Chapter 2 Chapter 1 Finding Genes
Humans first received genes through yellow and green peas, thanks to Mendner's presence in his botanical garden; Morgan then used black melon flies, no more than two millimeters long, to show that chromosomes are Gene-carrying best worker; finally Watson and Crick model the double-helix gene (DNA)...
Mendel was born in 1822 in a poor peasant family in Hayzendorf, Austria. In 1843 he entered the monastery in Brno as a monk.He had originally studied for a science degree but never completed it because, like Darwin and Galton, he suffered from depression and was unable to work for months at a time.Even so, he never gave up on the experiment at hand, and finally discovered that genetic information is transmitted through simple rules, and this rule is the grammar of genes.However, in his later years, he was pressured by the administrative department to continue the experiment, which became a precedent for modern science.Thus, genetic research was shelved for nearly half a century.
Mendel proposed a conceptual breakthrough. Unlike his predecessors in biology, who only focused on the study of the inheritance of traits, such as height and weight, he focused on reasoning.He was also the first biologist to do serious math, which led to his great discoveries.
Peas, like other garden plants, have so-called true-breedinslines, in which every pea looks exactly the same.As for different strains, there will be different characteristics, such as the shape of the seeds, some are round, some are wrinkled; and the color of the seeds may be yellow or green.Another advantage of peas is that each pea plant has male and female organs, and with a light touch of a paintbrush, pollen can be transferred to the stamens and the pistils can be fertilized.Even stamen pollen from the same plant can use this process of plant incest, which we call self-fertilization.
Mendel added yellow pea pollen (equal to male sperm cells) to the pistils of eight green pea flowers, and found something interesting in the next generation of pea: the next generation of pea did not appear mixed as expected The color, on the contrary, is only like one of the parents, all of which are yellow peas.If the "blood" of the two strains were really mixed together, then the second-generation pea should have a combined color of yellow and green, but it obviously didn't.
The second step in the experiment was to self-fertilize the first generation of yellow peas (that is, the offspring of mating yellow peas and green peas), using pollen from the same plant to fertilize the egg cells of the pistil.Later, unexpected results appeared:
The two original colors, yellow and green, appear simultaneously in the next generation of peas.That is to say, whatever the substance that caused the green peas to appear, its effect continued to occur despite the intervening generation of all yellow peas.This result is completely inconsistent with the theory that the traits of the parents can be mixed together. The mechanism of inheritance seems to be through particles rather than fluids.
Mendel's experiments were not over yet. He added some yellow peas and green peas to each generation of peas.It was found that the first generation of peas, that is, the next generation of two purebred lines, were all yellow; by the second generation, that is, the next generation produced by the self-fertilization of the first generation of yellow peas, yellow peas The appearance ratio of green peas is three to one.Thus, Mendel deduced the basic rules of genetics from the results of this simple experiment.
He believed that pea color is controlled by a pair of factors (that is, genes that were later known), and each growing pea plant has two factors that control color, one comes from pollen and the other comes from egg cells.At the time of fertilization, that is, when the pollen hits the egg, another new plant is born. The new plant also has these two factors in it, and the color of the pea is determined by these two genes.In the original purebred line, all peas carry either two "yellow" or two "green" genes.After mating between purebred strains, each offspring produces a new family that is identical to their parents.
Pollen from one purebred line, combined with eggs from a different purebred line, produces new plants that contain different factors from each parent.In Mendel's experiments, although all peas looked yellow, each yellow pea contained a set of recessive factors that could produce green peas.In other words, the yellow gene covers up the green gene, so we call the yellow gene a dominant gene (ddrinantgene), and the green gene a recessive gene (recessivegene).
Plants with both genes produce two types of pollen or eggs.Half of the pollen, or eggs, carried the genetic instructions to produce green peas; the other half contained the genetic instructions to produce yellow peas.So when two plants mate, the pollen and eggs have four different combinations of genes: a quarter of the fertilized eggs are yellow plus yellow, a quarter are green plus green, and two quarters, That is half, yellow plus green.
Mendel's experiments have confirmed that plants with a yellow gene plus a green gene will grow yellow peas; and yellow plus yellow will naturally grow yellow peas; only plants with both genes are green can grow green peas. green peas.
Therefore, the color ratio of the second-generation peas is three yellow peas to one green pea.Mendel developed the basic rules of heredity based on this ratio he discovered.
Mendel also cross-experimented with many other different traits, such as flower color, plant height, pea shape, etc., and found that all of them fit this three-to-one ratio.In addition, he experimented with mating peas with different characteristics, for example, mating a plant that grew yellow peas with a smooth surface with other peas that grew green and had a wrinkled surface, and the results still met his rules.Moreover, the inheritance of pea color is completely unaffected by the inheritance of shape.From this, he deduced another corollary: each genetic trait is controlled by a single gene, rather than different variations of the same gene, whether it is different forms of the same trait (such as yellow or green in color), Or quite different traits (such as the color and shape of peas) are based on separate physical units.
Mendel was the first biologist to demonstrate that offspring are not composite averages of their parents, and he was also the first to demonstrate that heredity is based on differences rather than similarities.
Biologists from Mendel onwards have constantly discussed his experimental results, repeatedly argued, and occasionally accused him of fraud because his theories fit the actual situation too well.These biologists debated exactly what Mendel's so-called factors were, and speculated why his discovery had been ignored for so long.Regardless of the reason why Mendel's theory has been hidden for many years, his works were re-discovered by several experts in plant cultivation at the beginning of the 20th century, and it was quickly discovered that Mendel's laws are consistent with hundreds of animal and plant genetics. idiosyncratic.It is of course his talent and good luck that Mendel was able to correct the mistakes of his predecessors for many years in one fell swoop.After all, in the history of science, the origin of no science can be directly traced back to individuals like genetics, and Mendel’s works are still the basis of this huge discipline.
Mendel solved Darwin's theoretical dilemma, although neither of them knew anything about it.Neither the gene for green pea color nor the gene for white skin, no matter how rare, would be diluted by the presence of many other copies of it.Conversely, the gene can persist through generations and, given the chance to take advantage, is likely to flourish and become common.
Not long after scientists rediscovered Mendel's laws, the 5!Use these laws to interpret human genetic patterns.Of course, it is impossible for biologists to conduct reproduction experiments on humans because it would take too long; instead, they rely on experiments that have been attempted in the past to study human sexuality.They use family trees (ftilltree) or pedigrees (pedigrees) to conduct research.Some genealogies are full of imagination.Strange enough to go back to Adam as their ancestor.Usually geneticists have only a few generations of data available to them.But in reality, as long as there is one or two generations, it can be traced back hundreds of years.
The first human genealogy was published in 1905. This genealogy shows that the villagers in a small village in Norway all have the genetic characteristics of short palms and short fingers, and there is an obvious genetic pattern in the family, and no generation slips through the net. fish.
In other words, if anyone has the genetic trait of short fingers, his parents, grandparents, and even great-grandparents, in every generation of direct blood relatives, at least one person has the same trait.If such a person marries someone who does not have the genetic trait, about half of their children will have the genetic trait and the other half will be normal.If these unaffected children marry normal people, their offspring will be completely normal, and the genetic trait will disappear in this branch of the family.
Such a pattern of inheritance, known as dominant inheritance, requires only one gene (as in the case of yellow peas) for its effects to show.Most of the children with short fingers are the result of marriage between normal people and those with this genetic trait. Therefore, a pair of genes controlling short fingers in their bodies come from the father and mother respectively, one is normal and the other is Not normal.Therefore, their own sperm or eggs also have two forms, one half is normal and the other half is abnormal. After they get married and have children, at least half of the children will have the gene that causes the short fingers.Therefore, after a normal person marries a person with short fingers, the probability of having a child with short fingers is 1/2.As for couples who are both normal, it is absolutely impossible to have a child with short fingers, because neither of them has the gene that causes short fingers.
However, other genetic characteristics are not so straightforward, because they are affected by recessive genes.For the inheritance of recessive genes, one factor must be inherited from both parents in order to show its influence.Usually only one of the parents has a recessive gene, looks completely normal on the outside, and has no idea that they will have a child with the genetic trait.Sometimes, they give birth to children with genetic traits that look more like distant relatives or ancestors. Before Mendel, the biological world was quite troubled by such children, not knowing why they formed, sometimes called them It is "thorbacks" and sometimes it is said to be due to "atavism".But now we all know that they just followed Mendel's law, and they happened to inherit one recessive gene from both parents, while their parents had only one recessive gene each.
The most typical example of recessive genetic inheritance is albinism.In Britain, there is only one white child in about a few thousand children.Baizi's eyes, hair and skin do not have any pigment.In other regions outside the UK, the phenomenon of Baizi is more common.Among North American Indians, the probability of white sons appearing is about 0.67%.According to the Bible "Book of Enoch" (the Book of Enoch, which is a chapter of questionable authenticity in the Bible), Noah himself was albino. If so, Noah's descendants show no signs of this genetic inheritance.
Almost all albino parents have normal skin color. One of their genes must be a recessive albino gene, coupled with another dominant gene that can provide complete pigmentation.Half of Baizi's father's sperm carry the recessive albino gene.If a sperm carrying this recessive gene is fertilized with an egg carrying a recessive albino gene, then the child will have two recessive genes and thus become an albino child.In such a marriage, the probability of giving birth to a white son is about 1/4.But every pregnancy has the same 1/4 chance of giving birth to an albino child. It is not like some parents think that after giving birth to an albino child, they will definitely give birth to three normal children in a row.
In fact, the genetic rules of peas also apply to human genetic patterns.It's just that the rules of biology are seldom so pure and simple. Therefore, in the history of human genetics research, it has long been common to find exceptions that break Mendel's laws of inheritance.
For example, genes do not necessarily have to be dominant or recessive.Like some blood types, both genes will be expressed. For example, a person who has both type A and type B blood genes, his blood type is AB type, and the characteristics of both blood types are included.
If we further study molecular inheritance, the concepts of dominant and recessive genes will be wiped out.We can now easily pinpoint where changes have occurred in the sequence of DNA bases.Because a person with both normal genes is very different from a person with a normal strand of DNA and an abnormal DNAM, and a person with changes in both DNA sequences.Molecular biology allows us to directly observe the behavior of genes, without having to guess what is going on based on the inheritance of the next generation like Mendel did.
Another discovery in modern biology that astounded Mendel was the discovery that a single gene might control several traits.A variant of sickle cell heme, for example, has several side effects: People with two of these variants can develop brain injuries, heart failure or bone deformities, among other symptoms.In contrast, some traits, such as height and weight, are controlled by many genes.In addition, the genetic ratio proposed by Mendel sometimes changes, probably because one of the genotypes (genetroe), or other genotypes, is a lethal gene or is more dominant.
All of these indicate that genetic research has become a complex subject.Still, there are those who routinely use Mendel's laws to explain the phenomena of heredity in humans and other organisms that seem straightforward.
However, after the biological community rediscovered Mendel's laws, they began to expect that these laws could explain all imaginable, and some unimaginable, patterns of family inheritance.And so came lengthy genealogies that purported to show that sudden outbursts of bad temper were attributable to a single dominant gene, or to explain which genes made people want to go to sea, which genes caused adrift pain (draPetornania, pathologically known as runaway slaves).
Even today, there are still people who demand a simple explanation for everything, but they are not biologists!
Most geneticists once believed that Mendelian theory could explain everything, and tried to use simplicity to control complexity, but they suffered a lot.
At that time, Mendel only regarded the genetic factors as the genetic units passed from parents to children, and did not study the components of genetic factors in detail, nor did he explain where to find these factors.So other scientists began to ask, what are these things?
In 1909, when American geneticist Morgan was looking for objects for breeding experiments, he found the humble fruit fly. His choice inspired the genetic research of later generations.His experiments on Drosophila melanogaster were the first step in mapping the human genome.
Morgan (1866-1945) was born in an old family full of legends in Kentucky, USA.
He has been fond of collecting specimens since he was a child, including exotic birds, horse eggs, butterflies, fossils and so on.In addition to serving as a biology teacher at Bryn Marr College and a visiting professor at Stanford University, his academic career has mainly two periods:
The Columbia period from 1904 to 1928 and the MIT period from 1928 to 1942.
Drosophila is small in size, less than two millimeters in length. It only takes about 10 days for a period from burial to larvae to emergence to adulthood. Each female fly can lay hundreds of eggs, and it is convenient to raise, which is conducive to the research work. .There are thousands of species of fruit flies, and the fruit fly that Morgan used as research material is called Drosophila melanogaster.It is a kind that can be seen everywhere in the world, and it is often found wherever there is fruit.
Most of the genetic traits of fruit flies operate according to simple Mendelian laws.But Morgan discovered that there are some weird genetic patterns that are not as clear as Mendel's research.For example, in a pea cross experiment, which parent carried the green or yellow genetic factor did not affect the color change of the next generation.In other words, regardless of male green and female yellow or male yellow and female green, the mating result is the same.But certain genetic traits in fruit flies have different results.Because some specific genes, such as the gene that makes the eyes change from red to white, must be seen from the father or mother to determine whether they have an impact on the next generation.If a white-eyed father mates with a red-eyed mother, all offspring will be red-eyed.If it were the other way around, that is, if a white-eyed mother mates with a red-eyed father, the result would be the same, with sons all white-eyed and daughters all red-eyed.Parents of different genders carry specific genes, which will affect the appearance of offspring, even Morgan himself was surprised!
Morgan knew that male and female fruit flies also differ in another way.The chromosomes of the cell nucleus are all paired with two black lines. Most of the chromosomes of the two sexes are similar, and only one pair of sex chromosomes is different.Females have two large X chromosomes; males have one large X chromosome and one. In addition, Morgan also found that the color of the eyes of fruit flies is inherited along with the X chromosome.Male fruit flies have only one X chromosome (inherited from the mother, the father provides the Y chromosome), so they all look like the mother.
Female fruit flies, on the other hand, have one X chromosome inherited from their mother and another X chromosome inherited from their father.So in matings of white-eyed females and red-eyed males, all female offspring have one X chromosome with a "white eye" and another X chromosome with a "red eye."As Mendel speculated, the offspring would have the same eye color as one of the parents, in this case, red eyes.
The gene controlling eye color and the X chromosome happen to have the same inheritance pattern, so Morgan deduced that the gene controlling eye color must be on the X chromosome, and he called this inheritance pattern "sex-linked inheritance".Since there are only half as many chromosomes in sperm and eggs as there are in other cells, chromosomes, like the factors Mendel postulated, are the best vehicles for carrying genes.
The same pattern occurs in humans as well.There are forty-six chromosomes in each human cell, forty-four of which are in pairs, making a total of twenty-two pairs; but the sex chromosomes X and Y are different.Because there are few genes on the Y chromosome, Mendel's theory of dominant and recessive genes does not apply to men.And any gene on the X chromosome, whether recessive or dominant in females, will show influence in males.
For example, color is inherited in humans in the same way that eye color is inherited in fruit flies.If a colorblind man marries a normal woman, the offspring will not be affected.But when a colorblind woman marries a normal man, she usually passes her colorblindness on to her sons, not her daughters.Because all males, as long as there is an abnormal X chromosome, will show its influence, but in most females, this recessive gene will be covered by another normal dominant gene, so boys are more likely to become X-chromosomes than girls. color blind.
Other birth defects have the same inheritance pattern, such as Duchenn muscular dystrophy (DUchennmusculardysrOPh), a disease that causes muscular tissue wasting. Wearing a brace, starting to use a wheelchair at the age of eleven, and usually do not live beyond the age of twenty-five.Because the gene that causes this disease is also related to gender inheritance, like color blindness, boys are more likely to suffer from this disease.Parents who watched their sons die from muscular atrophy had to endure yet another bit of gut-wrenching ambition, as there was a one-in-two chance that other sons would also suffer from the genetic disorder.
Sex-linked inheritance causes some interesting differences between the sexes.Since women have two X chromosomes, men have only one, so women have more information than men.Human beings have two different receptor factors for the red color, and because this receptor factor is on the X chromosome, many women have two kinds of receptor factors, each with different sensitivity to subtle differences in the spectrum, while men can only limited to a receiving factor.So, when it comes to color, women have access to a wider range of sensory experiences than men.
While women can see the world differently, there are many potential problems with sex-linked genetics.Usually, anyone who has an extra chromosome as large as an X chromosome is enough to be fatal, not to mention that as long as the information on one X chromosome is enough to create a person (at least a man can be created), then how do women adapt to two? What about the X chromosome?The answer came as a surprise. One of the two X chromosomes in almost every cell in a woman's body must be turned off.This process was first discovered by the geneticist Leon (anrywr), hence the name "leonization"
(LyoniZatbo), the best example to illustrate the process of lyonization is the cat.The mottled coat color of the tabby domestic cat (tortoise shllcat) is formed by mixing a patch of yellow and a patch of black.All tabby domestic cats are female cats who inherit the black gene from one parent and the yellow gene from the other.The coat color gene is sexually linked, so in a developing kitten, half of the skin cells turn off the X chromosome with the black gene, and the other half of the skin cells turn off the X chromosome with the yellow gene, and the result is It becomes black and yellow hair mixed together.As for the size of the spots, they vary.
The same happens with humans.For example, if a woman gives birth to a son who is congenitally colorblind, it means that of the two red receptor factors in her genes, one must be normal and the other must be abnormal.When a tiny red or green light is swept across her retina, her ability to perceive colors changes as the light sweeps across different cell groups. About half of the time, the colors are clearly discernible, and the rest of the time. , just like her color-blind son, can't distinguish between red light and green light. This is because in each color sensory cell, different X chromosomes are turned off. Sometimes the normal chromosome is turned off, and sometimes the color-blind gene is turned off. of chromosomes.
Another important difference between the genetic patterns of the sexes is related to mitochondrial genes.When the egg is fertilized, most of the cytoplasm inside the egg cell, including the mitochondria, is transferred to the developing embryo, but the sperm has no mitochondria.Mitochondrial DNA has its own set of inheritance patterns, which are all inherited from the maternal line, including the history of the mother of the world, and are completely free from male interference.The mitochondrial DNA of Queen Elizabeth II was not inherited from Queen Victoria, but from Anne Caroline (died in 1881), who was relatively unknown at the same time as Queen Victoria. , because Queen Victoria is the paternal ancestor of Elizabeth II.As for some genetic diseases caused by mistakes in mitochondrial genes, such as blindness caused by damage to the optic nerve, they are naturally inherited from the mother.Mothers pass genes to sons and daughters, but only daughters pass on to the next generation. This mode of inheritance is very different from the way of sex-linked inheritance.
That's the game of genetics, and the rest is molecular biology, more mechanical than physical.
As for the true composition of genes in the end what is it?This problem was not found until scientists discovered that taking a mutated substance (transfondllgprincghe) from a bacterial colony and sending it into another colony with a different shape, but related to it, could change the shape of the latter. Answer.This mutated substance is DNA. Many years ago, human beings found DNA on bandages stained with pus and blood. This kind of experiment sounds disgusting, but DNA is a very important substance in biology.
Since Morgan, with the further development of genetics, people have been eager to understand whether the function of genes is limited to the transmission and expression of genetic information between generations.What is the chemical composition of the gene itself?How do genes act on organisms to express biological traits?How cells replicate themselves when they divide...and so on.Questions such as these, from the 1920s onwards, along with the growth of knowledge on the material structure, biochemical function, physical properties of genes, and genes as carriers and transmitters of genetic information, as developmental units and mutation units controlling hereditary traits, etc. It's time for a solution.
A prelude to the discovery of the double helix structure of DNA In 1935, M. Debrick, a student of the famous theoretical physicist Bohr, discussed the physical properties of genes and their effects on cells from the perspective of physics.He believes that the reason why genes are passed down from generation to generation and maintain their structure is that chromosomes are connected with surrounding atoms or molecules like non-periodic crystal structures, so they are relatively stable, due to the particularity of the arrangement of different parts , it may contain specific genetic information.Ten years later (1945), the physicist Schrödinger, in his book "What is Life", played up Debrick's point of view, pointing out that "...the most important part of a living cell—the chromosome filament— It can be properly called a non-periodic crystal", which is the "carrier of living matter" (Xie Dingzhen: "What is Life" Shanghai People's Publishing House, 1973 edition, pages 5-6), he also believes that chromosomes should be Realize the "original code" of individual development and expression of all biological traits, "every set of chromosomes contains all codes" (p. 72 of the same book).The gene on the chromosome is a kind of biological macromolecule, which changes or mutates, and originates from the isomer molecule formed when the atoms are rearranged.It is the macromolecular structure of the gene that "provides every possible (heterogeneous) arrangement within its small spatial extent to embody a hybrid 'determination' system" (ibid., p. 67 ), which means that differences in the arrangement of atoms form the genetic code.
He thought of using Morse's dots and bars to represent gene activity (that is, the expression of the genetic code).The extent to which Schrödinger's views influenced the field of genetics and caused revolutionary changes in this field is difficult to estimate.After the 1930s, Debrick turned to the research on the genetic information transmission of bacteriophages, and some people overly focused on the research on the activities of protein macromolecules, ignoring the effects of genes in biochemical reactions , so the research on the activity of genetic information has not achieved significant results in the field of biophysics for a while.
About the same time as Schrödinger's "What is Life" was published, in 1944, bacteriologist Avery and his colleagues McLeod and McCarty were engaged in research on the transformation of pneumococcus.This work had been previously studied by the British physician and bacteriologist Griffith (1929), who found that heat-killed virulent bacteria (type S) and non-toxic bacteria (type R) were simultaneously injected into the In mice, only S-type bacteria were isolated from the mouse blood, which indicated that the R-type bacteria obtained something from the S-type bacteria that transformed the non-toxic R-type bacteria into the virulent S-type bacteria.But he didn't understand what the mechanism of transformation was, so he didn't understand the significance of his discovery.When Avery and others re-conducted this experiment, they firmly grasped the main contradiction and focused their attention on the transformation mechanism. They isolated the active transformation factor from S blood group pneumococcus, and then clarified the chemical composition of this factor. properties, they are "a highly polymerized and sticky DNA sodium salt" (Avery et al.: A study of the chemical properties of the substance that causes the type transformation of pneumococcus in trees", contained in "Selected Classical Papers on Genetics", Science Publishing Press, 1984 edition, p. 107), which makes it clear that nucleic acids (at least deoxyribonucleic acid-type nucleic acids) have the characteristics of transformation and inheritance.This transformation factor is the basic unit that makes the SJ type of pneumococcus play a transformation function, which can be compared to a gene.However, this discovery was diluted under the great influence of orthodox cytogenetics, and it was limited to discussing gene characteristics from biochemical pathways, focusing only on how genes control biological metabolic processes, so it has not been determined that genes are DNA biomacromolecule.
From 1951 to 1952, Hershey and Chase used radioactive S to label the semi-uric acid and methionine in the phage protein, and "P" to label the phosphoric acid in ENA, and then used raw P to infect bacterial cells. It was found that the DNAilliN of eP in the phage was transferred to the host bacterium, which indicated that only the DNA molecule was related to the replication of the new phage, while the protein amino acids containing S remained in the empty shell of the phage, thus proving that DNA is the real genetic material.
If the above research focuses on the study of genes as the bearer and transmitter of genetic information as genetic material, which reflects the characteristics of the "Information School" research, then the study of how genes work, or the study of gene functions Problems are the main subjects of the biochemical school, and both of them are preparations for the study of the material structure and biochemical characteristics of genes.
To study the function of genes from the perspective of biochemical pathways, the starting point is to understand how genes control or regulate biological metabolism.In other words, it is used to study and determine the interaction between nucleic acid macromolecules and other molecules in cells, that is, to determine the interaction between DNA macromolecules and proteins (enzymes).As early as 1908, the British doctor Garrod wrote the famous article "Congenital Defects of Metabolism" on the study of black urine, explaining that this disease is caused by an enzyme deficiency caused by a gene mutation, That is, at a certain point in the middle of normal biochemical metabolism, the gene mutation causes the loss of homogentisate oxidase, which causes metabolic failure, resulting in alkapia.This sort of thing convinced Garrod that a change in a gene somehow affected a particular chemical product of metabolism in the body.Geneticists such as Düller, Wright and Haldane all believe that genes control the metabolic process of biological cells in a certain way.Later, people gradually learned that the enzyme that plays a specific catalytic role can make the metabolic reaction between the two related molecules reach a balance state.Due to the specificity of enzyme catalysis, there are dozens of metabolic pathways or steps from substrate to final product.The intermediate molecular product in the metabolic pathway is catalyzed by the previous enzyme, and its reaction steps are one-way equilibrium. As long as there is a problem in one step, it will affect the subsequent process and the final product.An obvious example is: In 1936, geneticists Biddle and Iferis discovered that the eye color pigments changed according to the genetic composition of buds and recipients when they transplanted the eyes of Drosophila larvae, and the pigment molecules were not only determined by the genes of the transplants Controlled, and also affected by the foreign matter obtained by the chromatophore in the synthesis pathway, it is proved that the synthesis of eye pigment is realized through several intermediate products, and its synthesis process is:
Precursor—V substance—CAs substance—pigment
vw due to Culs due to
The two substances V" and Cn" determine the color of the eyes. If the eye color is vermilion, it means that one of these two substances is missing. Body V" is the precursor, that is, cinnabar eye itself can not provide the missing Cn" substance, if both are lacking, then the biochemical pathway will be interrupted, showing white eyes. It can be inferred that the production of eye color in Drosophila goes through Several steps controlled by genes, if one of the genes is mutated, the metabolic pathway is inhibited there, and a certain trait is also affected. However, since Drosophila is a higher animal, it is controlled by dominant and recessive in the experiment. The mutual interference of genes affects the experimental results. To truly understand the role of genes in controlling the metabolic process, more and better experimental materials are needed.
What kind of material is suitable?Biddle and Tatum believe that the selected experimental materials should have the following advantages:
Reproduction conditions are simple, and can be reproduced in large quantities under artificial culture conditions; this material has the characteristics of fast-reproductive sexual generations, and the adult is a haploid chromosome, and mutants can appear phenotypically, and mutants are easy to distinguish.They finally found the most suitable experimental material of Lypospora among fungi.他们借助链抱霉的生化反应去探究基因功能问题，比得尔和塔特姆这样认为：“从生理遗传学观点来看，一个生物体的发育和功能主要是由一个完整的生化反应系统构成的，这些生化反应以某种方式受到某些基因的控制，据推测，这些基因本身就是这个系统的一个部分，它们或者是以酶的方式直接起作用，或者是决定着酶的特异性，从而控制或调节这个系统中的特异反应”
（G．W．比得尔等：《链抱霉生物化学反应的遗传控制》，载《遗传学经典论文料，科学出版社1984年版，第2页）。鉴于过去的实验无论对植物的花青式色素、酵母的蔗糖发酵，或者对果蝇眼睛色素变化的研究都因材料上和方法上的局限性，只能选择具有明显表到的个体当实验材料，而对它们的生化反应难以分析和辨认，所以比德尔和塔特姆用链抱霉当作研究对象是十分睿智的。
他们制定研究键抱霉的方法是：第一步，用X射线诱发键抱霉突变，并假定哈果菌体必须完成某种化学反应才能在一种特定的培养基中生存下来，那么一个不能完成这种反应的突变体，在这种培养基中显然会死亡……如果在这种培养基中加入这个遗传阻断反应的主要产物突变体就能生长的话，突变体就能保存下来”（同上书第90页）。根据上述假定，他们把用X射线处理过的单抱子培育物，先置于完全培养基中，然后再置于基本培养基中，使一个失掉合成任何一种必须物质能力的菌株，只能生存于含有必须物质的培养基中，而不能生存于缺少必须物质的基本培养基中，形成一个生化突变型菌株。
因为它们与正常菌株的生化差别就在于不能合成某种必须物质，所以，下一步的工作则是对形成的抱子作遗传分析，这个过程应用了比较方法，即利用几个不同的突变菌株，在培养基上补足它们各自不同的需要物，分别补加某种氨基酸、维生素或核劳酸……等等，然后作断代培养，以鉴别各该突变菌株生长时必须的某种物质。
判断生化代谢发生缺陷的关键是：由菌株从完全培养基到基本培养基中的继代培养来确定的。某菌株需要某种氨基酸，就在基本培养基中添加该种氨基酸，用这种方法鉴别该突变型菌株在合成该种氨基酸时的缺陷，证明它不能完成这一步生化反应。再用这类突变型菌株与野生型菌株杂交，经分离后就显示出团单个基因发生突变，出现了突变的表型。由此可推测一个基因的功能相当于一个特定的酶的作用。基因本身决定酶的特异性，因此也控制或调节着孩过程的特异反应，基因发生突变就导致了酶的突变，或者说，酶的特异性是由基因所包含的某种信息决定的。比德尔和塔特姆据此提出“一个基因一个酶”的假说。这个假说虽然说明了基因在遗传中的作用和功能，但问题是有一些基因指导合成的物质并非是酶，而是象血红蛋白或胰岛素之类的蛋白质。此外，一个基因一个酶的结论亦是归纳推理的产物，前提虽然是真，结论未必也真，因为确实存在这样的事实，一个基因是否只决定一个酶，抑或一个基因可以指导或决定多种酶的产生，或者由若干个基因决定一个酶……如此等等，比德尔和塔特姆的假说是无力解释这些问题的。所以后来有人提出一个基因决定一个多肽的假说。
1944年，索勒和霍洛维茨对突变型链抱霉需要依赖精氨酸供给才能存活的代谢反应作了遗传和生化分析，进一步明确了生物细胞内生化合成过程的全貌，证明基因突变与特定的酶的存在或不存在有密切关系。基因决定多肽链氨基酸排列顺序的工作则是在DNA双螺旋结构模型提出后，由美国分子生物学家英格拉姆对镰状红细胞的研究后确定的。
建立DNA双螺旋结构的第三个知识来源，则是晶体分子X衍射分析技术的发展和建立有关模型，即结构化学的兴起。特别是从本世纪40年代以来有关蛋白质化学结构模型建立后，进而对基因形态结构（化学结构）所作的研究和分析所得到的启示。主要借助于DNA双螺旋立体化学的最适构型照片和X衍射资料的证据。
由于把X衍射晶体技术应用于结晶蛋白质和核酸上，对认识有机大分子的性质和推定它的三维结构起了重要作用。这个工作在30年代就开始了。英国生物化学家阿斯特伯里等人利用X衍射方法取得了有关蛋白质结构的许多资料，并计算出蛋白质中相邻原子间的距离和相邻键的夹角，弄清了键角内各原子呈线形排列的方式，称为p构型。纤维蛋白的原子排列则较为复杂，有效多的折叠或较多致密，称为a构型。到了50年代初，鲍林和考雷等人提出a构型的多肽呈螺旋型，他们制作了许多。构型蛋白质模型，计算了键长和键夹角，单一的多肽链在自身基因之间借助氢键折叠成螺旋型。他们还计算出这种螺旋每圈有3．6个氨基酸，各圈间的距离为5．4A，借助氢键来维持它的形状。鲍林建立蛋白质的a螺旋模型应用了结构化学的规律！他所发现的a螺旋结构不是仅仅依靠研究X衍射图谱，主要方法是探讨了蛋白质大分子内原子间的相互关系，并且建立了一组象玩具似的分子模型，这种模型对了解蛋白质三维结构内在联系及其功能起到十分重要的作用（参见L．D．沃森：《双螺旋》中文版，第29－30页）。大约与鲍林提出蛋白质a螺旋结构模型的同时，伦敦大学金学院的威尔金斯及其同事富兰克林正用X衍射方法进行着DNA的研究，他们拍摄了当时最好的DNA衍射图，积累了大量分析资料，为DNA模型的建立提供了极重要的根据。
建立DNA双螺旋模型的第四个知识来源，就是有关DNA本身的历史知识。最早确定DNA物理性质的是豆869年米歇尔提出的“核素”，19世纪末、细胞学家如O．赫特维希和威尔逊等人曾推测染色质的组成成分可能就是核素，赫特维希还推测核素可能承担着性状的传送职能。此后，柯塞尔系统地研究了核酸的分子结构，发现这类分子存在着两类核酸，一为脱氧核糖核酸报pDNA），另一类是核糖核酸（RNA）他把核酸水解，分离出各有四种含氮碱（即腺瞟吟、鸟瞟吟、胞啧啧，以上三种二类核酸都有，此外，DNA还含有胸腺嚷嚷，RNA含有尿陵牌）。19三五年，莱文等人进一步发现核酸里有五个碳原子组成的糖分子（在RNA中为核糖，在DNA中五碳糖缺一个氧原子，称脱氧核糖）。其后，又发现核酸的磷酸组分。于是由一个含氮碱基一个磷酸和一个脱氧核糖共同组成了一个接着酸。莱文等人还对核酸作定量分析，测定四种含氮碱基的克分子数相等，莱文由此推测在一切生物来源的DNA中四种碱基数是等量的，这意味着核酸是由固定和重复排列的核音酸组成，所以不论核酸的来源如何，它们的成分总是相同。根据这种推论，便认为核酸不可能携带极复杂的遗传信息，它们仅仅是简单的线性排列的四核音酸多聚体。莱文的四核音酸说从此成了核酸的生化范式，以致影响到1944年艾维里已明确证实DNA是遗传物质时，人们还不把它看成是遗传物质。
1952年，美国生物化学家查哥夫应用理化分析和测量技术证明四种核音酸的含量是不等的，DNA不是由四种核青酸单调重复排列的多聚体，四种碱基在DNA中的相对数量因物种不同而有其特异性，即在不同的物种中DNA含量各不相同。他进一步测定了源晗和啧啧的总的克分子比为1。而腺瞟吟与胸腺喷陡、鸟瞟吟与胞陵牌的充分子量之比也大都是1。这表明DNA四种碱基是两两互补；此外，它们依次作顺序排列，这意味着储存遗传信息的编码。但是，有关DNA传导遗传信息、控制或调节生物的生化反应、表达生物性状、以及实现自我复制等问题，只是在彻底弄清DNA三维结构（基因的具体形态）后才有可能解答。
二DNA双拐旋结构模型的发规模型是人为摹似自然现象物态相似的一种认识方法，它是对自然界宏观客体或微观世界客观对象的模仿。依据客观对象的规模和大小，人们借助有关理论的指导，可以按比例缩小或放大原型的尺寸制造模型，可以间接地研究原型的规律。在生物界用动物等实物模拟人的生理生化或病理过程，以弄清人的生理或病理机制。但是，模拟自然现象的模型无论是缩小或放大，都能近似或比较近似地再现对象实体，符合原型的规律。通过思维设计放大的微观模型，需要严格验证，必须将模型与用理化手段取得的实物图象或用其他方法来检测，以证实模型的确实性。从这个意义上讲，模型是对自然现象的一种人为仿制品。
模拟自然现象的模型，它的作用在于：第一，给人以感性直观的明晰性、简洁性的认识。第二，使人们直接研究参与构成模型各种因素及其矛盾关系，找出它在模型中的作用和由此产生的种种效应，并将这种认识应用到原型上，第三，根据这种认识，用来解决原型中出现的种种问题。所以模型在人们认识自然和解决问题过程中起到了中介的作用。
任何模型都是解决实际对象中出现的种种问题而制造的，水库模型为求得相似条件下有关因素的各类参数，据此可作为实际设计的参考根据。建立DNA模型时需要考虑这个模型的设计不是单纯地建立它的化学结构，还要考虑它必须具备遗传物质的生物学特性。按照这个要求，这个模型至少要解决这样一些问题：第一、模型要反映出具有携带和传递遗传信息的功能；第二，模型能说明DNA自我复制机制；第三，模型能说明引起生物突变的原因；第四，模型必须符合化学规律，特别是要符合查哥夫规则。总之，这个模型应是实实在在的基因的反映或基因的模式。沃森和克里克正是出于这种认识，提出了DNA双螺旋模型。
50年代初，人们已普遍肯定DNA是生物的遗传物质。为搞清楚DNA的机制，需要先弄清楚DNA的化学组成和它的三维结构。这两者对了解基因（DNA）的性质是个关键问题。
1951年春天，沃森在那不勒斯参加生物大分子会上看到威尔金斯的DNA结晶体X衍射图象，给他以极深刻的印象，他认定了这张照片将能成为“解决生命奥秘的钥匙”埃森：
《双螺旋》，中文版第20页）。这张照片表明DNA是一种可用简单方法来测定的有规则的结构，因为它能结晶。这就解除了沃森原先认为基因有异常不规则结构的思想顾虑。
在这之前，美国的鲍林已成功地建立了蛋白质X螺旋结构模型，鲍林建立这个模型时不完全依靠X衍射图谱，他更着重探讨原子间的相互关系，制造了一组分子模型（沃森称它象儿童玩具的模型），然后用X衍射图数据来检验模型的效果，并从理论上证明这两者的一致性。鲍林制造模型的举动引发沃森和克里克也想用同样方法来建立DNA分子结构模型。沃森说：“我们看不出为什么我们不能用同样的方法解决DNA问题！我们只要制作一组分子模型，开始摆弄起来就行了”（同前书第30－31页）。当鲍林建立蛋白质a螺旋模型时，探讨每条蛋白质多肽链都由自身基团间的氢键自主地折叠成螺旋状的情况，他注意到每条氨基酸借助氢键连接起来，并固定在各自的位置上。这个发现至少成为启发沃森等人在探讨DNA分子多维度时的重要方法。
沃森和克里克初步设想：因DNA是结晶聚合体，它可能是一种含有许多核音酸并作有规则直线排列的东西，因为DNA的糖和磷酸骨架是非常有规则的，这种情况能最好解释DNA分子结构。可是威尔金斯根据DNA衍射图谱指出：DNA分子直径比一条单一核音酸链直径大，所以DNA分子可能是一个包括有几条绕在一起的多核昔酸链的复杂螺旋。
此后，沃森和克里克认识到DNA分子的特异性应是碱基的差别，而它的糖和磷酸都是共同的，核音酸之间的联系只与糖和磷酸相关。于是他们又假设有一种相同的化学键联结着所有的核青酸，它的分子结构表现为糖和磷酸的有规则性和碱基顺序不规则性的混合体（作这样的安排为的是体现基因的多样性）。但克里克认为制作模型先要弄清楚DNA分子核音酸链的数目，从衍射图谱上看，可能是两条、三条或四条多枚着酸链。于是他们设想DNA是以糖和磷酸骨架为中心、多枚苛酸链排列在外面的结构。51年冬天，他们着手建立模型，先把模型搭成几条多孩背酸链围绕着糖和磷酸骨架的形状，并假定多接管酸链之间借助盐键联结起来。理由是盐键的“两价正离子如Mg——可以维系两个或更多的磷酸基团”（同前书第54页）。但是因这个设想在DNAX衍射图中没有看到两价正离子的镁或钙，所以假定镁或钙离子嵌进了糖和磷酸骨架中，他们专门设计了模型中磷酸H图滚形状，制作成由三条多核青酸链纠缠在一起的螺旋模型，并确定沿螺旋轴每隔28A绕一周。他们当时认为这个设计图案和X衍射图谱相符，并且还用富兰克林的定量分析法加以验证，螺旋参数的选择与富兰克林提出的数据相吻合。
但是，以糖和磷酸骨架为中心的模型，要把参差不齐的碱基排列和组装在这个骨架上，问题就大了。由于原子堆集过密，组装的结果既不符合化学规律，也构成不了DNA有规则的模型，这个模型是失败的。
他们继续通过各种途径，把探讨建立模型的工作再深入一步。沃森转入对TMV（烟草花叶病毒）的研究，这项工作启发他对生物晶体结构的螺旋有对称的想法。他进一步思考查哥夫测定的DNA化学特性（即由直哥夫测定的腺源吟和胸腺晓健、鸟瞟鸣和胞陵牌的充分子量比值都是1，总的瞟岭和喷晚的充分子量的比值也相同），这表明两类不同碱基之间可能是互补配对，他猜测DNA分子结构的基本组成形式就是配对的。当时，和他们相识的化学家格里菲斯曾提到，“基因复制是在互补表面交替形成基础上进行的”
（同前书第78页），这个提示意味着遗传学家和物理学家们曾设想过的，基因复制是正本和负本的互补。格里菲斯计算过一个DNA分子碱基的相互吸引力（弱相互作用），计算结果表明：它们是不同类碱基间的相互吸引力，这表明“腺瞟哈和胸腺噙牌的平面应该粘在一起的”（同前书第79页），这种情况也适用于鸟瞟吟和胸腺喷院的互补。这个计算结果给查哥夫提出的不同类碱基配对互补的规则提供了有力佐证。
1952年，富兰克林用X射线拍下了DNA分子结构的B型照片，经威尔金斯鉴定，证明只有螺旋结构才能出现交叉形的反射线条，这张照片还可精确确定DNA分子多核音酸链数目。沃森根据B型照片就DNA应是单链、双链、三链或三条以上的核音酸链形成螺旋的事进行苦心推敲。B型照片给他的启示和测得的数据使沃森联想起生物界繁衍配对的现象，预示DNA分子结构也可能是配对成双链的构型。所以他决定要做一个双链的模型。
现在需要解决三个问题：第一，DNA碱基是怎样排列的？是有规则排列还是无规则排列？从X衍射图谱来看，螺旋每隔34A重复一次，表示了碱基沿螺旋轴方向完全旋转一周的距离，这个距离表示了螺旋角度最合适的键角角度，它预示着碱基应是有规则的排列。还有，富兰克林曾推测DNA磷酸和糖骨架在外部，碱基在骨架中心。如果碱基是有规则的排列，那么它应该表明每个核音酸糖—磷酸基团都有完全相同的三维结构。但是，碱基是不相同的，连接的多核音酸的碱基顺序也不可能有规则，若把大大小小的碱基拼在一起，外部的糖一磷酸骨架就会变形。这是一个难题，如果不能解决，螺旋模型就建立不起来。
第二，多孩着酸又是如何联结在一起的？靠什么力把碱基连接起来？沃森和克里克长久以来未曾考虑过氢键的作用，他们过多地考虑金属离子盐键的作用，在鲍林建立蛋白质a螺旋结构模型和明确指出氢键的连接力作用时，他们仍然在离子键上打转转。然而根据X衍射图，双链碱基间的连接是靠很多不规则的氢键完成的，在理论上，戈兰德和约尔丹提出碱基间能形成相连氢键的理论。这样，才使他们明白碱基上一个或几个氢原子可以移位形成相连的氢键，而正是这种氢键才能把同一个分子中的碱基连接起来。
第三，要解决碱基间的键合问题，哪个碱基与哪个碱基键合？这个问题一度把沃森5队歧途，沃森经过长期思索得不到答案。有一次他无意中画出腺源吟结构时，突然想到同类碱基间可能形成两个氢键，并实现键合。更重要的是他也曾设想过在瞟吟碱与呼唤碱之间可能也形成氢键，并把二者连接起来。这个推测是构成双螺旋结构模型关键的一步。但是，当时他更热衷于设想DNA分子都是由相同碱基的双链构成，每个DNA分子都可能是同类碱基配对的双链，而两条链则是由同类碱基对的氢键将它们连接起来，互相缠绕在一起形成螺旋结构。这个构型按沃森的想法可能说明复制问题，他设想两条链的其中一条可能是合成时另一条的模板，这个模型虽然可解释生物遗传上的若干问题，但是同类配对的方法解决不了不规则的碱基顺序问题。这样做，整个模型由于碱基大小不一，就会显得凹凸不平，而且完全不符合查哥夫的等量规则。由此看来，同类配对的双螺旋结构模型的设想也是行不通的。
在此情况下，沃森用纸板制成碱基模型，来回拼凑，移来移去突然发现通过二个氢键维系的一个腺瞟吟同一个胸腺喷晚的形状，竟然同一个鸟漂岭和一个跑呼峻联系的形状相同。这个发现无疑是一个重大突破，但当时他错误选择了碱基的互变异构体（酿醇式），这种结构的碱基间不能形成氢键。美国晶体学家多纳休及时指出了这种错误，并指出通常情况下四种碱基都以酮式结构存在而不是酿醇式结构，后者却因两个碱基间距离过远而无法形成氢键。
沃森和克里克吸取了失败教训后，就改进了他们的方法。沃森用硬纸剪成的碱基模型作了多种配对的可能尝试，采用碱基的酮式结构后，发现由二个氢键联系的腺瞟呼和胸腺嘴徒对的形状，和以同样方式维系的鸟瞟吟和胞喷晚对的形状相同，这种互补的联系不仅能形成氢键，还表明DNA螺旋的直径是一样的，这种互补关系还正好说明了查哥夫提出的两类碱对1：1的对等关系。因此，他们认定了DNA接着酸链只有两条。此外，有关X衍射图诺表明，两条链应呈螺旋形的，其直径约为20A，相邻核音酸间的距离是3．4A，旋转一周（正好十个核音酸）为34A，根据这些情况，他们制成了DNA金属立体模型。
沃森和克里克指出：“在这种结构中两条链围绕着一条共同的轴线缠绕，并通过核音酸碱基之间的氢键彼此连接起来……。两条链都是右手旋转的螺旋，但原子在糖一磷主链上的顺序是反方向的，并成对地垂直于螺旋轴线。糖和磷酸基因在外侧，而碱基在内侧（沃森、克里克：《核酸的分子结构》，载《遗传学经典论文选集》，科学出版社1984年版，第148页），全部结构象沿轴心旋转的梯子，形成了一个特定的螺旋模型。根据计算和分析，这个模型既符合X衍射图谱有关结晶分子的各个数据，又和立体化学的原则一致。沃森和克里克终于建立生命史上具有巨大意义的基因（DNA）模型。人们把这个发现誉为分子生物学新时代的开端。
DNA双螺旋结构作为遗传物质，它的生物学特性在以后若干年中陆续得到证实，这种特性具体表现在DNA的功能上。确定DNA的基本功能大致有以下几个方面：第一，它的自我复制机制。沃森和克里克在制作DNA模型时已经想到DNA的自行催化的繁殖机制。由于双螺旋的对称性，它们的互补性质十分明显，当基因增殖时两条链分开，每条链实现自我复制，即各自成为配对物的模板，借助其互补特性形成新的双链，构成了新的DNA分子链。沃森和克里克掼出：“……我们的脱氧核糖核酸模型实际上是一对样板。这两条样板是彼此互补的。我们假定，在复制之前氢键断裂，两条链解开并彼此分离。然后，每条链都可以作为样板，在其上形成一条新的互补链。这样我们最后得到了两对链，而此前我们仅有一对链，而且在复制过程中，也是严格符合碱基对顺序的”（沃森：《双螺旋》，中文版第155页）。这种复制称半保留复制，即原先的链保留，而后分开来分别到子分子中成为新链的模板。1958年，梅塞尔森和斯塔尔证明DNA的复制确如沃森和克里克所描述的是一种半保留的复制机制。
第H，DNA指导蛋白分子的合成。蛋白质是按照DNA分子的结构合成的，所以DNA是蛋白质合成时的模板。它的实现分两个步骤，第一步，DNA先转录到特殊的核酸——信使核糖核酸（InRN）单链上。因为核音酸是专一配对的，信使核糖核酸上的碱基排列顺序同DNA上的碱基排列顺序互补配对，rnLRNA就成为了DNA的“副本”。这就是说InRNA的核音酸排列顺序是DNA核昔酸排列顺序的翻板。每三个核音酸组成一个“密码子”，对应于某一种氨基酸，即三个核音酸决定一个特定的蛋白质氨基酸。第二步，这条InRNA移到细胞质的核糖体里什RNA），借助既能识别mRNA密码子又能识别氨基酸顺序的转移核糖核酸（tR－NA）单链“翻译”成蛋白质氨基酸。由于每个tRNA都有一个特定的“反密码子”，能认别遗传密码，它的另一端和特定的氨基酸相结合。处在核糖体内的mRNA，由每个特定的tRNA携带着某种氨酸，借助反密码子在mRNA上找到自己的位置，按照mRNA核音酸排列顺序，把不同的氨基酸排列起来组成多肽（蛋白质或酶）。
由此可知，从DNA到蛋白质是一个单向的信息流。沃森在从事DNA结构模型设计时已想到基因指导蛋白棋会成过程，当时，他记下了DNAnRNAn蛋白质这样单向性流动公式，表示遗传信息从DNA传到蛋白质的作用过程。这种遗传信息传递过程称为“中心法则”。
后来，梯明等人发现了“反向转录酶”，可指导RNA中的信息转录到DNA上，表明DNA与RNA之间在少数情况下可以发生逆转。但是，核酸指导蛋白质合成的法则依然是正确的。
第三，基因突变的分子基础是DNA核音酸排列顺序发生了变化。早在1949年，鲍林曾推测镰状红细胞贫血症的起因是血红蛋白多肽链内部发生变化所致。1957年，英格拉姆证明镜状红细胞贫血症是因为在血红蛋白分子中的B链上，第六位上的谷氨酸突变成激氨酸造成的，如果追溯组成谷氨酸的密码，它是GAA，突变成绿氨酸后密码子为GUA，其中的A（腺瞟吟）变成了U（尿障院），正是这个碱基发生了突变才引起氨基酸成分的变化，从而5！起了镰状红血球贫血症。以后，人们了解到：通过核音酸碱基的代换，或者通过核音酸碱基的添加或缺失，发生碱基序列的变化，从而引起基因突变，并影响到有机体表型以及有机体生理生化反应等方面的变化。
总之，DNA双螺旋结构模型在揭示生命的基本问题上已取得了极其辉煌的成就。由于DNA双螺旋的发现，现在知道：基因就是DNA分子上的多核高酸片段，它决定特定的多肽链氨基酸顺序，即指导蛋白质或酶的合成，是实现基因自我复制和发生突变的基本单位。这样的单位也叫一个“顺反子”，基因就是一个“顺反子”。
随着时代的进展和科学的发展，基因从假定中的“诞生子'和承担专一遗传作用的“种质”，到孟德尔实验中推导出的遗传因子，再到摩尔银通过果蝇杂交后代中出现的重组频率推导出基因的重组的存在，把基因落实到染色体上作直线排列的领料。但自DNA双螺旋结构模型建立后，人们终于找到了遗传和发生变异的实在物，找到了生物的遗传和变异的机制。（张乃烈）