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Deletions may cause cancer by removing or disrupting genes that suppress tumors; inversions and translocations may break tumor-suppressing genes or they may move genes to positions next to different regulatory sequences erectile dysfunction with age cheap viagra soft 50mg mastercard, which alters their expression erectile dysfunction keywords purchase online viagra soft. Additional mutations allow the polyp to enlarge impotence cure cheap 100 mg viagra soft, invade the muscle layer of the gut erectile dysfunction drugs used discount generic viagra soft canada, and eventually spread to other sites. Retinoblastoma results from at least two separate genetic defects, both of which are necessary for cancer to develop. In sporadic cases, two successive mutations must occur in a single cell, which is unlikely and therefore typically affects only one eye. In people who have inherited one of the two required mutations, every cell contains this mutation, and so a single additional mutation is all that is required for cancer to develop. Given the millions of cells in each eye, there is a high probability that the second mutation will occur in at least one cell of each eye, producing tumors in both eyes and the inheritance of this type of retinoblastoma. Mutations in oncogenes are usually dominant because a mutation in a single copy of the gene is usually sufficient to produce a stimulatory effect. Mutations in tumor-suppressor genes are generally recessive, because both copies must be mutated to remove all inhibition. Tumor-suppressor genes, on the other hand, suppress cell proliferation and act in a recessive manner; a single copy of a tumor-suppressor gene is sufficient to prevent cell proliferation. Give some examples of the functions of proto-oncogenes and tumor suppressers in normal cells. Briefly outline the events that control the progression of cells through the G1/S checkpoint in the cell cycle. Briefly outline the events that control the progression of cells through the G2/M checkpoint of the cell cycle. Why are mutations in components of signal-transduction pathways often associated with cancer? Explain how chromosome deletions, inversions, and translocations may cause cancer. Briefly outline how the Philadelphia chromosome leads to chronic myelogenous cancer. Briefly outline some of the genetic changes that are commonly associated with the progression of colorectal cancer. If cancer is fundamentally a genetic disease, how might an environmental factor such as smoking cause cancer? Briefly outline how you might go about determining if these differences in the incidence of prostate cancer are due to differences in the genetic makeup of two populations or to differences in their environments. The mother is free from cancer, but the father has unilateral retinoblastoma and he has a brother who has bilateral retinoblastoma. If the couple has another child, what is the probability that this next child will have retinoblastoma? The palladin gene, which plays a role in pancreatic cancer (see the introduction to this chapter), is said to be an oncogene. Which of its characteristics suggest that it is an oncogene rather than a tumor-suppressor gene? Cells in a tumor contain mutated copies of a particular gene that promotes tumor growth. Gene therapy can be used to introduce a normal copy of this gene into the tumor cells. Would you expect this therapy to be effective if the mutated gene were an oncogene? Genes in cancer cells are frequently amplified, meaning that the gene exists in many copies. Would you expect to see gene amplification in oncogenes, tumor-suppresor genes, or both? They used antibodies to 658 Chapter 23 stain for acetylation at three different sites and for methylation at two different sites on histone proteins. They found that the degree of histone acetylation and methylation helped predict whether prostate cancer would return within 10 years in the patients who had a prostate tumor removed. Explain how acetylation and methylation might be associated with tumor recurrence in prostate cancer. Radiation is known to cause cancer, yet radiation is often used as treatment for some types of cancer. Some cancers are consistently associated with the deletion of a particular part of a chromosome.
The shoot grows upward and the roots downward erectile dysfunction age statistics cheap 100mg viagra soft with amex, a compact rosette of leaves is produced and impotence pills buy viagra soft 100mg mastercard, under the right conditions lloyds pharmacy erectile dysfunction pills cheap viagra soft line, the shoot enlarges and differentiates into flower structures erectile dysfunction diabetes causes discount viagra soft 100mg with amex. Genetic techniques with Arabidopsis A number of traditional and modern molecular techniques are commonly used with Arabidopsis and provide it with special advantages for genetic studies. Arabidopsis can self-fertilize, which means that any recessive mutation appearing in the germ line can be recovered in the immediate progeny. Cross-fertilization also is possible by removing the anther from one plant and dusting pollen on the stigma of another plant-essentially the same technique used by Gregor Mendel with pea plants (see Figure 3. As already mentioned, many naturally occurring variants of Arabidopsis are available for study, and new mutations can be produced by exposing its seeds to chemical mutagens, radiation, or transposable elements that randomly insert into genes. The large number of offspring produced by Arabidopsis facilitates screening for rare mutations. Genes from other organisms can be transferred to Arabidopsis by the Ti plasmid from the bacterium Agrobacterium tumefaciens, which naturally infects plants and transfers the Ti plasmid to plant cells (see Chapter 19). The Mouse Mus musculus The common house mouse, Mus musculus, is among the oldest and most valuable subjects for genetic study. Advantages of the mouse as a model genetic organism Foremost among many advantages that Mus musculus has as a model genetic organism is its close evolutionary relationship to humans. Being a mammal, the mouse is genetically, behaviorally, and physiologically more similar to humans than are other organisms used in genetics studies, making the mouse the model of choice for many studies of human and medical genetics. Other advantages include a short generation time compared with that of most other mammals. Mus musculus is well adapted to life in the laboratory and can be easily raised and bred in cages that require little space; thus several thousand mice can be raised within the confines of a small laboratory room. Finally, a large number of mutations have been isolated and studied in captive-bred mice, providing an important source of variation for genetic analysis. Life cycle of the mouse the production of gametes and reproduction in the mouse are very similar to those in humans. Diploid germ cells in the gonads undergo meiosis to produce sperm and oocytes, as outlined in Chapter 2. Male mice begin producing sperm at puberty and continue sperm production throughout the remainder of their lives. If mating takes place during estrus, sperm are deposited into the vagina and swim into the oviduct, where one sperm penetrates the outer layer of the ovum, and the nuclei of sperm and ovum fuse. An important tool for determining the function of an unknown gene in humans is to search for a homologous gene whose function has already been determined in the mouse. Furthermore, the linkage relations of many mouse genes are similar to those in humans, and the linkage relations of genes in mice often provide important clues to linkage relations among genes in humans. The mouse genome is distributed across 19 pairs of autosomes and one pair of sex chromosomes. Genetic techniques with the mouse A number of powerful techniques have been developed for use in the mouse. These techniques are made possible by the ability to manipulate the mouse reproductive cycle, including the ability to hormonally induce ovulation, isolate unfertilized oocytes from the ovary, and implant fertilized embryos back into the uterus of a surrogate mother. The ability to create transgenic, knockout, and knock-in mice has greatly facilitated the study of human genetics, and these techniques illustrate the power of the mouse as a model genetic organism. Mouse and human cells can be fused, allowing somatic-cell hybridization techniques (see Chapter 7) that have been widely used to assign human genes to specific chromosomes. Mice also tolerate inbreeding well, and inbred strains of mice are easily created by brothersister mating. Members of an inbred strain are genetically very similar or identical, allowing researchers to examine the effects of environmental factors on a trait. The use of mice as a model genetic organism has led to many important genetic discoveries. In the early twentieth century, mice were used to study the genetic basis of coat-color variation in mammals. More recently, they have figured prominantly in research on the genetic basis of cancer, and potential carcinogens are often tested in mice. Mice have been used to study genes that influence mammalian development, including mutations that produce birth defects in humans.
In humans erectile dysfunction 2015 discount viagra soft 100mg with amex, for example erectile dysfunction natural buy 50 mg viagra soft otc, many body structures respond to growth hormone impotence lack of sleep purchase 50 mg viagra soft visa, and there are genes that affect the amount of growth hormone secreted by the pituitary gland erectile dysfunction rates age buy discount viagra soft online. People with certain genes produce high levels of growth hormone, which increases both height and hand size. Others possess genes that produce lower levels of growth hormone, which leads to both short stature and small hands. Height and hand size are therefore phenotypically correlated in humans, and this correlation is due to a genetic correlation-the fact that both characteristics are affected by the same genes that control the amount of growth hormone. Genetically speaking, height and hand size are the same characteristic because they are the phenotypic manifestation of a single set of genes. When two characteristics are influenced by the same genes they are genetically correlated. A positive genetic correlation between two characteristics means that genes that cause an increase in one characteristic also produce an increase in the other characteristic. Thorax length and wing length in Drosophila are positively correlated because the genes that increase thorax length also increase wing length. A negative genetic correlation means that genes that cause an increase in one characteristic produce a decrease in the other characteristic. Milk yield and percentage of butterfat are negatively correlated in cattle: genes that cause higher milk production result in milk with a lower percentage of butterfat. Genetic correlations are important in animal and plant breeding because they produce a correlated response to Chicken Mouse Fruit fly Source: After D. Correlated responses to selection are due to the fact that both characteristics are influenced by the same genes; selection for one characteristic causes a change in the genes affecting that characteristic, and these genes also affect the second characteristic, causing it to change at the same time. Correlated responses may well be undesirable and may limit the ability to alter a characteristic by selection. From 1944 to 1964, domestic turkeys were subjected to intense selection for growth rate and body size. These correlated responses were due to negative genetic correlations between body size and fertility; eventually, these genetic correlations limited the extent to which the growth rate of turkeys could respond to selection. Genetic correlations may also limit the ability of natural populations to respond to selection in the wild and adapt to their environments. When two characteristics are genetically correlated, selection for one characteristic will produce a correlated response in the other characteristic. If greater milk yield is selected in this herd, what will be the effect on the percentage of butterfat? For many quantitative characteristics, the relation between genotype and phenotype is complex because many genes and environmental factors influence a characteristic. Regression can be used to predict the value of one variable on the basis of the value of a correlated variable. Heritability is based on the variances present within a group of individuals, and an individual does not have heritability. The heritability of a characteristic varies among populations and among environments. Even if the heritability for a characteristic is high, the characteristic may still be altered by changes in the environment. Heritabilities provide no information about the nature of population differences in a characteristic. Genes influencing quantitative traits can also be located with the use of genomewide association studies. Cross two individuals that are each homozygous for different genes affecting the traits and then intercross the resulting F1 progeny to produce the F2. Determine what proportion of the F2 progeny resembles one of the original homozygotes in the P generation. This proportion should be (1/4)n, where n equals the number of loci with a segregating pair of alleles that affect the characteristic.
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