Chapter 18, Problem 21
Because the degree of DNA methylation appears to be a relatively reliable genetic marker for some forms of cancer, researchers have explored the possibility of altering DNA methylation as a form of cancer therapy. Initial studies indicate that while hypomethylation suppresses the formation of some tumors, other tumors thrive. Why would one expect different cancers to respond differently to either hypomethylation or hypermethylation therapies?
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Trace the relationship between the methylation status of the glucocorticoid receptor gene and the behavioral response to stress.
Prader–Willi syndrome (PWS) is a genetic disorder with a clinical profile of obesity, intellectual disability, and short stature. It can be caused in several ways. Most common is a deletion on the paternal copy of chromosome 15, but it can also be caused by an epigenetic imprinting disorder, and uniparental disomy, an event in which the affected child receives two copies of the maternal chromosome 15. A child with PWS comes to your clinic for a diagnosis of the molecular basis for this condition. The gel below shows the results of testing with short tandem repeats (STRs) from the region of chromosome 15 associated with the disorder.
Is this case caused by a deletion in the paternal copy of chromosome 15? Explain.
Prader–Willi syndrome (PWS) is a genetic disorder with a clinical profile of obesity, intellectual disability, and short stature. It can be caused in several ways. Most common is a deletion on the paternal copy of chromosome 15, but it can also be caused by an epigenetic imprinting disorder, and uniparental disomy, an event in which the affected child receives two copies of the maternal chromosome 15. A child with PWS comes to your clinic for a diagnosis of the molecular basis for this condition. The gel below shows the results of testing with short tandem repeats (STRs) from the region of chromosome 15 associated with the disorder.
Based on your interpretation of the data, what is the cause of PWS in this case? Explain your reasoning.
From the data in Table 19.3, draw up a list of histone H3 modifications associated with gene activation. Then draw up a list of H3 modifications associated with repression.
Are there any overlaps on the lists?
From the data in Table 19.3, draw up a list of histone H3 modifications associated with gene activation. Then draw up a list of H3 modifications associated with repression.
Are these overlaps explained by different modifications?
From the data in Table 19.3, draw up a list of histone H3 modifications associated with gene activation. Then draw up a list of H3 modifications associated with repression.
If not, how can you reconcile these differences?