EARTH LOG ENTRY EARTH LOG METADATA EL-ID: 0005 Title: Inheritance and Change Author: Marquez Comelab Date Published: - Date (Gregorian): 2026-04-27 - Cosmic Time ≈ 13,800,000,000 Location: Planet Earth → Europe → Belgium Cosmic Address: Pisces–Cetus Supercluster Complex → Laniakea Supercluster → Local Group → Milky Way → Orion Arm → Local Interstellar Cloud → Solar System → Planet Earth Language: English Medium: Text Series: Earth Log Purpose: A chronological record of human civilization written during the lifetime of the author and preserved on the BitcoinSV (BSV) Blockchain. Origin BSV Pay Address: 12ifVfVfPxBPshVz3t1ZaixDzsBmH4ZJ3f Origin BSV Ordinal Address: 12Ub5i2MXLcBwTed8ssm4VGDAdkfpdGJfo BSV Blockchain Transaction ID, TXID: Pending (assigned after BSV Blockchain inscription, cited in the next Earth Log inscription) Preceding Earth Log's BSV Blockchain, TXID: 4451e8e0c86adaa5555f7110e67b68d7fb81b6c020b61a18d65959f0199c4cbb BSV Tipping Address: 194NLjH58MYVZ846jmNXSpobVZK72NZXJD Subject Timeframe - Years Ago: Start: 4,000,000,000 End: 0 - Cosmic Time: Start: 9,800,000,000 End: 13,800,000,000 - Gregorian Date: Start: N/A (pre-human history) End: 2026 CE CLASSIFICATION Category: Life Questions: • How did life arise? • How does evolution shape life? • How does the universe work? Tags: • genetics • heredity • inheritance • DNA • RNA • genes • chromosomes • alleles • mutation • genetic code • double helix • Mendel • epigenetics • CRISPR • gene editing • variation • biology • molecular biology • life • science • scientific discovery • evidence • reason • knowledge systems Context: Emergence of Life Series: • How We Came About Cosmic Narrative Stage: • Life References: #0004 Corrections: None Copyright © 2026 Marquez Comelab. All rights reserved. =============== EARTH LOG #0005 =============== -------- COMMENT: In the previous entry I described what humanity at this time understands about how life began on Earth — the chemistry that produced the first replicating molecules, and the moment at which ordinary matter first acquired the property of making copies of itself. This entry continues the *How We Came About* series. Once a molecule that copies itself exists, two questions follow immediately: what is the copy actually made of, and how does the information get faithfully transmitted from one generation of replicators to the next? This is the domain of genetics — the study of inheritance, of the molecule that carries it, of the small mistakes that introduce variation, and of the structures that turn that variation into the diversity of every living thing. I write this entry in the spring of 2026 of the Common Era. The science of heredity is among the most rapidly developing fields in our era; substantial parts of what follows would have been unknown or only dimly suspected fifty years before, and parts of it are still being worked out as I write. I have set out the picture as it is broadly understood at this moment, noting where the picture is settled and where it is still being argued over. -------- ------ ENTRY: ------ THE QUESTION What carries the form of a parent into a child? For most of human history, the answer was obvious only by what one could observe: children resemble their parents. They have a parent's eyes, a grandparent's nose, the shape of a great-grandfather's forehead. Some traits skip a generation. Some seem to come from neither side and surprise everyone. Whatever was being transmitted, it was being transmitted somehow — and yet for thousands of years the mechanism was completely unknown. The solution turned out to be a molecule. This entry describes what we now know about that molecule, about the rules by which the information it carries is passed on, about the small errors that creep in during copying, and about the way those errors — far from being a defect of the system — are the engine that drives every change in the living world. THE PUZZLE NO ONE COULD SOLVE The first person to make real progress on the mechanism of heredity was a monk named Gregor Mendel, working in the garden of an abbey in Brno, in what is now the Czech Republic, between 1856 and 1863. Mendel grew tens of thousands of pea plants. He counted the offspring of carefully arranged crosses, noting whether the seeds came out wrinkled or smooth, the flowers white or purple, the plants tall or short. What he found, in the patterns of those numbers, was that the traits of his peas behaved as if they were carried by discrete particles — units that did not blend together when a tall plant was crossed with a short one, but instead were inherited intact, distributed to offspring in predictable mathematical ratios [1]. A tall × short cross did not, as common sense suggested, give rise to plants of intermediate height. The first generation was uniformly tall; the next generation reproduced the original short plants in roughly one-quarter of the offspring. The "short" instruction had not vanished. It had been carried, hidden, through the first generation, and re-emerged in the second. Mendel published his results in 1866, in the proceedings of a small natural-history society. They were almost entirely ignored for the next thirty-four years. When they were rediscovered around 1900 and properly understood, they founded the modern science of heredity. The hereditary particles Mendel had inferred were eventually given a name: *genes*. But what *was* a gene, physically? For another half-century, no one knew. THE MOLECULE The answer was identified, in stages, between the 1940s and the 1950s. In 1944, Oswald Avery, Colin MacLeod, and Maclyn McCarty showed, by careful purification work on bacteria, that the substance which carried hereditary information was deoxyribonucleic acid, or DNA [2] — a molecule that had been known to chemists for decades but had been considered too uniform, too repetitive, to plausibly carry the diversity of life. Most biologists of the day expected the answer to be a protein instead. In 1953, James Watson and Francis Crick — drawing crucially on X-ray crystallography work by Rosalind Franklin and Maurice Wilkins — proposed the structure of DNA that has stood ever since [3]. DNA is two long, thin strands twisted around each other in a regular spiral. Each strand is a backbone of alternating sugar and phosphate units. Attached to each sugar, pointing inward toward the partner strand, is one of four small molecules called *nitrogenous bases*: adenine, cytosine, guanine, and thymine — abbreviated A, C, G, and T. Inside the helix, the bases pair up across the gap: A with T, C with G, always. The two strands are not identical; they are complementary. Where one strand reads ACGT, the other reads its mirror image: TGCA. This complementarity is what makes inheritance possible. To copy a DNA molecule, the cell unwinds the helix, separates the two strands, and uses each one as a template — running along it base by base, slotting in the complementary partner each time. From one double helix, two are produced, each consisting of one old strand and one new one. Each daughter molecule is, to a very high degree of fidelity, identical to the parent. The chemical composition of the four bases is the same in every living thing. A T-base in a worm is the same molecule as a T-base in a human. The only difference between species, and between individuals within a species, is the sequence in which those four bases appear along the strand. Life on Earth is written in a four-letter alphabet, and the differences between every organism that has ever lived are differences in spelling. A typical human body cell contains two complete copies of the genome — about 6.2 billion base-pairs of DNA in total — distributed across forty-six chromosomes (twenty-three pairs). A single haploid set, such as that carried in a sperm or an egg cell, contains about 3.1 billion base-pairs across twenty-three chromosomes [4]. If the DNA from a single ordinary body cell were unwound and laid end to end, it would extend roughly two metres — folded, in life, to fit inside a cell nucleus only a few micrometres across. The human body, at adult size, is built of around thirty-seven trillion cells [6]; almost every one of them carries a complete copy of the same DNA. THE CODE AND THE GENE The sequence of bases in DNA is not a passive archive. It is read. A particular stretch of DNA — typically thousands of bases long — encodes the instructions for building a single specific protein. That stretch is what is meant, in modern usage, by a *gene*. (Some genes encode functional RNA molecules rather than proteins; the protein-coding case is the canonical one and the path we will follow here.) To execute the instructions, the cell first transcribes the gene into a working copy made of a closely related molecule, ribonucleic acid (RNA) — the same molecule that, in the era described in the previous entry, was likely the original replicator. The RNA copy then leaves the cell nucleus and is fed into a molecular machine called a *ribosome*, which reads the sequence three bases at a time. Each three-base "word" — known as a codon — specifies one of twenty standard amino acids, the building blocks from which proteins are assembled. As the ribosome moves along the message, it joins the specified amino acids together in order, producing a chain that folds, often spontaneously, into a working protein. This sequence of operations — DNA copied to RNA, RNA translated into protein — is so fundamental that it was given the name *the central dogma of molecular biology*, by Crick himself in 1958 [7]. It is, with some now-known exceptions (such as reverse transcription, by which RNA can be copied back into DNA) and refinements, how every cell on Earth runs its inherited information. The genetic code — the table that maps each three-base codon to a specific amino acid — is essentially the same in bacteria, fungi, plants, and animals. The reason is simply that all living things on Earth descend from a common ancestor that was already using this code, and any large-scale change to it would be catastrophic for any organism that adopted it. Minor variations exist — most notably in mitochondria and in a few microbial lineages — but the deep machinery is universal. The complete set of genetic information carried by an organism is called its *genome*. The specific combination of alleles an organism carries is its *genotype*. The actual collection of physical and behavioural traits that emerge when those instructions are executed in a particular environment is called the *phenotype*. The relationship between the two is not one-to-one. Most traits are shaped by many genes, often in combination with conditions during development; a single gene rarely produces a single trait neatly on its own. In humans, the protein-coding portion of the genome — the portion that contains genes in the strict sense — is now known to comprise only about 1 to 2 per cent of the total DNA sequence. The other 98 to 99 per cent was for many years dismissed as "junk DNA". It is now known that a substantial fraction of it is involved in gene regulation — switching genes on and off, controlling when and where in the body each protein is produced, controlling the timing of development [8]. The picture of the human genome as a list of around 19,000 to 22,000 protein-coding genes is correct as far as it goes, but the regulatory machinery surrounding those genes is at least as important to what an organism becomes [9]. CHROMOSOMES AND CELLS Inside a cell, DNA does not float free. It is wound around proteins called histones and packed into discrete bundles called *chromosomes*. The DNA molecules of a single human cell, if uncoiled, would each be too thin to see directly under any optical microscope; the chromosome packaging brings them up to a scale at which, with appropriate staining, they become visible. Different species have different numbers of chromosomes. Mosquitoes have 6. Onions have 16. Carp have 104. Humans have 46, organised in 23 pairs. The pair structure reflects the central fact about heredity in most animals and many plants: every individual carries two complete copies of the genome — one inherited from each parent. When a cell divides for ordinary growth or maintenance — a process called *mitosis* — the chromosomes are first duplicated and then split evenly between the two daughter cells. Each daughter ends up with the full set. This is how a single fertilised cell, the *zygote*, becomes, in time, an entire body. Every adult human began as one cell; the trillions of cells that constitute the body are the descendants of that first cell, produced by something like forty to fifty rounds of division. The exception is the production of sperm and egg cells. Those cells must carry only one copy of each chromosome — twenty-three in humans — so that when sperm and egg combine, the resulting zygote has the correct full set of forty-six. The specialised division that produces single-copy reproductive cells is called *meiosis*, and it is in meiosis that some of the most important shuffling of inherited material takes place. SEX, ALLELES, AND DOMINANCE Because every individual carries two copies of each gene — one from each parent — there are, in principle, two versions of every instruction inside every cell. The two versions may be identical, or they may differ. Different versions of the same gene are called *alleles*. Most of the time, when the two alleles disagree, the body produces a phenotype shaped by both — but not always equally. In many cases, one allele is *dominant*: when it is present, it is the one that is read into the trait. The other is *recessive*: it is present in the genome and can be passed to offspring, but it does not show up in the bearer's phenotype unless both copies of the gene are recessive. This is the rule Mendel inferred, before any of the molecular detail was known. A child carrying one allele associated with blue eyes and one associated with brown will, generally, have brown eyes — because the brown allele tends to be dominant — and will still carry the blue allele intact, ready to be passed on. If two such carriers reproduce, roughly a quarter of their children will have inherited the recessive blue allele from both parents and will therefore have blue eyes. This is the dynamic by which a trait can disappear from one generation and re-emerge in the next. The simple model is a useful entry point. In reality, only a small minority of traits are governed by a single gene with clean dominance. Most traits — height, skin tone, susceptibility to many diseases, behaviour — are *polygenic*, shaped by tens or hundreds or even thousands of genes acting in concert, modulated by conditions during development. Eye colour itself is now known to involve dozens of contributing genes. The arithmetic Mendel discovered remains correct for the simple cases, and the underlying logic of dominant and recessive alleles still applies; but the picture of human variation as a series of clean two-allele switches is no longer how the geneticists of this era describe what they see. WHY CHILDREN ARE NOT EXACTLY THEIR PARENTS A child receives a complete set of DNA from each parent and is therefore, in the strict molecular sense, made entirely of inherited material. And yet the child is never an exact copy of either parent, nor of an older sibling. The reasons for this are now well understood. The first reason is that *every* sperm and *every* egg already carries a different sample of the parent's DNA. During meiosis, the two members of each chromosome pair are not simply distributed at random into separate sex cells. They first physically swap segments with each other in a process called *recombination*, or *crossing over*. The chromosome that goes into a sperm cell is therefore a patchwork — partly inherited from the man's father, partly from his mother, stitched together in a unique combination that has never existed before and will never exist again. The second reason is that, when sperm and egg combine, they are bringing together two such patchwork sets, drawn from two different family lines. The child's genome is a fresh mosaic: chromosomes from one grandparent on the maternal side mingled with chromosomes from another grandparent on the paternal side, each chromosome itself a recombined patchwork. The third reason is that copying is never perfect. Every time a cell divides, several letters in its DNA are copied incorrectly. The molecular machinery that copies and proof-reads DNA is extraordinarily accurate, but at the scale of three billion base pairs, even an error rate of one in a billion produces a handful of changes per cell division. Most of these errors are caught and repaired. A small number escape repair and become permanent. The vast majority of these surviving errors — *mutations*, in the standard term — fall in regions of the genome where they do nothing measurable. A small fraction land in places that matter. An even smaller fraction matter in a way that improves the carrier's chances of surviving and reproducing. This last fraction is the hinge on which the whole story of life turns. MUTATION Mutations are the ultimate source of new hereditary variation. Without them, recombination could shuffle existing alleles into new combinations, but no truly new variant could ever appear. With them, every generation introduces some genuinely novel material into the population. Mutations come in many sizes. The simplest is the *point mutation*: a single base swapped for another (an A becomes a G, say) at a single location. Sometimes a base is dropped or an extra one is inserted, shifting the reading frame from that point on and garbling everything downstream. Sometimes whole stretches of chromosome are duplicated, deleted, inverted, or transposed elsewhere — the *chromosomal rearrangements* that Mendel could not have known about but whose existence the modern reader can take for granted. Most mutations are neutral. Many are mildly harmful and tend to be removed from the population over generations because their carriers leave fewer descendants. A few — quite rare — are beneficial in the carrier's environment, and these tend to spread because their carriers leave more descendants. The accumulation of beneficial mutations is the raw material on which the process described in the next entry, natural selection, acts. In humans, the rate of new point mutations is now reasonably well measured: each newborn child carries on the order of seventy new point mutations that were not present in either parent's genome [10]. Across the population of every living thing on Earth, every generation, the total number of new variants introduced is staggering. It is not a malfunction of the system. It is the system's most important property. WHAT RECENT DECADES HAVE REVEALED The account so far would have been broadly recognisable to a working geneticist of fifty years ago. Several pieces of the picture, however, have come into focus only recently, and a reader of 2026 should be aware of them. The first is *epigenetics*. The same DNA sequence can be expressed very differently in different cells — a skin cell, a neuron, and a liver cell in the same body have identical genomes but produce very different proteins — because the cells carry different patterns of small chemical marks on top of the DNA, and on the proteins around which the DNA is wrapped. These marks influence which genes are switched on and which are switched off. The marks can change over the course of an individual's life in response to diet, stress, exposure to toxins, and other environmental factors [11]. In some cases — especially in plants and in some animal lineages — a subset of these marks can be transmitted to offspring, allowing a kind of inheritance that is not encoded in the DNA sequence itself [12]. The scope and stability of epigenetic inheritance in mammals, including humans, remains an active research question; clear-cut transgenerational effects are documented in some laboratory organisms but have proven harder to nail down in humans, where most parental marks are erased and reset early in development. The second is the *non-coding genome*. The view that 98–99 per cent of human DNA was useless was largely abandoned in the 2010s, after large-scale projects mapped the regions of the genome that are biochemically active. A great deal of the non-coding sequence is now known to be involved in regulating when, where, and how strongly the protein-coding genes are read [8]. The exact functional fraction is still debated — some biochemical activity may be noise rather than meaningful regulation — but the casual dismissal of "junk" has not survived contact with the data. The third is *horizontal gene transfer*. The classical picture of inheritance is vertical: parents transmit genes to offspring along a continuous family tree. Bacteria and archaea — the single-celled organisms that dominated the first three billion years of life on Earth, and still dominate it by mass and by number — also exchange genes sideways, between unrelated lineages, by several different mechanisms. A bacterium can pick up a useful gene from a different species in its environment and incorporate it into its own genome [13]. This is how antibiotic resistance, once it arises somewhere in the bacterial population, can spread between species rather than being confined to descendants of the original carrier. For most of the history of life, in other words, "inheritance" was not exclusively a matter of parent to child. The tree of life has tangled roots, and its earliest branches are, more accurately, a network. The fourth is *gene editing*. In 2012 — within the lifetime of many readers of this entry — researchers learned to use a bacterial defence system called CRISPR–Cas9 as a programmable tool for cutting DNA at any chosen location [14]. CRISPR was originally identified as part of the immune system that bacteria evolved to defend themselves against viruses; the discovery that it could be repurposed to perform precise edits on the genomes of essentially any organism transformed molecular biology within a decade [15]. By 2026, gene editing is in clinical use for several inherited diseases — notably sickle-cell disease and beta-thalassaemia [5] — in routine use in agricultural and laboratory research, and increasingly capable in its precision. Earlier methods of programmable genome editing existed, but CRISPR's combination of precision, accessibility, and ease of use brought the practice within reach of any well-equipped laboratory. For the first time, our species can write deliberately, and increasingly at scale, in the same molecular alphabet that natural variation has been writing in for four billion years. The implications — medical, agricultural, ethical, and otherwise — are still being worked out. THE LONG-LIVED THING There is one more idea worth pausing on before moving forward. The physical molecules of DNA inside any one body do not last long. The cells that contain them die continually; the body itself, in time, will die. The four bases that spell out a particular gene at this moment will, before too many decades have passed, be dispersed back into the ordinary chemistry of the planet. What persists is not the molecule but the *pattern* — the sequence. Every time a DNA strand is copied accurately, the pattern is preserved into the next molecule. Every time an organism reproduces, the pattern is preserved into the next generation. A particular gene — a particular sequence of bases — can in principle continue to be copied, generation after generation, for millions of years, hundreds of millions of years, even when no individual organism that ever carried it lived more than briefly. The gene is the long-lived thing. The body, it has been said, is the gene's way of getting more genes into the future [16]. This framing — sometimes called the *gene's-eye view* of life — was articulated most influentially in the 1970s. It is not the only useful way to think about heredity; whole organisms, populations, and ecosystems are also doing things that the gene-level description does not always capture cleanly. But it is one of the most powerful frames available for understanding why life behaves the way it does. Anything that happens in a living thing that helps the genes inside it get copied into the next generation will, over time, become more common. Anything that gets in the way of that copying will, over time, fade. The implications of that single observation, when it is applied with patience to four billion years of replicating life, are the subject of the next entry. WHAT FOLLOWS We now have, in front of us, the materials needed to understand the rest of the story. A planet has produced, by ordinary chemistry, a self-replicating molecule. That molecule is being copied with very high but imperfect fidelity, generating variation in every generation. The variants are sorted into the patchwork combinations that arise from sexual reproduction, then into individual bodies, then into populations of individuals. Some of those individuals leave more descendants than others. Some of those descendants carry the mutations that helped their parents succeed. What this whole arrangement amounts to, when it is allowed to run for hundreds of millions of years, is the topic of the entry to come. — Marquez Comelab Earth Log Project Planet Earth Year 2026 REFERENCES: [1] Mendel, Gregor. "Versuche über Pflanzen-Hybriden." Verhandlungen des naturforschenden Vereines in Brünn 4 (1866): 3–47. English translation: "Experiments in Plant Hybridization," in The Origin of Genetics: A Mendel Source Book, ed. Curt Stern and Eva R. Sherwood. W.H. Freeman, 1966. [2] Avery, Oswald T., Colin M. MacLeod, and Maclyn McCarty. "Studies on the Chemical Nature of the Substance Inducing Transformation of Pneumococcal Types: Induction of Transformation by a Desoxyribonucleic Acid Fraction Isolated from Pneumococcus Type III." Journal of Experimental Medicine 79(2) (1944): 137–158. [3] Watson, James D., and Francis H.C. Crick. "Molecular Structure of Nucleic Acids: A Structure for Deoxyribose Nucleic Acid." Nature 171(4356) (1953): 737–738. See also Franklin, Rosalind E., and Raymond G. Gosling. "Molecular Configuration in Sodium Thymonucleate." Nature 171(4356) (1953): 740–741. [4] International Human Genome Sequencing Consortium. "Initial sequencing and analysis of the human genome." Nature 409(6822) (2001): 860–921. For the parallel Celera publication, see also Venter, J. Craig, et al. "The sequence of the human genome." Science 291(5507) (2001): 1304–1351. For the gapless reference assembly, see also Nurk, Sergey, et al. "The complete sequence of a human genome." Science 376(6588) (2022): 44–53. [5] Frangoul, Haydar, et al. "CRISPR-Cas9 Gene Editing for Sickle Cell Disease and β-Thalassemia." New England Journal of Medicine 384(3) (2021): 252–260. [6] Bianconi, Eva, et al. "An estimation of the number of cells in the human body." Annals of Human Biology 40(6) (2013): 463–471. [7] Crick, Francis H.C. "On Protein Synthesis." Symposia of the Society for Experimental Biology 12 (1958): 138–163. See also Crick, F.H.C. "Central Dogma of Molecular Biology." Nature 227(5258) (1970): 561–563. [8] ENCODE Project Consortium. "An integrated encyclopedia of DNA elements in the human genome." Nature 489(7414) (2012): 57–74. [9] Salzberg, Steven L. "Open questions: How many genes do we have?" BMC Biology 16(1) (2018): 94. [10] Kong, Augustine, et al. "Rate of de novo mutations and the importance of father's age to disease risk." Nature 488(7412) (2012): 471–475. [11] Bird, Adrian. "Perceptions of epigenetics." Nature 447(7143) (2007): 396–398. [12] Heard, Edith, and Robert A. Martienssen. "Transgenerational epigenetic inheritance: myths and mechanisms." Cell 157(1) (2014): 95–109. [13] Boto, Luis. "Horizontal gene transfer in evolution: facts and challenges." Proceedings of the Royal Society B: Biological Sciences 277(1683) (2010): 819–827. [14] Jinek, Martin, et al. "A Programmable Dual-RNA-Guided DNA Endonuclease in Adaptive Bacterial Immunity." Science 337(6096) (2012): 816–821. [15] Doudna, Jennifer A., and Emmanuelle Charpentier. "The new frontier of genome engineering with CRISPR-Cas9." Science 346(6213) (2014): 1258096. [16] Dawkins, Richard. The Selfish Gene. Oxford University Press, 1976 (40th-anniversary edition 2016). END of Earth Log - A record of humanity, written in its own time.