Read an Excerpt from “Disputed Inheritance” by Gregory Radick
In 1900, almost no one had heard of Gregor Mendel. Ten years later, he was famous as the father of a new science of heredity—genetics. Even today, Mendelian ideas serve as a standard point of entry for learning about genes. But in Disputed Inheritance: The Battle over Mendel and the Future of Biology, Gregory Radick shows that Mendelian ideas became foundational not because they match reality—little in nature behaves like Mendel’s peas—but because a ferocious debate ended as it did in the early twentieth century. On one side was the Cambridge biologist William Bateson, who, in Mendel’s name, wanted biology and society reorganized around the recognition that heredity is destiny. On the other side was the Oxford biologist W. F. R. Weldon, who, admiring Mendel’s discoveries in a limited way, thought Bateson’s “Mendelism” represented a backward step, since it pushed growing knowledge of the modifying role of environments, internal and external, to the margins. Weldon’s untimely death in 1906, before he could finish a book setting out his alternative vision, is, Radick suggests, what sealed the Mendelian victory.
In this excerpt from the introduction, Radick begins to detail the history underpinning his argument.
“A Scotch soldier, when I was lecturing in Y.M.C.A. huts, said: ‘Sir, what ye’re telling us is nothing but Scientific Calvinism.’ Sometimes I think that would serve.”—William Bateson, 1920, on what to call a volume collecting his “lay” papers on Mendelism
“Scientific Calvinism” never took hold as a name for the science of inheritance that boomed its way into biology in the early years of the twentieth century. “Mendelism” fared much better, and “genetics”—William Bateson’s coinage in 1905—better still, along with an associated word that arrived in 1909, “gene.” Nowadays, talk of genes is everywhere, in and out of biology: genes for aggression, alcoholism, and autism; for baldness, blue eyes, and breast cancer; for caffeine consumption, curly hair, and cystic fibrosis. You name it, and there is, we are told, a gene for it, invisibly pulling the strings, determining how our bodies grow and our lives go. How and why did such talk become so pervasive?
A familiar answer runs like this. We came to talk of inheritance as genic for the same reason that we came to talk of species as evolved and matter as atomic: because genes and evolution and atoms are real, and whatever is real is bound to get discovered eventually. Gregor Mendel (1822–84) discovered the gene through experiments that he conducted with varieties of the garden pea in the garden of the monastery where he lived and worked in Brünn, in the Austrian Empire (now Brno, in the Czech Republic). He reported his discovery in 1865, publishing it the next year. But alas, Mendel was ahead of his time, and his achievement went unrecognized. Only in 1900, well after his death, were biologists ready to appreciate the significance of what he had done. They made up for lost time, however, swiftly establishing a new science based on the gene. The rest is history: of science, but also of medicine, agriculture, and domains almost undreamt of in Mendel’s day, such as forensics. What we now know about inheritance, and what we know how to do with it, we owe to the discovery of the gene. Mendel got there first, but the discovery was inevitable, along with the central role that biologists assign to genes in understanding and controlling life.
This book aims to replace this answer with a rather different one. We came to talk of inheritance as genic, I will suggest, not because the invisible string-pullers are real but because, in the early years of the twentieth century, a debate over Mendel’s experiments and their interpretation went as it did. The debate was centered in England, indeed, in its two ancient universities, Cambridge and Oxford. On the one side was the Cambridge-based William Bateson (1861–1926). From 1900, he made it his mission to reshape biology in the image of Mendel’s experiments. For Bateson, what Mendel had done in that monastery garden was to sweep away all of the hitherto distorting complexity surrounding inheritance, exposing its underlying simplicity: a vision kept alive in our textbooks. On the other side was the Oxford-based Walter Frank Raphael Weldon (1860–1906). Admiring Mendel’s experiments in a limited way, Weldon nevertheless regarded them as profoundly misleading if taken as a guide to inheritance as such. In Weldon’s view, Mendel had shown not how heredity at its most basic works, but what it looks like in lineages from which almost all ordinary sources of variability, internal and external, have been eliminated. To generalize from Mendelian experiments, in which context had been made to look ignorable and hereditary characters made to look well described by x-or-y (yellow-or-green, round-or-wrinkled, purple-flowered-or-white-flowered) categories, was thus to mistake the exception for the rule.
The debate between Bateson and Weldon drew in others, but no one else cared as deeply, fought as bitterly, or—in consequence—thought as creatively about what was at stake in reorganizing the science of heredity around Mendel’s peas. Nor was the Mendelian victory a foregone conclusion. Indeed, by winter 1905–6, Weldon seemed, in Bateson’s eyes, to be worryingly close to winning the argument. But then, in spring 1906, Weldon died, with a book manuscript setting out his alternative vision unfinished. I shall argue that had Weldon lived, and had Bateson’s fears been realized, our present understanding of how heredity works, and our ability to make use of that knowledge in ways we value, would have been none the poorer. Indeed, in some crucial respects, we might now be better off. We might still talk of “genes,” but without even a hint of that string-puller notion, as though the presence of a particular DNA variant in itself, and by itself, can determine whether or not someone is born to be aggressive, alcoholic, or autistic; to be bald, blue-eyed, or doomed to breast cancer; to crave caffeine, have curly hair, or suffer from cystic fibrosis. Instead, our gene talk would be routinely hedged with talk of contexts, internal and external, because our concept of the gene—“our” meaning everybody’s, no matter how glancing their contact with biological science—would be of an entity whose effects on bodies and minds can be variable depending on the mix of other causes in play. Change those other causes, and you potentially change a gene’s effect, or even extinguish it: something you would hardly guess if you think of inheritance as Mendel’s peas writ large. No wonder that, on hearing Bateson lecture, a Scottish soldier recalled fatalist theology at its most grim.
* * *
Ever since Bateson’s day, introductory lectures in genetics typically deal early on with Mendel’s experiments. Mendel, the student will learn, was a scientifically inclined monk who, in the mid-1850s, having become interested in the mystery of the biological ties binding offspring to their parents—the mystery of inheritance—turned the garden of his monastery into a laboratory devoted to experimental hybridizing. With uncommon shrewdness, he judged the garden pea to be an especially suitable choice for these experiments because it has a suite of easily tracked, sharply differentiated, either/or hereditary characters. The color of a garden-pea seed is either yellow or green. Similarly, the surface of the seed is either smoothly round or unsmoothly wrinkled; the color of the flower on the plant that grows from the seed is either purple or white; the plant itself is either tall or “dwarf”; and so on, with seven such characters tracked in all. Next, and again shrewdly, before beginning to make hybrid plants, Mendel spent a very long time purifying his originating stocks, making sure that—to stick with flower color for now—his purple-flowered pea plants only ever gave purple-flowered progeny, and his white-flowered pea plants only ever gave white-flowered progeny. The stocks became, in other words, “true-breeding.” Only at that point did he begin the experiments per se: first cross-fertilizing; then collecting the hybrid seeds produced; and then planting them. He did all this not with a handful of plants but (showing yet another sign of shrewdness) with lots of them—indeed, ultimately, over the eight years of his work in the garden, over ten thousand of them. And what he found is that the plants grown from the hybrid seeds, when they produced their own flowers, produced flowers that were not lilac, nor mottled purple and white, nor a mixture of purple and white, but uniformly purple.
Here was a remarkable empirical discovery: a regularity new to science, uncovered thanks to the care Mendel took to purify his starting stocks, and thus—as the student is encouraged to see it—to have removed the baffling clutter, the signal-muffling noise that defeated previous investigators. And once Mendel had made this discovery, he went on to make others, in the course of explaining that regularity simply and powerfully. Suppose, he reasoned, that underlying the purpleness of the purple-flowered pea plants there is a purple-making factor, “P.” Since his purple-flowered stocks only ever gave purple-flowered offspring (thanks to his purification efforts), there seemed to be nothing in those stocks, when it came to flower color, except P. Similarly, for his white-flowered stocks, there seemed to be nothing in them colorwise but a factor for whiteness, “p.” Now, on those suppositions, what happened in the course of cross-fertilization was that P and p were brought together, making Pp hybrid plants. And yet, as noted, those plants all had purple flowers only. According to Mendel, what that showed was that, in the pairing of P and p, the effects of the former are visible while the effects of the latter are not. In Mendel’s enduring terms, purpleness is thus “dominant” and whiteness “recessive.” As he saw, an important corollary immediately followed. The dominant version of a character can arise in two ways: if the dominant factor alone is present (as in the purple-flowered parents), or if there is a mixture of dominant and recessive factors (as in the purple-flowered offspring). The recessive version of a character, however, can arise only if the recessive factor alone is present (as in the white-flowered parents).
From that impressive opener, Mendel proceeded, as described in his remarkable 1866 paper on his inquiry, to uncover and explain further regularities within his experimental lineages by further extending this same set of basic methods and concepts. After he had bred into being all those purple-flowered hybrid plants, he let them self-fertilize, and got a generation in which, along with purple flowers, white flowers came back, in the ratio of 3 purple to 1 white. (Mendel’s methodological innovations, the student learns, were not merely to purify and experiment and scale up, but to count.) That ratio, in turn, Mendel explained by way of two additional suppositions. The first concerned what he called “segregation”: that is, when the purple-flowered hybrid plants generated pollen and egg cells, each pollen grain and each egg cell contained either a P factor or a p factor, but not both factors together. The second concerned chanciness: it was a matter of chance whether a particular sex cell (or “gamete”) got a P factor or a p factor, and also a matter of chance which factor came together with which in the union of a pollen grain and an egg cell in the making of an offspring plant. Summing the possible outcomes, one thus expects, Mendel reasoned, to find equal numbers of four factor combinations in the next generation: male P with female P, male P with female p, male p with female P, and male p with female p. Since P is dominant to p, that gives flowers that are, respectively, purple, purple, purple, and white, or 3 purple-flowered plants to 1 white-flowered plant (see fig. I.1).
Anyone even remotely susceptible to the charms of explanatory science will, at this point, feel a little pop of pleasure. So that is what is going on! How elegantly simple on nature’s part, as on Mendel’s. But even those not so susceptible will, sooner or later, encounter Mendel’s peas. They are a staple of scientific education all the way through, in formal schooling as well as outside of it. My children have a Horrible Science Annual that conveys the Mendelian essentials, purple flowers and all, in a good-humored way, including the inevitable pea jokes. (Brother Mendel ladles out pea soup but withholds it from his naughtier brethren, since, he admonishes, there can be “no peas for the wicked.”) In the wider culture too, Mendel’s position as begetter of genetics is reinforced in all kinds of ways, subtle and not-so-subtle. There is Mendelian kitsch: ties, mouse mats, and baseball caps bearing his face, above and below the commandment “Obey Mendelian Principles: It’s the Laws of Inheritance.” In newspapers and their online successors, a standard accompaniment to the latest biotech wonder-story is a history lesson on Mendel and those who have built on the foundation he laid. Such linkings of the Mendelian past to the biotech present can be found well beyond the sphere of popular science. “Since Gregor Mendel first suggested the existence of a gene in the 1860s, genomics research has progressed at an incredible speed. Recent technological advances have moved genomics out of research labs and into the real world.” So reads a posting on an investment blog, advising readers to consider the commercial potential of genetic tests, and noting their recent applications ranging from use in identifying future champion athletes to the much-publicized decision by Angelina Jolie to have her breasts removed after a test revealed a mutation associated with an increased risk of breast cancer.
Thus does a traditional, Mendel-venerating, Mendelism-based education in genetics, informal as well as formal, tend to strengthen the notion that traits are “all in the genes,” even when teachers and textbook writers would disclaim any such agenda. And the lessons stick. A friend of mine told me about a married couple she knows. Both husband and wife have light-colored eyes, green and blue respectively. They had a daughter with brown eyes. On learning that fact, the husband’s mother blew the whistle. According to Mendelian principles, she announced, no child of that couple could possibly have brown eyes, since, according to the version of those principles she (like everyone else) learned in school, dark-colored eyes in humans are dominant and light-colored eyes are recessive, so that light-eyed people, including her son and his wife, could only ever pass on the gene variants for light-colored eyes. Any other outcome implied a violation, and probably not of Mendel’s laws . . . Her son and daughter-in-law, of course, reacted furiously to the implied insinuation, and did what anyone else nowadays would do in their shoes: they turned to the internet. After some searching, they found the reassurance they sought, to the effect that eye color did not, in fact, always follow the Mendelian rules. “Blue-eyed parents can have brown-eyed kids and other eye-oddities” is the title of a currently available online newspaper column, which goes on to explain that, contrary to the simple Mendelian explanation of eye color so widely believed, eye color in humans is not determined by just one gene in one of two states, light-making or dark-making. Like more or less every other hereditary character, eye color is multifactorial in its causation and variable in its expression. To look back on the Bateson-Weldon debate over Mendel is to return to the moment when such complexity, rather than becoming unquestioned common knowledge, became permanently surprising.
Adapted and excerpted from Disputed Inheritance by Gregory Radick, published by the University of Chicago Press. © 2023 by The University of Chicago. All rights reserved.
Gregory Radick is professor of history and philosophy of science at the University of Leeds.