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Ch. 19 - Epigenetics
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All textbooksKlug 12th EditionCh. 19 - EpigeneticsProblem 19

Chapter 18, Problem 19

A developmental disorder in humans called spina bifida is a neural tube defect linked to a maternal diet low in folate during pregnancy.

Should researchers be looking for mutant alleles of genes that control formation and differentiation of the neural tube?

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Hello everyone here We have a question telling us scientists were able to artificially induce spina bifida in mice by inactivating the V. A. N. G. I two gene identify which statement correctly states the relationship between genetic defects and spina bifida. A. This gene is part of a cellular signaling pathway that cells cells which way they're facing within the tissue for the cellular signaling pathway to function. Normally, sales must interact with their neighbors in order to communicate directional information. Up to 10% of spina bifida, which were detected during the first trimester, also presented with additional chromosomal anomalies like trisomy 13 and 18, tranquility and single gene mutations, which means that A and B. Are both correct. So our answer is C. Both A and B. Thank you for watching. Bye.
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How are mutations in histone acetylation (HAT) genes linked to cancer?

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Textbook Question

A developmental disorder in humans called spina bifida is a neural tube defect linked to a maternal diet low in folate during pregnancy.

What does this suggest about the cause of spina bifida?

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Textbook Question

A developmental disorder in humans called spina bifida is a neural tube defect linked to a maternal diet low in folate during pregnancy.

Does this exclude genetic mutations as a cause of this condition?

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Textbook Question

Trace the relationship between the methylation status of the glucocorticoid receptor gene and the behavioral response to stress.

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Textbook Question

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.


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Textbook Question

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. 

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