary base pairing, and D1 and D2 re-bonding afterward to close the zip. We thus have R1 being similar to D1 except for U replacing T. This forms the template used for the next step, the translation, during which the proteins will be synthesized based on the codon sequence of the mRNA.

We will go into more details on that front in Chapter 4 but what interests us for the time being is that the information encoded in the DNA is effectively being copied and read to generate biological products such as proteins and ultimately turned into a function. I have only mentioned protein as yet but, with some difference in modalities, the central concept remains similar for other kinds of output. In the jargon, this process is called “gene expression”.

Nevertheless, having the information required to create functional products doesn’t mean such manufacturing should take place in every part of an organism all the time. Therefore, the DNA also needs to enclose information serving as instructions to turn on and off a particular gene expression. This control aspect is called “gene regulation”; it is information about the time and place to express function.

You may or may not be surprised to know that all cells have the same genome, and therefore the same information stored in their DNA. Hence, it is gene regulation that is behind cell differentiation in terms of their shape (morphogenesis) and role (cellular differentiation) in an organism. Furthermore, the expression of some genes can also be induced depending on environmental context and triggers, thus ensuring the adaptability of an organism and improving its odds of surviving and thriving by means of reproduction.

Over the course of an organism’s life, the coding of the regulation of gene expression may be altered without a change to the DNA sequence itself. This type of molecular overlay falls in the category of “epigenetics” and is not inherited by the offspring of animals (it works a little differently for plants) unless it occurs in the gamete – the eggs and sperm, the carriers of genetic information from the parents during the reproduction process. In that case, it can be transmitted one generation down for males and two for females due to exposure of the germline in the womb – germline refers to those cells that form the gametes. Side note: the term epigenetics is somewhat ill-defined and very often ill-used, do not believe everything you hear about heritability.

At this point, we should not omit to discuss the end result of gene expression, its observable characteristics, what is called a phenotypic trait or “trait” for short. Think eye or hair colour or blood group or even more complex aspects of our biology such as how tall one is. This can be the result of a single gene expression or the outcome of thousands of them expressed simultaneously; such is the case for our size or our individual propensity to gain weight, or not.

A particular variation of a gene is called an “allele” and having two chromosomes in our genome, one from each parent, the observable trait an individual exhibits depends on biochemistry (the chemistry of living organisms). Before providing an example, let me introduce the relevant nomenclature for a specific gene X corresponding to the presence or not of antigens in red blood cells: in the case where antigen A is produced, the letter “a” in superscript will follow X in capital letter and where no antigen is produced the lower-case version of the letter representing the gene is used. So antigen A would be noted as X^A, antigen B would be noted as X^B and the no-antigen variation would be written as “x”, this last case would be caused by the silencing of the gene through regulation. These are the three possible alleles for this specific genes in humans. As a result, with one allele from each parent, there are six (3!) possible genotypes: X^AX^A, X^AX^B, X^Ax, X^BX^B, X^Bx, and xx. Because X^A and X^B are dominant over x, somebody with the xx combination will be “Type O”, either of the X^AX^A and X^Ax combinations will yield “Type A”, those of X^BX^B and X^Bx constitute “Type B”, and when both Antigen A and B are present for genotype X^AX^B we have “Type AB”. In reality, there are dozens of alleles but many of the proteins they produce have identical properties so the grouping into three works in practical terms. Similarly, the colour of our eyes, which is determined by traits including the amount of the melanin pigment in our iris, owes mostly to two genes but there are at least another 10 involved so the end result ultimately depends on their interaction, on the biochemistry of the expressed genes at the molecular level. What we have been told at school about the blue eye allele is an oversimplification (a kind way to say it is wrong), both in terms of how many genes are involved and with regards to an allele being dominant and the other recessive. That said, this concept of dominance does help with estimating probabilities of eye colour depending on that of the parents.

When many or all traits are considered together, we talk about phenotype. Because gene expression can be impacted by environmental factors such as temperature, diet or light cycles, so is our phenotype. A well-known example of this is the influence of the temperature at which a reptile’s eggs are incubated on the sex of the new-borns through the expression or repression of particular genes.

Before wrapping up this section, and prior to exploring the notion of organisms in Chapter 5, I would like to make a short digression on the topic of extended phenotype, a biological concept introduced by Richard Dawkins in his namesake book The Extended Phenotype. Essentially, this considers the effects of a gene expression on the organisms’ environment, beyond their strict physical boundary. The classic examples would be a beehive or a beaver dam, both direct modification of an animal’s habitat. However, the idea of phenotype can also encompass direct and indirect manipulation of other organisms. The former would include parasites being carried by their hosts or perhaps even pollen transferred between flowers by birds or butterflies. The poster-child example for the latter is the genes determining the looks and shape of a cuckoo’s egg ultimately tricking another host species to feed the cuckoo’s chick hatching in their nest. This widens the scope of evolutionary fitness and firmly cements the place of the gene at its centre.

d) Reproduction and inheritance

This would have been a perfect segue to seamlessly move to the topic of natural evolution, nonetheless, before we do so, we need to spend some time on the notion of inheritance and the technicalities of reproduction – the how, not the why, which will be covered in the next section. I won’t spend too much time on this topic though, nor provide too many details, because no matter how interesting each variation is, I prefer to focus on the big picture of what it does to information and the fit within evolution.

Reproduction refers to the production of a new organism, the offspring, from one or two parents. We distinguish two forms of reproduction: asexual and sexual. The term “sexual” doesn’t refer to sexual intercourse, which may or may not occur. Instead, the key aspect lies in the offspring being the result of the interaction between one female gamete and one male gamete, coming in most cases from two different organisms, thus resulting in a gene mixing and an offspring with a genome different from those of its parents. This is unlike asexual reproduction where typically only one organism is involved and the outcome is an offspring effectively identical to the parent, barring any error in the process.

For prokaryotes, single-cell organisms without nucleus, the asexual reproduction involves the replication of DNA within the cell followed by an elongation of this cell and then its division resulting into two cells with identical genetic material. This is called “binary fission”, if you wish to know. For background, prokaryotes encompass bacteria and archaea, two out of the three-domain taxonomic system, the other one being the eukaryotes. They can be found everywhere including in volcanic hot springs or in animal microbiomes.

Another common form of asexual reproduction, in particular among vertebrates such as fishes and reptiles, is parthenogenesis. This process consists in the development of an egg without fertilization, hence there is no combination of male and female gametes. Parthenogenesis can serve as a reproduction back up mechanism when the opportunities for sexual reproduction are limited. Other types of asexual reproduction include, but are not limited to, budding, vegetative propagation, sporogenesis. I have inserted the link towards the Wikipedia entry for “reproduction” in case you with to know more about these.

For eukaryotes, organisms with cells that have a nucleus such as plants, animals or fungi, the prevalent mode of reproduction is sexual. The single most important aspect of the process is “meiosis”, the cell division producing gametes, and it is truly fascinating. Meiosis takes place in the germ cells (those cells destined to become male or female gametes) and involves 4 steps. In Step 1, the pairs of chromosomes are all duplicated to form “sister chromatids” joined together at the centre. Let’s use the example of Chromosome “C” represented by the pair consisting of “C1” and “C2” – so after replication we have 2 of each, i.e. 4 chromosomes C. During Step 2, C1 and C2 exchange genetic material – think cutting DNA strands and swapping them, so that no new gene is created but each chromosome has been altered. At this stage we still have 4 chromosomes C. Step 3 involves the homologous chromosome pairs moving to opposite sides of the cell and a division of the cell into two, thus forming two cells each containing a set of sister chromatids. In Step 4, these sister chromatids split to form single chromosomes that again move to opposite sides of the cell, which undergoes a second split to form two cells with single chromosomes. Consequently, after meiosis, there are 4 cells (2×2) with a single set of recombined chromosomes (this is called the “haploid” phase), and each of those cells can potentially become a gamete.

Upon fertilization, the objective of sexual intercourse, the male and female gametes will fuse thereby reconstituting chromosome pairs (the “diploid” phase). The result will be an offspring with statistically half of its genetic material coming from each parent. Now, if you followed carefully, because the chromosome in the parent’s gamete was recombined, it included genetic material from both parents of the parent, i.e. from the grandparents. Thus, with each generation, every member in the lineage will contribute some of its own genetic material – which is why we can identify genes and phenotypic traits from any of our grandparents and beyond. Crucially, it also ensures genetic variability between individuals.

e) Evolution and natural selection

We now find ourselves in evolution territory. First off, scientists talk about theory of evolution and a theory can be defined as a system of ideas offered to explain phenomena and events. The reason why using this word is technically accurate is because no theory can ever be proven and therefore is never completely certain. That said, this aspect is unfortunately often misinterpreted (and this happens intentionally in most cases) because it says nothing about probability, and so far, whilst there are still some unexplained phenomena, none goes against the theory of evolution. No case of an ugly fact slaying a beautiful theory. Neither is there any competing theory that would accord to the facts observable around us on a daily basis and to the fossils buried in the Earth’s crust.

The theory of evolution advances that today’s biodiversity is the result, over generations, of generic drift and natural selection. Let’s tackle generic drift first since we have already touched upon the matter and it plays a part in natural selection. We should think of drift as a change in the information content from one generation to the next. This can take place, as we have seen in the previous section, through sexual reproduction, which involves the combination of parts of the parents’ genome, yet in reality it consists in the combination of parts of the recombined grand-parents’ genome. This makes for some serious mixing of genes and therefore new properties and new phenotypes depending on the respective gene expressions and regulation. Here we have our probable answer to the question of why our genome includes two chromosomes: ensuring genetic diversity by inheriting information from each parent.

Yet, this doesn’t account for the creation of new genes. For this, we must point our finger at mutations, the alteration of genomic information due to errors during replication or some damage, such as can be caused by ultraviolets or x-rays. By the way, since some mutations can be lethal, we must thank the presence of the Earth’s magnetic field for deflecting charged particles such as cosmic rays (think DNA shredding) – without this protection life as we know it would not be present at the surface of the globe. This is still an unsolved challenge for space exploration, including would-be human missions to Mars and beyond.

At this point, we understand how mutations, resulting in the creation of new genes, and the random combination of new genes through sexual reproduction come about. This begs the question of their relevance, which would also provide the most likely explanation behind the development of said sexual reproduction – not an obvious outcome from the perspective of a single gene. The underlying driver of evolution is natural selection, defined in Wikipedia as the “differential survival and reproduction of individuals due to differences in phenotypes”. In a way, this is the answer, but rather than explain why this is so and then have to repeatedly clarify the dynamic between genes and organisms as well as the passive aspect of evolution, it might be more insightful to follow nature’s pathfinding process. This might be a little long, indeed it took a few billion years to get to the current pool of species.

And so, in the beginning was the macromolecule. No evolution is required to go from the elementary particles to this self-assembly of atoms, it all obeys fundamental interactions. At some stage, in the primordial soup, some of those macromolecules would somehow have developed the ability to self-replicate; we are not talking complex organisms here nor are we talking just a handful of atoms but still, considering the trillions of billions of macromolecules forming, it is very conceivable that serendipity would struck here and there. Whether the first replicators were nucleic acids such as RNA or if there were proteins isn’t really important, although it is one of the first big unanswered questions in the emergence of life. What matters is the idea that if a macromolecule can replicate, even if some of its instances get destroyed, some will survive, unlike non-replicating entities. This ability to replicate is one way to preserve information over time.

If in the long run and probably on the back of some random mutation, one of those replicating entities develop a specific function providing it with an edge in terms of survival over those that do not, then eventually it will outnumber those replicators lacking the same advantage – note here that the relevance and superiority of this function are context-dependent so a specific development cannot be considered favourable in the absolute, its usefulness may vary drastically in a different environment or ecosystem. It is easy to demonstrate the outnumbering dynamic by running some simple maths with one generation defined as one replication from a parent to an offspring entity. Let us assume each parent replicates twice and the survival rate of each entity until it replicates itself is 50% in the standard case and 51% in the case with an advantageous mutation. Over one generation, the standard replicator will have 2×50% = 1.00 offspring that end up replicating itself. Over two generations this becomes 1.00*1.00 = 1.00. For the mutated replicator, the expected number of offspring reaching replication is 2*51% = 1.02. Over two generations this becomes 1.02*1.02 = 1.0404. Over 100 generations the standard entity could expect to have yielded 1.00 (1.00 raised to the power of 100) 100^th-generation offspring and for the mutated variant, this would be about 7.24 (1.02^100). If we have one replication per day, this means after 100 days there would be 7 times more mutated entities than standard ones. After 1 year (365 days), the ratio becomes 1,377, and after 2 years it would be 1,377*1,377, which is close to 2 million. Effectively, the mutated version would have become the new standard, what is called the “wild type” when it comes to gene alleles (we have not reached the gene stage yet but the notion is the same). This explains why tiny increments can make such a difference and it also gives a sense of the number of generations involved in timespans in the order of hundreds of millions of years. Of course, the inter-generational time span between generations increases as organisms grow more complex, yet even assuming inter-generational periods of 10 years, every 100 million years represent 10 million generations, plenty enough to accommodate the evolution from macromolecules to humans.

Eventually one can imagine many replicating units binding together as long polymers, this would be the RNA we introduced a few sections ago that is still being used in our cells as template for creating proteins. Further along, evolution, through mutations or chance assemblage, would have given rise to the first DNA macromolecules, thus providing an edge to the replicator (the RNA). But what is this edge exactly if RNA also stores information? Well, edge should be in the plural form: DNA is chemically more stable as well as less error-prone during replication as compared to RNA. From now on, we will think about gene both as not only the macromolecule able to indirectly code for function and therefore phenotypes but also as the base replicating unit. A stance similar to that of Richard Dawkins in his seminal book The Selfish Gene.

So far, we have covered the importance of replication, survival, mutation and information storage. At first sight, sexual reproduction doesn’t seem to obey the same logic since the odds of a specific gene being passed on to one of its offsprings is halved. The truth is that sexual reproduction obeys all the above dynamics when they interact and sometimes compete with each other. Before I clarify this statement, I must sprint through the process of development of sexual reproduction: through generic drift the mechanism of genomic recombination is “discovered” and since it proves useful it becomes more prevalent and continues evolving towards the model of male and female gametes coming from two different parents. The rest is history. So why is genomic recombination such an ace in evolution’s sleeve?

The answer is quite straightforward, it is a supercharged engine of genetic variability, the fastest method to try new gene combinations, though as I already pointed out, it is not a way to create new ones (that would be mutation and other types of genetic drift). Imagine genetic recombination improves the survival rate from 50% to 60%, however a gene’s replication rate gets halved from 2 to 1 since it is only present half the time in the recombined genome of the offspring. The non-recombining version would therefore on average be present in 2*50%*100% = 1.0 surviving offspring and the recombining one would be present in 2*60%*50% = 0.6 surviving offspring. Non-recombining wins in this scenario. Over one generation, assuming only one common pool, and no competition between organisms. In reality, replication rates are much larger than two and survival rates much lower than 50-60% so in a specific ecosystem, a particular genetic variation behind a new phenotype could provide an organism with a sufficient edge to completely outcompete other organisms not endowed with this particular phenotype. If survival rate for the organism with the standard gene drops significantly when faced with organisms carrying the mutated gene then the maths quickly turn into the latter’s favour. And so the chances of this occurring are (almost) infinitely higher for organisms that are more susceptible to genetic variation, hence the clear long-term advantage of sexual reproduction in terms of natural selection. Also, once a particular gene becomes the wild type and is carried by most of the population, it stands a very high chance (much more than 50%) of being present in the offspring in one of its allele forms even with genomic recombination in the picture.

Finally, as population spread geographically, the genetic drift and mixing through sexual reproduction eventually leads to different phenotypes, especially as the environment varies and the types of organisms sharing an ecosystem also differs. Throughout thousands of generations, these incremental changes reliably give rise to organisms differing markedly from their common ancestors, thus the branching out into what scientists call “species” for convenience’s sake, notably the benefit it introduces in terms of taxonomic organisation. Indeed, I would like to highlight that species are much more of an intellectual concept than a natural one and the main differentiating factor between two species, as nature goes, is the inability to create viable offspring through inter-species sexual reproduction due to the existence of some genomic incompatibilities. So, do not be surprised next time you hear about the percentage of similarities between the genomes of humans and some other species. Case in point, it is close to 99% for chimpanzees and 80% for bovines. This is also a clue about how much information relates to functions and organism-wide processes not visible from the outside and driven by microscopic chemical interactions such as synthesizing proteins as opposed to phenotypic traits like size, shape of limbs or even the make-up of the brain.

f) Rewarding cooperation

Whether reproduction involves gene recombination or not, the fact that it involves the entire genome rather than individual genes has a consequence that cannot be underestimated: it indirectly encourages cooperation via the development and spread of genes working for the benefit of the entire organism because all genes find themselves in a shared outcome scenario – and this doesn’t suggest they have a mind of their own, the dynamic is a passive one, as I spelled out previously. Indeed, this favours the persistence over generations of random mutations favouring the survival of the organism, rather than simply the replication of the mutated gene itself. Now it should become clear why there is no contradiction between the idea of “selfish genes”, in the sense that genes do not actively seek to help other genes, and the patterns of coordination and complementarity resulting from genes’ expression and regulation. This joint effort may even become intergenerational since generations from the same lineage partly carry the same set of genes so if a gene induces parents to care after their offspring, even to the detriment of their own survival rate, you can be sure that this gene has made it into the species’ genome because the maths worked in its favour, at least in the ecosystem in which the species evolves.

This idea of shared outcome and cooperation within an organism also explains why we would expect to see differentiation and specialization emerge. It is quite obvious how the ability to perceive the outside world through a visual system such as the eyes and brain (for processing of the data), the development of specialized organs and muscles to allow the organism to evade predators and hunt preys would be beneficial to the organism. However, those could never have evolved if each differentiated set of cells did not share the same outcome as the others; the eye by itself would be easy prey and the muscle without the lungs and the eye would also have a low survival rate.

g) Trivia – The making of a theory

It took a surprisingly long time for the concepts of evolution and speciation (the formation of new species) to emerge and become a serious area of enquiry. Undoubtedly, the main reason lay in the fact that the idea ran counter to the prevalent religious dogma stipulating the divine origin and design of living forms so not only was there no further explanation required but advancing one would have been seen as blasphemous, heretical and very possibly akin to a death warrant.

In the early 1800s Jean-Baptiste Lamarck proposed the idea of inheritance of acquired characteristics by the offspring from the parents, which obviously doesn’t accord with what we know now but at the time genes and DNA had not yet been discovered so there was no obvious competing theory. It is Charles Darwin and Alfred Russel Wallace, independently in the mid-19^th century through their observation of various species, who posited the idea of evolution, speciation and natural selection. Gregor Mendel in the 1860s and some of his intellectual successors worked out the mechanisms of inheritance, in particular Hugo de Vries who advanced the hypothesis of mutation.

As for DNA structure, the double helix model came to light in 1953 with credits to James Watson, Francis Crick, Rosalind Franklin and Raymond Gosling.