A boy with Klinefelter syndrome (47,XXY) is born to a motherwho is phenotypically normal and a father who has the X-linkedskin condition called anhidrotic ectodermal dysplasia. The mother’sskin is completely normal with no signs of the skin abnormality.In contrast, her son has patches of normal skin and patchesof abnormal skin. Question: Using the appropriate genetic terminology, describe themeiotic mistake that occurred. Be sure to indicate in whichdivision the mistake occurred.
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A:
A boy with Klinefelter syndrome (47,XXY) is born to a mother
who is
skin condition called anhidrotic ectodermal dysplasia. The mother’s
skin is completely normal with no signs of the skin abnormality.
In contrast, her son has patches of normal skin and patches
of abnormal skin.
Question: Using the appropriate genetic terminology, describe the
meiotic mistake that occurred. Be sure to indicate in which
division the mistake occurred.
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- A boy with Klinefelter syndrome (47,XXY) is born to a motherwho is phenotypically normal and a father who has the X-linkedskin condition called anhidrotic ectodermal dysplasia. The mother’sskin is completely normal with no signs of the skin abnormality.In contrast, her son has patches of normal skin and patchesof abnormal skin. Using the appropriate genetic terminology, explain theson’s skin phenotype.A female patient 19 years old, whose symptoms areanemia and internal bleeding due to a massive buildupof leukemic white blood cells, is diagnosed withchronic myelogenous leukemia (CML). Karyotypeanalysis shows that the leukemic cells of this patientare heterozygous for a reciprocal translocation involving chromosomes 9 and 22. However, none of thenormal, nonleukemic cells of this patient contain thetranslocation. Which of the following statements istrue and which is false?a. The translocation results in the inactivation (loss offunction) of a tumor-suppressor gene.b. The translocation results in the inactivation (loss offunction) of an oncogene.c. There is a 50% chance that any child of this patientwill have CML.d. This patient is a somatic mosaic in terms of thekaryotype.e. DNA extracted from leukemic cells of this patient,if taken up by normal mouse tissue culture cells,could potentially transform the mouse cells intocells capable of causing tumors.f. The normal function of the…A boy with Klinefelter syndrome (47,XXY) is born to a motherwho is phenotypically normal and a father who has the X-linkedskin condition called anhidrotic ectodermal dysplasia. The mother’sskin is completely normal with no signs of the skin abnormality.In contrast, her son has patches of normal skin and patchesof abnormal skin. Question: Which parent contributed the abnormal gamete?
- In retinoblastoma, a mutation in one allele of the RB1 tumorsuppressorgene can be inherited from the germ line, causingan autosomal dominant predisposition to the developmentof eye tumors. To develop tumors, a somatic mutation in thesecond copy of the RB1 gene is necessary, indicating that themutation itself acts as a recessive trait. Given that the firstmutation can be inherited, in what ways can a second mutationalevent occur?The gene controlling ABO blood type and the gene underlying nail-patella syndrome are said to show linkage. What does that mean in terms of their relative locations in the genome? What does it mean in terms of how the two traits are inherited with respect to each other?Fragile-X syndrome causes the most common form of inherited intellectual disability. What is the chromosomal abnormality associated with this disorder? What is the phenotype of this disorder?
- Prader-Willi syndrome and Angelman syndrome are both caused by deletion of a set of genes onchromosome 15. The symptoms of Prader-Willi syndrome are short stature, small hands andfeet, hypotonia (floppiness), hypogonadism, mild mental retardation, and an uncontrollabledesire to eat (polyphagia). Angelman syndrome is characterized by an intellectual anddevelopmental delay, sleep disturbances, seizures, hand-flapping and other jerky movements,frequent laughter or smiling, and usually a happy demeanor.Please explain how the deletion of the same set of genes can result in such different diseases. Inyour answer, be sure to discuss the role of genetic imprinting and epigenetics.The maternal-effect mutation bicoid (bcd) is recessive. Inthe absence of the bicoid protein product, embryogenesis isnot completed. Consider a cross between a female heterozygousfor the bicoid mutation (bcd+/ bcd-) and a homozygousmale(bcd-/ bcd-). How is it possible for a male homozygous for the mutationto exist?Glucose-6-phosphate dehydrogenase deficiency/G6PDD (g) is an X-linked recessive conditionwherein the red blood cells of affected individuals undergo premature hemolysis. Fragile X syndrome(F), on the other hand, is an X-linked dominant mutation characterized by a mild to moderateintellectual disability. Amelogenesis imperfecta (A) is a congenital disorder affecting the formation ofthe teeth enamel making affected individuals at higher risk for dental cavities and related problems.Only male offspring inherit this condition. Jane is heterozygous for both X-linked traits like her mother. Her father is normal for both X-linked traits. James has a mother who suffers from G6PDD but not from fragile X-syndrome. His fatherdoes not exhibit any X-linked disorder but has amelogenesis imperfecta. A. What are the genotypes of the following: Jane: ______________________ James: ______________________Jane’s mother: _________________ James’ mother: ________________Jane’s father: __________________…
- Fragile X syndrome why is interesting Fragile X syndrome What are the symptoms or characteristics of this disorder or trait? What is the prevalence of the trait or disorder? What are the main genetic factors? s the genetic cause of this disorder or trait known? What gene(s) have been proven to be involved? Or, if not known, what genes are thought to be involved? Is it caused by a single gene? polygenic? Multifactorial? Devote a few paragraphs to this This could be one of the longest parts of the paper, if you choose to focus on this. If multiple genes are thought to be involved, discuss the specific role of at least one of them in depth (if known). Is the gene you’re discussing thought to play a major or a minor role in the phenotype? What chromosome is it on? What protein does it code for, and how might the protein possibly contribute to the phenotype? If no genes have yet been identified, indicate this, and devote at least one paragraph to any current efforts to determine which…Six months pregnant, an expectant mother had a routineultrasound that showed that the limbs of the fetus wereunusually short. Her physician suspected that the babymight have a genetic form of dwarfism called achondroplasia,an autosomal dominant trait occurring with a frequency of about1 in 27,000 births. The parents were directed to a genetic counselorto discuss this diagnosis. In the conference, they learnedthat achondroplasia is caused by a mutant allele. Sometimes itis passed from one generation to another, but in 80 percent ofall cases it is the result of a spontaneous mutation that arisesin a gamete of one of the parents. They also learned that mostchildren with achondroplasia have normal intelligence and a normallife span. It has been suggested that prenatal genetic testing for achondroplasiabe made available and offered to all women. Wouldyou agree with this initiative? What ethical considerationswould you consider when evaluating the medical and societalconsequences of offering…Six months pregnant, an expectant mother had a routineultrasound that showed that the limbs of the fetus wereunusually short. Her physician suspected that the babymight have a genetic form of dwarfism called achondroplasia,an autosomal dominant trait occurring with a frequency of about1 in 27,000 births. The parents were directed to a genetic counselorto discuss this diagnosis. In the conference, they learnedthat achondroplasia is caused by a mutant allele. Sometimes itis passed from one generation to another, but in 80 percent ofall cases it is the result of a spontaneous mutation that arisesin a gamete of one of the parents. They also learned that mostchildren with achondroplasia have normal intelligence and a normallife span. What information would be most relevant to concluding whichof the two mutation origins, inherited or new, most likelypertains in this case? How does this conclusion impact on thiscouple’s decision to have more children?