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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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?
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?
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?
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 following table, 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?