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[1] Oak Ridge National Laboratory; A Department of Energy science and technology laboratory in Oak Ridge, Tennessee founded in 1943. It was initially created to separate plutonium for the Manhattan Project. See http://www.ornl.gov/ornlhome/about.shtml for more information.

[2] Marie Curie (1867-1934); A famous Polish physician and chemist who was awarded two Nobel Prizes, one for physics and one for chemistry. She discovered two elements and worked extensively on radioactivity and isotopes. See http://nobelprize.org/nobel_prizes/chemistry/laureates/1911/marie-curie-bio.html for her life story.

[3] Gymnasium; Equivalent to high school in the United States, it is the secondary part of one’s education in some parts of Europe.

[4] Thixotropic; Certain fluids become less viscous when they are shaken or disturbed. Such a fluid is thixotropic.

[5] Social Democracy; A left-leaning political philosophy which stresses political action over economic determinism. Historically this philosophy originated from the socialist movement.

[6] Putsch; A German word meaning a sudden attempt to overthrow the government.

[7] Englebert Dollfuss; The Chancellor of Austria from 1932 to 1934 who lead an authoritarian style of government based on conservative Roman Catholic ideas.

[8] Christian Socialist Party; An Austrian right wing political party from 1893 to 1933 that drew most of its constituents from the rural peasantry.

[9] The festival of Sukkoth celebrates the harvest with the construction of “booths”, temporary shelters which are then used as an outdoor room, often the site of a family meal.

[10] The festival of Purim celebrates the deliverance of the Jewish people from a plot to destroy them. The full story is told in the biblical book of Esther. Today the festival celebration includes dressing up as characters in the story, feasting, and the exchange of gifts among other things.

[11] The SS; The notorious Nazi police force which originally served as the personal bodyguard for Adolf Hitler.

[12] Thomas Mann; A German Nobel Laureate who was famous for his deeply profound novels.

[13] Franz Werfel; An Austrian novelist and playwright.

[14] Neville Chamberlain; British Prime Minister from 1937 to 1940. He is best known for signing the Munich Agreement, thereby giving the Sudetenland to Adolf Hitler and buying temporary peace with Germany.

[15] “Peace in our time”; A phrase from the speech Neville Chamberlain gave following the Munich Agreement.

[16] Historically billets were the sleeping quarters that a soldier was assigned to. In this context, billets designated the arrangements made for a place to sleep for children to keep them safe in the country while British cities were being heavily bombed.

[17] The Blitz; A period of heavy and destructive bombing by the Germans of British cities (especially London) from 1940 to 1941 during World War II.

[18] The Anschluss; The Nazi occupation and annexation of Austria by Germany in 1938.

[19] Gemütlich; German for warm and friendly.

[20] U-boats; Military submarines used by the Germans in World War I and World War II. They particularly targeted non-military merchant convoys in order to break the supply lines to the Allied powers.

[1] Germ layers; A collection of cells formed during the embryonic stage. There are three germ layers, the ectoderm, mesoderm, and the endoderm. They give rise to an animal’s tissues and organs.

[2] Jackson Laboratory in Bar Harbor, Maine is well known for its long history training scientists in genetics, cancer research, and fostering excellence in scientific research.

[3] William L. Russell (1927 – 2003); Liane Russell’s husband and a well known scientist. He is most noted for his work on acceptable levels of radiation. He is a recipient of the prestigious Enrico Fermi Award. For an article written about him in the New York Times, see http://www.nytimes.com/2003/07/25/us/william-l-russell-92-radiation-pioneer.html.

[4] Dopa Reaction; A staining seen in tissue when dopa has been administered. This may indicate dopa oxidase in the cells.

[5] Clarence Cook Little (1888 – 1971); An esteemed American geneticist who studied mouse and Mendelian genetics. He went on to found the Jackson Lab.

[6] Sewall Wright (1889 – 1988); A noteworthy American geneticist who was one of the fathers of theoretical population genetics. See http://www.harvardsquarelibrary.org/unitarians/wright-sewall.html for more information.

[7] Phenotype; The outward characteristics of a cell or an organism. It includes appearance, behavior, and development.

[8] Genotype; The genetic makeup of a cell or an organism, as opposed to its appearance.

[9] Milk factor; A substance transmitted from mother to offspring in some inbred mice strains via milk or tissues transmitted through nursing. It inhibits production of mammalian cholesterol.

[1] Curt Stern (1902 – 1981); A German-American geneticist most noted for his work on homologous chromosomes and mitosis research. He also was head of the group that declared that there was no “safe” level of radiation.

[2] Herman B. Chase; For an example of this geneticist’s work see http://bjr.birjournals.org/cgi/content/abstract/31/362/65.

[3] Herluf H. Strandskov; For an example of this geneticist’s work see http://www.genetics.org/cgi/reprint/24/5/722.pdf.

[4] Manhattan Project; Created in 1942, this was a secret project established by the US Government which developed the first atomic bomb. It ended in 1946.

[5] Atomic Energy Commission; A commission created by the Atomic Energy Act of 1946 to regulate nuclear energy development and use during peacetime.

[6] Clastogens; Substances that cause breakage within chromosomes thereby causing various genetic disorders.

[7] Paula Hertwig (1889 – 1983); A German biologist who was a pioneer in radiation genetics and one of the first to see the dangers of radium and roentgen radiation.

[8] George D. Snell (1903 – 1996); An American geneticist and immunologist who shared the Nobel Peace Prize in Medicine for his work on immunological markers on the cell membrane.

[9] Hermann J. Muller (1890 – 1967), A noted American geneticist who was awarded the Nobel Prize in Physiology or Medicine for proving artificial mutations can occur as a result of X-ray manipulation. See http://nobelprize.org/nobel_prizes/medicine/laureates/1946/muller-bio.html.

[10] Mutagenesis; The process by which chemicals or radiation causes a genetic mutation.

[11] Teratogenesis; The study of atypical processes in physiological development, especially those occurring in a fetus.

IV. Work with Radiation and Embryology; Chromosome Research at Oak Ridge Lab in Mice and Drosophila

Q: What techniques could -- let me ask another question first. What was driving your science? Was it just circumstance that you had a situation in which you could create -- to look at the effects of radiation on embryos or embryological development? Was it an interest in embryology? Was it an interest in basic genetic principles. What was it that was driving your interest at this point?

A: Well, at that point, for my thesis, which was not typical of my later work at all, it was certainly the fact of relating it to events of normal embryology. Very soon, it became a very practical thing because of the hazard, the human hazard. Several of my papers were devoted to that and trying to find out also, just in library research, what kind of doses people were normally getting in medical practice for diagnostic radiation, and what type of precautions were taken.

Then I came up with this fourteen day rule that if you -- and that roused the ire of the radiological community. The fourteen day rule essentially says that if a patient has to have diagnostic radiation that's not urgent, that's not an emergency or anything like that, and you can time it, you should time it in relation to the menstrual cycle and give the radiation at a time when there's no possibility of -- in other words, the first half of the cycle, before ovulation, when you don't have the possibility of an unsuspected pregnancy. As soon as I published that, I was horribly attacked by all radiologists, I think mostly because they were worried about being sued. I'll get you that publication.

Q: If this is [the publication] from Radiology, I may have it here with me. Okay. Yes, I do have a copy of that one. [Russell, LB and Russell, WL. Radiation hazards to the embryo and fetus. Radiology. 1952;58(3):369-77.]

A: Somebody by the name of Chamberlain? No, it was President of the Radiologists of America or something. Richard [H.] Chamberlain. There were several letters of all of the -- anyhow, you're welcome to read them. [handing Maestrejuan the letters]

Q: Okay. Well, who was your audience at this point? Who did you think your audience was?

A: Well, the funding audience was the AEC [Atomic Energy Commission]. At that point, it was the medical community.

Q: Okay. And in this particular article, you were very explicit that, okay, these are experimental results from mice, but this is what it would look like in humans. And you made the direct connection on how applicable this would be for human medicine. What was motivating to make that connection between the mouse and basic genetic principles in mammals?

A: This wasn't really genetics. This was teratogenesis. I found one case in the literature. There were lots of human medical publications about various odd babies after radiation, but the time of radiation was usually not very well known or so, it wasn't published. I found one paper where it was exactly known when conception occurred because the woman was married to a guy who was in the army, and he came home for one weekend, or something like that. So it was a very exact timing of conception, and the radiation too. And the abnormality, which was an upper arm abnormality, was exactly like it would been in the mouse at a certain stage. So there was a stage comparison.

Then -- I don't know if that's in this paper somewhere. No, it must be somewhere else. Somebody had done a mouse and human comparison of embryonic events.

A: I have it somewhere. So when you do that, then you can tell when the major organogenesis[1] stages would be in humans. In the mouse, they're between day six and thirteen. In humans, it's from week two to week seven or something. It gives you a very good cross-reference point. The stages that I was never very happy with knowing more about were the post major organogenesis ones, when they were much more subtle things than gross malformation.

I did come back -- this was my main excursion into teratogenesis, but later on I came back to the area via developing a test for teratogenic effects that would pick up very small doses of either radiation or chemicals. It was based on what I drew for you, what I call the homeotic shifts. I'm not sure, I'll have to find out what publications, but you may already have those.

I just really loved it, but I didn't do much more with it, other than publishing it as a relatively easy method. What it was based on was, again, the axial formula, so many thoracic, so many lumbar, so many sacral, and also things like the number of components of the sternum. In the mouse, you have five little bones, and then you have the base of the sternum, and a number of ribs. So easily quantitatable, very easily countable changes.

If you pick the strains that straddle a threshold like that, then very small disturbances would push them one side or the other of the threshold, and you count the number of the vertebrae and you see if you've had a small disturbance. I call that the homeotic shift method, and I have about four or five papers on that. But that was my only subsequent way back into embryology. Except, of course, the spot test[2] which is also involved in embryosis, but it's purely genetic.

Q: At this point in the late forties, how were you identifying yourself? By the 1950s, say. What kind of scientist were you?

A: A geneticist. As I said, the only other time I got into teratogenesis was probably in the late fifties or early sixties when I did the homeotic shift.

The other thing that I profited from was the mutations that were being induced as part of the mutagenesis tests. Bill's work was essentially counting the mutations and finding things that affected the rate of induction, whereas I grabbed them. So I was very fortunate that he had decided to keep propagating them as stock, not just counting them but setting up -- so by the time I got into sort of milking the results of his labors, there were a lot of stocks to work with.

I think I got back in a big way into genetics when I started doing the complementation tests[3] with the mutations, because, as you probably know, you probably didn't read too much of his stuff, but he was using the specific locus test[4] and it was essentially using seven loci, not for their own sake, but because they were a good indicator, an easy indicator of mutation rates. But this resulted in our having multiple mutations at any one locus. They may have twenty or thirty at the B locus, the may have fifty or sixty at some other locus. So that gives you a lot of good genetic material to do complementation[5] with.

And I milked his weird cases in other ways. For instance, a lot of the X-chromosome work I did came out of that. And really, the best thing that ever happened to me was finding the variegated mutants. I would say in the genetic area, a lot of things that I did had a common interest, and that was in mosaicism[6] coming from different directions.

And you know, the book that I edited, Genetic Mosaics and Chimeras? [Russell, Liane B., ed. Genetic mosaics and chimeras in mammals. New York: Plenum Press, 1978.] They had found -- I've forgotten in what order now, but anyhow, that some of the specific locus mutations were not whole-body, but they were mottled or variegated. So those are the ones I picked up for special interest.

A: Because they were unusual and potentially of genetic interest. I was very much, at that time -- I had mentioned Ed [Edward B.] Lewis.[7] I thought he was great, and he had done quite a bit of work on position effect[8] on Drosophila[9], and he had a review on position effect, which I read every word of and I thought it was great.

But anyway, I was pretty sure that there was some kind of position effect because in Drosophila, if you have heterochromatin[10] next to a gene, it makes the -- not just next, but near -- it will make the action of that gene, quote, “uncertain.” So I thought that was what was happening here.

Well, I soon found -- and they're not that common. To start with we had one, and then a year later we had two more. I think eventually, even over all the years, we may have had twenty, which is not a big number. Because those aberrations turn out not to be as frequent. What we found was that they were -- the females were the only ones that were the variegated. And also, the females were what we then called semi-sterile. It means the litter size was roughly half of what it would have been. So immediately the suspicion is [that] they carry a translocation.[11] Of course, this is before the days of very good cytogenetics[12] but we did pretty soon get the cytogenetics, too. So, genetically, it was very clear they were translocations, and they were translocations of an X chromosome to an autosome.[13] I really don't know how much you want me to talk about this.

Q: Right. Well, one question I wanted to ask before, and I'll just insert now, because you're discussing really the Science article in '61.

Q: And we'll get back to that, because you and Mary [F.] Lyon[14] start to at the same time simultaneously develop a hypothesis on the --

A: Just making crosses. Just really progeny where the translocation bearing females were variegated, but the translocation bearing males were not. Then we found -- this is something else that I was working on at the same time was spontaneous and induced losses of sex chromosomes. Once in a while we would find a female that had a translocation but was not variegated, and she would turn out to have lost one of her sex chromosomes. So the only X chromosome she had would be in two pieces, each one attached to the --

A: And whatever the marker gene was wild type allele[15] of that particular marker gene, for instance, brown or pink or whatever, that piece of autosome was attached to a piece of X. But it was only when she had another X that she was variegated, and when she lacked another X, or when it was a male that only had that one broken X, was also not variegated.

So from that, I came at it from a very different way from Mary [Lyon]. I said that one X was needed to do its job, and the other X was surplus and was able to be on and off and induced the position effect, and I called it the position effect, if the X was inducing a position effect.

Q: And what I was reading is it would be more of an activation of one of the X's, and she described it as inactivation of one of the X's. Or is that too simplistic?

A: Well, I essentially said one X is needed to be active, and the rest of them are junk, I mean they're not needed. So that immediately brought the idea that the reason that it was variegated was because in some cells the one X was doing its job, and in others, the other. In the cells where the broken X was active, then that wild type marker was also active, and in the other cells, the intact X was active. So the broken X was not, and the piece of autosome attached to it also was not, so it was off, and that's what gave you the variegation.

Q: Okay. And were you aware of Lyon, what she was doing in Britain at that point?

A: No, because she was essentially -- the whole XO[16] thing started here with the scurfy[17] back in -- I don't know, but two or three years before that. That was interesting because scurfy was a mutation which was not one of our markers, it turned out to be an X- chromatization. At the time we didn't publish it, otherwise we would have published the first X-linked mutation, but we didn't.

A: Because Bill was lazy, or busy or something. But scurfy ended up with the same situation. Once in a while you'd find only the males with scurfy. I'm trying to remember - I know that Bill was doing ovarian translocation at that time to rule out one of the possibilities, and the upshot was that we found the XO, because of the situation in the scurfy strain where you sometimes got the wild type females, and they turned out to be XOs.

So that was published. Bill published that, and at the same time we published two papers together. The other one, I was also doing it with tabby,[18] which was a well known X-linked mutation. Then shortly thereafter, we found XXYs, and they would be variegated if they had the translocations or if they had whatever the mutant was.

Because if it had been like Drosophila, it would have been different because, in Drosophila, the Y chromosome will suppress the variegation. Because I had been reading the E.B. Lewis stuff, that's why I was pretty sure to start with that there was something to do with the Y, but then when we had the translocation both as XOs and as XXYs, the XXYs were much later -- not much later, maybe a year later, it turned out that it wasn't whether or not you had a Y but it was how many Xs you had that made a difference, so it wasn't like Drosophila. The Y didn't have anything to do with it.

Q: So Drosophila had been used as a model organism for genetics for quite a long time. How much of the understanding of genetics based on the Drosophila model influenced the way you thought genetics would work?

A: It did. Immediately, we found the XOs and everything. It turned out that sex determination was not like Drosophila. In Drosophila, it's the ratio of autosomes to X chromosomes, and that's how I was conditioned to think. But it wasn't. It was whether you had a Y or not. So the Y determination shattered the parallelism with Drosophila, and so did the position effect. The Y had nothing to do with whether or not you got the position effect.

Q: And how long did it take you to figure this out? Or was it just that when you identified the first XXY mouse that you realized that things were different than flies?

A: No, I think it was even before we had the XXY, when we just had the XO and XX that we figured it out. But, you know, the relation to the human -- because just about that time Charlie [Charles E.] Ford and others were doing XO humans. But in the humans, it was all cytogenetic evidence. There was no genetic evidence. In the mouse, we had the genetic and the cytogenetic, so I think that was a nice clincher. I mean, that showed when modeled organisms are important. Also, human XOs are non-fertile, but mouse XOs are, so you're able to do genetic work with them.

A: We had a cytogeneticist by the name of Ernie [Ernest H.Yi] Chu, who is still at [University of] Michigan, I think. He was pretty good. I think that the mouse cytogenetics was never as good as the humans because the mouse chromosomes are all acrocentric, so before the banding came in you really could not identify individual mouse chromosomes. They make a continuum in length, and the centromeres[19] are all at the end, or near the end. And humans, you could identify individual chromosomes. So I think the mouse cytogenetics was lagging at the time, but it certainly was good enough to tell whether you had an X or not.

Q: So the model here at Oak Ridge, rather than to do postdocs, was to bring in people with different expertise?

A: Yes, it was. And Dr. [Alexander] Hollaender[20] was a great genius that way. He was the division director. He was the one that hired Bill, but he was here not very long before Bill came, I think, maybe a year or so. He wanted to make the division very genetics-oriented. Before he came here, whoever had been in charge of biology, it was mostly radiation effects on different organ systems, that kind of stuff.

But Hollaender wanted to make a genetics division. He built up some really great young people. Drosophila, Neurospora,[21] maize.[22] He had all sorts of organisms represented. He also went out and started to become international. He got our group, our division people, invited along to foreign meetings, or to take sabbaticals abroad. And then he would bring in foreign investigators for a year or two years. He brought in a great many people for short durations. I think that's where we got our broad experience. Bill and I never got a sabbatical because we had to stay with the -- there's no one else has a mouse colony like that size. But we had a lot of people come in.

Q: Okay. I think we're going to get back to that topic, but I wanted to -- just because this is an interesting issue for priority debates in science, yours and Lyon's work come out the same year. One comes out in Nature -- they're simultaneous. How do you account for the fact that you basically came up with the same conclusions at the same time working completely independently of each other?

A: And working totally different projects, yeah. It's maybe because she had got at that time the fact that sex-linked mutants came to be known. There really weren't any sex-linked mutants in a mouse. Well, the scurfy was there, but it hadn't been published, and it wasn't a good thing to work with because it was so lethal. Tabby was really the one that became a good mutant to work with. That wasn't very long, and then the whole XO situation, which we published, but that she made use of.

A: Well, I think it was because I didn't capitalize on it, and I think that was -- I was not very good at publicizing myself. And also, I really didn’t do all the work I could have done on it because of other things in my life. My kids were like eight and ten, and I had a lot of things that involved them. We were talking last night. I was never able to become single focused on something because I was too diffused, and I didn't do as much work as I could have.

Q: And what do you think the implications have been for you that it's not the Russell-Lyon Hypothesis or the Russell Hypothesis?

A: It did bother me some, but it didn't really make me sick or anything. It did bother me.

[1] Organogenesis; The process by which organs form from embryonic cells.

[2] Spot Test; Dr. Russell’s fur-spot test identified chemicals likely to be mutagenic in reproductive cells.

[3] Complementation Tests; A test which determines if two different strains of an organism both have homozygous recessive mutations by seeing whether the two organisms produce the same wild-type phenotype when cross bred (for example, a change in wing structure in flies). This test is useful because it shows what a specific gene’s function is. For more detail, see http://www.ndsu.edu/pubweb/~mcclean/plsc431/mutation/mutation5.htm.

[4] Specific Locus Test; A test that shows recessive mutations in offspring when one parent is normal and the other is recessive at various loci.

[5] Complementation; Where two different homozygous recessive strains of an organism result in the same phenotype and where the cross of both genotypes results in the wild type.

[6] Mosaicism; A mutation where there are different sets of chromosomes within the cells of a single organism. This difference can result in genetic disorders such as Downs syndrome.

[7] Edward B. Lewis (1918 – 2004); A Nobel Prize co-recipient in medicine for demonstrating how genes direct embryonic development, Lewis was a well-respected geneticist. He also developed the complementation test and studied radiation effects.

[8] Position Effect; The effect of a gene’s position in the chromosome upon phenotype. For instance genes translocated to regions of heterochromatin are often not expressed.

[9] Drosophila; A genus of fruit fly, most commonly drosophila melanogaster, used as a model organism in many scientific experiments since it is relatively inexpensive, has a high fecundity and a short life span, and has a discernable phenotype and genotype.

[10] Heterochromatin; An intricately coiled piece form of DNA which is known for its relative genetic inactivity.

[11] Chromosomal translocation; Movement of gene segments between nonhomologous chromosomes.

[12] Cytogenetics; The study of the cell’s chromosomes.

[13] Autosome; A chromosome that is not a sex chromosome. Autosomes carry genes which determine the somatic characteristics and do not have any influence on determining the sex of the organism, unlike the sex chromosomes.

[14] Mary F. Lyon, FRS (Fellow of the Royal Society); An English geneticist famous for her work on radiation and its effect on mutation. She also formulated the Lyon Hypothesis, stating that an X chromosome can be inactive.

[15] Wild Type Allele; The most prevalent allele, the one with the highest gene frequency is the one deemed as wild type allele. The allele that is thought to contribute the typical phenotype seen in "wild" populations of organisms.

[16] XO Genotype; A case where there is only one sex hormone instead of two. XO individuals are females with Turner’s Syndrome.

[17] Scurfy; The scurfy mutation affects the autoimmune system. This mutation in mice is used to study the immune system. It causes mice to have scabby skin, open their eyes late, and die early.

[18] Tabby; Abbreviated as (Ta), is a mutation used as a marker gene in strains carrying the X-linked mutations jimpy (jp) and testicular feminization (Tfm) and in the XO chromosomal stock.

[19] Centromeres; The point where two sister chromatids meet is the centromere. From this point, the cell can engage in cell division.

[20] Alexander Hollaender (1898 – 1986); A radiation biologist who theorized that nucleic acids were the main component of genetic information. He is a recipient of the Enrico Fermi award. For more information see http://www.genetics.org/cgi/reprint/143/3/1051.

[21] Neurospora; Neurospora crassa is a model organism; it is a fungus of the phylum Ascomycot and the genus Neurospora. It is easy to grow and only has seven chromosomes making it ideal for genetics research.

[22] Maize; Also known as corn, maize is a model plant organism often used in genetics research from the genus Zea.

[23] Lyon Hypothesis; The hypothesis articulated by Mary Lyon maintaining that in organisms with more than one X chromosome, the other X chromosome may become inactive. The other X chromosome condenses into chromatin.

[1] Backcrosses; Breeding a hybrid offspring with its parent or an organism close in genetic makeup to its parent. This method is used to help identify the genotypes of the hybrid offspring.

[2] Y-12 National Security Complex; A building by the Oak Ridge Labs owned by the US Department of Energy. It deals with uranium and nuclear weapon parts production.

[3] Dose Rate Effect; Dose rate is the amount of radiation absorbed over time. The Dose Rate effect that William Russell wrote about in his paper Radiation Dose Rate and Mutation Frequency says that the amount of radiation received is correlated to the number of mutations. See http://www.sciencemag.org/cgi/content/abstract/128/3338/1546 for a link to the full text.

[4] Thomas Hunt Morgan (1866 – 1945); An esteemed American geneticist awarded the Nobel Prize in Physiology or Medicine for his work demonstrating how genes are the units of heredity in his work with Drosophila. See http://nobelprize.org/nobel_prizes/medicine/laureates/1933/morgan-bio.html.

[5] Thomas H. Roderick; A geneticist who worked at the Jackson Labs. He is most well known for using genetics in genealogy.

[6] N-ethyl-N-nitrosourea; Also known as ENU, this is a very strong mutagen that usually focuses on spermatogonial stem cells. The effect is genome wide. For William Russell’s paper on this topic see http://www.pnas.org/content/76/11/5818.abstract.

[1] United Nations Scientific Committee on the Effects of Atomic Radiation; Created in 1955 by the UN, this committee analyzes global levels of ionizing radiation and its effects. See http://www.unscear.org/.

[2] Biological Effects of Atomic Radiation, aka BEAR (1954 – 1964); An organization established to study the effects of radiation on living organism and to make sense of the data already published on radiation. There were six subcommittees under BEAR studying particular topics.

[3] National Research Council; A US governmental organization which seeks to educate public figures on matters of scientific policy.

[1] Rosalind Franklin (1928 – 1958); An English scientist and x-ray crystallographer who determined the structure of DNA.

[2] Barbara McClintock (1902 – 1992); An American cytogeneticist who was awarded the Nobel Prize in Physiology or Medicine for her work on maize cytogenetics.

[3] Pachytene; The third stage of prophase in meiosis, the cell division that results in gametes. It involves crossing over of genetic information.

[4] Charlotte Auerbach FRS (1899 – 1994); A Jewish German scientist whose work on the effects of mustard gas on fruit flies established the field of mutagenesis.

[1] Meiotic Cycle; A cell division cycle where the number of chromosomes is reduced by half.

[2] National Institutes of Health; The United States governmental organization in charge of regulating scientific research. It operates under the Department of Health and Human Services. See their website for more information: http://www.nih.gov/about/index.html.

[3] National Institute of Environmental Health Sciences; This institute is focuses on how the environment influences disease. It is part of the US Department of Health and Human Services.

[4] Chromosome Aberration; Any abnormality in a chromosome’s structure or the chromosome count. It can be deleterious, beneficial, or have no effect.

[5] Triclosan; An antibacterial substance commonly found in cleaning supplies.

[6] Richard P. Woychik; A noted geneticist who worked at the Jackson Labs. He is best known for his work on obesity-related genes. For a biographical sketch see http://www.jax.org/news/archives/2002/woychik_outline.html.

[7] Centimorgans; A measurement that signifies distance along a chromosome. Usually 1cM is equal to about 1 million base pairs

[8] Genetic Complementation Maps; A gene map that describes each mutation and shows whether it complements with other mutations.

[9] Dilute Short-Ear Region (d-se); A region of the mouse loci that is integral to development. For a sample of Liane Russell’s paper in this topic see http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1202704/.

[10] Nancy A. Jenkins and Neal G. Copeland; A husband and wife duo of geneticists noted for studying human diseases, particularly cancer, in mice.

[11] Hypermorphic mutation; a mutation which causes an increase in normal gene function.

[12] Charles DeLisi; Currently Professor of Science and Engineering at Boston University, DeLisi was head of the Department of Energy’s Health and Environmental Research Programs from 1985 to 1987.

[1] Proceedings of the National Academy of Sciences of the United States of America; PNAS is the journal of the US National Academy of Sciences specializing in printing biomedical sciences articles.

[2] Spermatogonia; A male germ layer that has not yet differentiated. It is the precursor to stem cells.

[3] Etoposide; A semi-synthetic product which can cause cell death, breaks in DNA, as well as a stop to DNA transcription.

[4] Crossing over; The process of exchanging genetic material between homologous chromosomes which happens in the prophase stage of meiosis.

[5] Pronucleus; A sperm or egg nucleus with only half the normal number of chromosomes. Pronuclei appear after the sperm enters the ovum but before the respective nuclei fuse.

[6] Perigametic Interval; The interval between the last pre-meiotic mitosis and the first post-meiotic mitosis. It contains a very high mutation rate. For an article by William and Liane Russell on the perigametic interval see: http://www.pnas.org/content/93/23/13072.full.pdf (Spontaneous mutations recovered as mosaics in the mouse specific-locus?test).

[7] Sibship; A group of persons all descended from a common ancestor, often siblings.

[8] Environmental Protection Agency; A US agency that administers the environmental policy passed by the government. See http://www.epa.gov/.

[9] Salmonella; A bacterium which causes many different afflictions in humans and animals.

[10] Oocytes; The female germ cell which is an integral part of reproduction. Also known as the egg cell.

[11] Genetic Lesions; Injuries or loss of function which occur in the DNA molecules which control a cell's proper operation, including the accuracy and appropriate rate of the cell's division. Genetic lesions in a cell can occur at any age.

[1] Irene Uchida; A Canadian scientist who is best known for her work on Down Syndrome. She has also studied the effects of radiation on mice.

[2] Frank Clarke Fraser, FRSC; A very important Canadian geneticist who is currently a Professor Emeritus at McGill University. An interview with Dr. Fraser is available in this collection.

[3] OncoMouse; A laboratory mouse that has been genetically altered to be more susceptible to cancer.

[1] Atomic Bomb Casualty Commission (ABCC); An organization created by Harry Truman in 1948 to study the effects of radiation from the atomic bombings at Nagasaki and Hiroshima.

[2] James V. Neel (1915 – 2000); An American geneticist who researched the genetics of sickle cell anemia and radiation from atomic bombings. Dr. Neel established the first human genetics department in the US at the University of Michigan and was very influential in the field.

[4] Duncan J. McDonald; The former chief of human genetics at the Atomic Bomb Casualty Commission.

[5] James F. Crow; A noted geneticist who is currently Professor Emeritus in Genetics at the University of Wisconsin-Madison. See James Crow’s interview in this collection.

[6] 2-Dimensional Gel Electrophoresis; A technique that allows infrequent proteins to be identified.

[7] ABCW Hypothesis; This postulate maintains that the rate of mutation (from radiation) for each locus is correlated directly to haploid DNA content.

[8] Leslie Clarence Dunn (1893-1974); A geneticist and former Professor of Zoology at Columbia.

[9] Salome Gluecksohn-Waelsch; A German geneticist noted for her work on developmental genetics.

[10] Hox Genes; A group of developmental genes that are responsible for the spatial arrangement of the body.

RUSSELL, LIANNE

INTERVIEW
JANUARY 18TH-19TH, 2007

RUSSELL, LIANNE

INTERVIEW JANUARY 18TH-19TH, 2007

INTERVIEW
JANUARY 18TH-19TH, 2007