Temperature-dependent sex determination (TSD) is the method of sex determination in sea turtles. In TSD, temperature experienced during embryonic development determines the sex of the offspring. TSD is only observed in reptiles and teleost fish. The molecular mechanisms are not well understood, but the production of estrogen, which causes female development, seems to be critical. A potential pathway is shown in Figure 1. EnvironmentCytoplasmInternalsignaling pathway(s)Activates or inhibitsTestosterone(substrate)Estrogen(product)AromataseFigure 1. One potential TSD metabolic pathway in sea turtlesWithin the TSD mechanism there are two distinct, genetically determined pattems, named pattemI and pattern II. The details of each pattern are presented below.Pattern I: Males develop below 82°F. Females develop above 88°F. A mix of males andfemales develop between temperatures of 82 and 88°F.Pattern II: Males develop between temperatures of 73 and 82°F. Females develop below73°F and above 82°F.

The answer to this question is solved in serial wise. A) Cellular Events

Temperature-dependent sex determination (TSD) is the method of sex determination in sea turtles. In TSD, temperature experienced during embryonic development determines the sex of the offspring. TSD is only observed in reptiles and teleost fish. The molecular mechanisms are not well understood, but the production of estrogen, which causes female development, seems to be critical. A potential pathway is shown in Figure 1.

Temperature-dependent sex determination (TSD) is the method of sex determination in sea turtles. In TSD, temperature experienced during embryonic development determines the sex of the offspring. TSD is only observed in reptiles and teleost fish. The molecular mechanisms are not well understood, but the production of estrogen, which causes female development, seems to be critical. A potential pathway is shown in Figure 1.

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter11: Genome Alterations: Mutation And Epigenetics

Section: Chapter Questions

Problem 8QP: Bruce Ames and his colleagues have pointed out that although detailed toxicological analysis has...

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Bruce Ames and his colleagues have pointed out that although detailed toxicological analysis has been conducted on synthetic chemicals, almost no information is available about the mutagenic or carcinogenic effects of the toxins produced by plants as a natural defense against fungi, insects, and animal predators. Tens of thousands of such compounds have been discovered, and he estimates that in the United States adults eat about 1.5 g of these compounds each daylevels that are approximately 10,000 times higher than those of the synthetic pesticides present in the diet. For example, cabbage contains 49 natural pesticides and metabolites, and only a few of these have been tested for their carcinogenic and mutagenic effects. a. With the introduction of new foods into the U.S. diet over the last 200 years (mangoes, kiwi fruit, tomatoes, and so forth), has there been enough time for humans to develop resistance to the mutagenic effects of the toxins present in those foods? b. The natural pesticides present in plants constitute more than 99% of the toxins we eat. Should diet planning, especially for vegetarians, take into account the doses of toxins present in the diet?
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Animals do not keep all their detoxification enzymes in aconstant state of readiness. Thus they depend on phenotypicplasticity to adapt to changing hazards. An example is providedby the enzyme alcohol dehydrogenase, which breaks down ethylalcohol. People who do not drink alcoholic beverages have littlealcohol dehydrogenase. Expression of the enzyme increaseswhen people drink alcohol, but full expression requires manydays, meaning that people are incompletely defended againstalcohol’s effects when they first start drinking after a period ofnot drinking. Consider, also, that muscles atrophy when notused, rather than being maintained always in a fully developedstate. Propose reasons why animals depend on phenotypicplasticity, instead of maintaining all their systems in a maximumstate of readiness at all times.
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Development of the nematode Caenorhabditis ele-gans generates exactly 959 somatic cells; it also producesan additional 131 cells that are later eliminated by apop-tosis. Classical genetic experiments in C. elegans isolatedmutants that led to the identification of the first genesinvolved in apoptosis. Of the many mutations affectingapoptosis in the nematode, none have ever been found inthe gene for cytochrome c. Why do you suppose that sucha central effector molecule in apoptosis was not found inthe many genetic screens for “death” genes that have beencarried out in C. elegans?
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