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6 The Discovery of the Egg in Higher Eukaryotes

Elof Axel Carlson Indiana University Press ePub

While it was known to almost all of humanity since antiquity that birds lay eggs, it was not known that the egg is a cell until cell theory was developed in the 1830s. In 1652, William Harvey (1578–1657) found two things of interest when studying reproduction in the fallow deer.1 One was that after copulation and conception in the fall, the gestation process of the fallow deer goes into an arrested state for several months. The process is called diapause and it allows seasonal regulation of when birth takes place. It occurs during the blastocyst stage and was observable to Harvey as a small spot that neither went away nor enlarged until the winter. Harvey’s other, more significant, observation was that after copulation the uterus of the deer was empty. There was no coagulum to be seen or evidence that anything had changed in the uterus. What Harvey did not know was he could not see the blastocyst that implants itself in the uterus of the fallow deer because it is transparent and microscopic. The mammalian blastocyst at implantation at best would be the size of a period in a sentence. It does not enlarge before implantation in the uterus. It receives no external nutrient to grow until it implants. In 1843, Theodor L. W. Bischoff (1807–1882) was able to demonstrate the presence of that blastocyst. Bischoff studied the egg in rabbits, dogs, guinea pigs, and the roe deer, following it through its cleavages, blastocyst formation, and early embryonic development.2

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12 The Discovery of Sex in Microorganisms

Elof Axel Carlson Indiana University Press ePub

When Anthony van Leeuenhoek observed the animalcules, as he called them, from different dips of water or from his own body, he did not discuss how they formed. Most of his contemporaries would have said that they formed from spontaneous generation. The idea is as old as written thought. Aristotle believed in spontaneous generation, and so did anyone watching rotting food or meat swarming with maggots. Before Rudolph Virchow and Robert Remak’s cell doctrine, biologists did not think of life coming from preexisting life. At least they conceived the process as far back as life goes: Genesis for the pious; after Charles Darwin, some sort of event that led to the formation of the first living cell; or after H. J. Muller, the formation of the gene, the first replicating molecule that could copy its errors.

Microscopy flourished in the last half of the nineteenth century. It spun off the field of histology in medical schools and the field of cytology that led to inquiries about heredity. It was a necessary tool for the field of microbiology that flowed from germ theory. Louis Pasteur (1822–1895) and Robert Koch (1843–1910) introduced the germ theory of infectious diseases in the 1870s and 1880s. It revealed even smaller organisms than those seen by Robert Hooke and Leeuenhoek. Pasteur and Koch’s theory brought microscopy back to the medical school to study infectious diseases caused by bacteria and other microorganisms. By the end of the nineteenth century, scientists inferred the existence of even smaller organisms, which slipped through filters that barred passage of bacteria. In 1892, the first virus, tobacco mosaic virus, was identified.1

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2 Wild Guesses in an Era of Scientific Ignorance

Elof Axel Carlson Indiana University Press ePub

Almost all of the topics taught in K–12 or undergraduate introductory science courses come from work published in the last two centuries. Before the nineteenth century, very little of the chemistry, biology, geology, astronomy, or physics (other than Newtonian) that is covered in a twenty-first century class had been discovered. Almost all of a medical school curriculum, with the exception of gross anatomy, is a product of work done in the past two centuries. However, humanity centuries ago had the same curiosity about life and the universe as those born today. One of the universally recognized experiences of all people born is that roughly half are males and about half are females. When it comes to classifying who is a male and who is a female at birth, almost every adult in the world will use the external genitals. In a male there are a penis and a scrotum containing two testes. In a female there is a vaginal passageway surrounded by labia and a clitoris. Except for rare occasions we do not see the genitalia of our fellow adult human beings. Usually we classify a person as male or female by characteristics such as body shape, the presence or absence of hair on the face, the length, distribution, and style of hair from the cranial part of the head, the bony structure of the limbs and face, the deepness or higher pitch of voice, the presence or absence of enlarged breasts, and the presence or absence of an “Adam’s apple.” To that, in most cultures, we add the clothing that people wear and the behavior we assign to males or females out of tradition or experience.

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15 The Discovery of Human Sex Chromosome Conditions

Elof Axel Carlson Indiana University Press ePub

When Michael Frederic Guyer (1874–1959) looked at human chromosomes in 1910, he estimated the diploid number was 24 in females and 23 in males.1 He thought the sex chromosome mechanism was XX female and XO male. Two years later, Hans Jean Chrysostome von Winiwater (1875–1949) doubled that estimate and claimed the human chromosome number was 47 in spermatocytes, but he agreed with Guyer about the XO status of males.2 That changed in 1921, when Theophilus Shickel Painter (1889–1969) at the University of Texas reported a chromosome number of 48 (although he said it could be 46 or 47). Painter used testes from freshly executed prisoners or from castrated patients in mental asylums. He also said there was a definite Y chromosome in the male cells he studied and thus 48,XY was the chromosome number and sexual status of males for another generation.3

The status remained stable because techniques did not change in cytology for human cells until the 1950s, when tissue culture techniques improved, hypotonic solutions were used to increase the volume of nuclei, and colchicine was used to arrest cell division at metaphase. In 1956, when two Swedish investigators, Joe Hin Tjio and Albert Levan, combined all these procedures, they got a consistent reading of 46 chromosomes, with very clear XX females and XY males.4 From then on, the human chromosome number was represented as 46,XX for females and 46,XY for males. By 1960, a standardized way of photographing, enlarging, and clipping out chromosomes was introduced. The chromosomes were measured and aligned in size, place, and by grouping within a particular size range of the location of the centromere that separates the two arms of the chromosomes. (The shorter arm of the chromosome is called “p” and the longer arm “q.”) The resulting mounted representation of the chromosomes is called a karyotype. The X chromosome is in the C group (chromosomes of moderate size), and it is slightly submetacentric. The Y chromosome is very small, and the q arm is at least twice as long as the p arm. In 1964, Lionel Sharples Penrose (1898–1972) estimated that the X accounted for about 6 percent of the total DNA of the sperm nucleus in humans, and the Y accounted for about 2 percent.5

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14 Dosage Compensation and the Sex Chromosomes

Elof Axel Carlson Indiana University Press ePub

Calvin Bridges and Thomas Hunt Morgan discovered the existence of dosage differences on the X chromosome of fruit flies when comparing the allele of white eyes called eosin to that of the allele of white eyes called apricot. They called the phenomenon bicolorism, but did not make a generalization about it. In a stock of eosin flies, females had a darker eye color than males. In a stock of apricot flies, the eye color of the male and the female was the same. Eosin arose in a bottle of white-eyed flies as a solitary male fly. It was interpreted as a partial reverse mutation from white to eosin. About a decade later, in 1926, Curt Stern (1902–1981) discovered a mutation called bobbed bristles. It was the first genetic character found on the Y chromosome in fruit flies that was not associated with fertility.1 As it turns out, the shorter and slightly elevated bristles are associated with a gene on both the X and the Y chromosome. This made the gene behave like an autosomal recessive. Normal males and females had two doses, but XO males had a single dose and XXY fertile females had a triple dose. Stern noted that as the number of bobbed alleles increases, there is a normalizing effect.

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