Introduction to Genetic Analysis
11th Edition
ISBN: 9781464109485
Author: Anthony J.F. Griffiths, Susan R. Wessler, Sean B. Carroll, John Doebley
Publisher: W. H. Freeman
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Chapter 1, Problem 17P
Summary Introduction
To determine: The reason for only twice the number of mutations in males, although the count of
Introduction: The formation of gametes undergoes a process of meiosis, which is followed by the mechanism of DNA replication. This process results in the doubling of chromosomes.
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We are not single celled organisms and multiple cell divisions occur between fertilization and production of gametes. In males there are an estimated 400 divisions before production of gametes and in females about 30 divisions.
Can you think of why this is? Is a new mutation arising from DNA replication more likely to occur because of errors in the male or the female germline?
Hundreds of DNA double strand breaks are created by SPO11, a topoisomerase type II like
protein.
(i)
Draw and explain how SPO11 can generate double strand breaks.
(ii)
What would be the consequences to the outcome of meiosis if SPO11 is absent?
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- The woman in Problem 24 has had two miscarriages. She has come to you, an established genetic counselor, with these questions: Is there a genetic explanation of her frequent miscarriages? Should she abandon her attempts to have a child of her own? If not, what is the chance that she could have a normal child? Provide an informed response to her concerns.arrow_forward. Early in development, most human cells turn off expression of an essential component of telomerase, the enzyme responsible for addition of telomere repeat sequences (5’-TTAGGG) to the ends of chromosomes. Thus, as our cells proliferate their telomeres get shorter and shorter, but are normally not lost over the course of a lifetime. If cells are removed from the body and grown in culture, however they ultimately enter a state of replicative senescence and stop dividing when their telomeres get too short. By contrast, most human tumor cells express active telomerase, allowing them to maintain their telomeres and grow beyond the normal limit imposed by senescence - good for them, bad for us. Anticipating a universal cure for cancer, you set up a company to screen chemical ‘libraries’ for telomerase inhibitors. The company share price takes a dive, however, when a rival group generates a strain of telomerase-knockout mice. These mice breed happily for several generations, but…arrow_forwardXX individuals can be sex-reversed males if one of their X chromosomes contains a translocated portion of the Y chromosome that includes the SRY gene. In light of what you now know about X-chromosome inactivation, it seems that this karyotype might have more complex consequences. In fact, although most such males are completely sex-reversed, X-chromosome inactivation can cause some of these XX males to have varying degrees of residual female characteristics. a. X-chromosome inactivation in normal XX embryos occurs earlier in development than SRY production in normal XY embryos. When present on a translocation X chromosome, SRY is subject to inactivation. Formulate a hypothesis to explain why many XX individuals with a translocation X chromosome that includes the SRY gene are not completely sex-reversed (male). b. Based on your answer to part (a), why do you think some individuals with this karyotype are completely sex-reversed?arrow_forward
- The nuclear DNA content of a single sperm cell in Drosophila melanogasteris approximately 0.18 pg. What would be the expected nuclear DNA content of a primary spermatocyte in Drosophila? What would be the expected nuclear DNA content of a somatic cell (non-sex cell) in the G1 phase? What would be the expected nuclear DNA content of a somatic cell at metaphase?arrow_forwardThe nuclear DNA content of a single sperm cell in Drosophila melanogaster is approximately 0.18 picogram. What would be the expected nuclear DNA content of a primary spermatocyte in Drosophila? What would be the expected nuclear DNA content of a somatic cell (non-sex cell) in the G1 phase? What would be the expected nuclear DNA content of a somatic cell at metaphase?arrow_forward"A deletion of a portion of a chromosome need not be very great before the effects become severe". Explain this ?arrow_forward
- Explain why, in humans, chromosomal mutation rates in females are much higher than in males.arrow_forwardA typical somatic cell from a badger, which is a diploid, sexually reproducing animal, contains a total of 32 chromosomes. Gametogenesis in badgers is similar to humans. What is the genome size for the badger in terms of chromosome number? How many DNA molecules would be found in a secondary oocyte before dividing? How many chromosomes would be found in a cell at metaphase? How many DNA molecules should be in a tetraploid liver cell from the badger?arrow_forward(a) How does the duplication of individual genes occur? (b) individual that inherit a genetic condition known as xeroderma pigmentosum exhibit an extreme sensitivity to sunlight exposure and often develop skin cancer by the age of 10. What repair pathway is most likely disrupted as a result of such mutation? Explain why?arrow_forward
- Please summarize and make the following paragraph about treacher collins syndrome disease into important bullet points. Thank you!! A mutation in the TCOF1 gene causes up to 93% of Treacher Collins syndrome cases. This gene, which is found on chromosome 5, is in charge of facial developnent. TCOF1 changes spontaneously in around half of all cases at conception, but no one knows what causes the change. In addition, Treacher Collins syndrome is inherited as an autosomal dominant condition in some cases. This indicates that the child inherits the Treacher Collins syndrome gene from one parent and an unaffected copy from the other. Changes in the POLRIC and POLRID genes may be responsible for another 2% of instances. It's unclear how the mutations in the genes create facial abnormalities. However, during weeks three to eight of embryonic development, they are thought to trigger apoptosis (cell death) of facial bone, cartilage, and soft tissue.arrow_forwardI am trying to understand DNA/chromosome structure and replication. I have a culture dish of human cells (NIH3T3) and expose them to radioactively labeled Thymidine, 3H-thymidine, during S phase of the cell cycle. How would my radioactivity be distributed over a pair of homologous chromosomes at metaphase? If i have to draw How the radioactivity would be distributed over a pair of homologous chromosomes at metaphase, how will my drwing look likearrow_forwardHypothetically, a cell has DNA that weighs 10 picograms. This cell goes through S phase and is about to undergo mitosis. How much does the DNA of this cell weight now? How much would the DNA of the two cells produced at the end of mitosis weigh? Explain your reasoning.arrow_forward
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Mitochondrial mutations; Author: Useful Genetics;https://www.youtube.com/watch?v=GvgXe-3RJeU;License: CC-BY