Question

In this chapter we focused on how genes that control the development, structure, and function of the nervous system and interactions with environmental factors produce behavior. At the same time, we found many opportunities to consider the methods and reasoning by which much of this information was acquired. From the explanations given in the chapter, what answers would you propose to the following fundamental questions: (a) How do we know there is genetic variation for a specific behavior that is present in strains of a species? (b) How do we know that Drosophila can learn and remember? (c) How do we know how the mutant gene product in Huntington disease functions? (d) How do we know that schizophrenia has genetic components?

Short answer

Answer: Researchers determine if there is genetic variation for a specific behavior in strains of a species by performing controlled experiments and comparative studies. They study different strains of the same species, which have been selectively bred, or they compare individuals with different genetic backgrounds. By isolating specific genetic contributions and controlling for environmental factors, researchers can observe behavioral differences among the strains, indicating a genetic influence on the observed behavior.

Step-by-step solution

(a) How do we know there is genetic variation for a specific behavior that is present in strains of a species?

To determine if there is genetic variation for a specific behavior in strains of a species, scientists perform controlled experiments and comparative studies. They often study different strains of the same species, which have been selectively bred, or they compare individuals with different genetic backgrounds. By isolating specific genetic contributions and controlling for environmental factors, researchers can observe behavioral differences among the strains, indicating a genetic influence on the observed behavior.

(b) How do we know that Drosophila can learn and remember?

Drosophila, also known as fruit flies, have been studied extensively for their learning and memory abilities. Researchers use various conditioning paradigms, such as classical conditioning and operant conditioning, exposing Drosophila to certain stimuli and observing their responses. Fruit flies can be trained to associate specific stimuli with positive or negative outcomes, and they can demonstrate that learned association when later exposed to that stimulus. Their ability to form these associations and recall them later on indicates that Drosophila are capable of learning and retaining memories.

(c) How do we know how the mutant gene product in Huntington disease functions?

Researchers have discovered that Huntington disease is caused by a mutation in the Huntingtin (HTT) gene. This mutation leads to an abnormally long stretch of repeating CAG nucleotide units, which results in an abnormal Huntingtin protein that contains an extended polyglutamine tract. The mutant protein forms aggregates within neurons and interferes with normal cellular functions, ultimately leading to neuronal death and dysfunction. By studying cellular models, animal models, and post-mortem human brains, scientists have been able to identify some of the key molecular and cellular pathways affected by the mutant Huntingtin protein.

(d) How do we know that schizophrenia has genetic components?

Evidence supporting the genetic basis of schizophrenia comes from various sources, including twin studies, family studies, and large-scale genome-wide association studies (GWAS). Twin studies, in particular, have shown that when one identical twin develops schizophrenia, there is a significantly higher chance that the other twin will also develop the disorder compared to fraternal twins. This demonstrates a strong genetic component to the disease. Additionally, family studies reveal that individuals with a family history of schizophrenia have a higher risk of developing the condition. Large-scale genetic studies (GWAS) have identified specific genetic loci that are associated with an increased risk of schizophrenia. These findings support the notion that schizophrenia has a strong genetic component to its etiology.