**Question:** Fredrich's ataxia is caused by which type of mutation-

A. Dominant mutation
B. Recessive mutation
C. De novo mutation
D. X-linked mutation

**Correct Answer:** B. Recessive mutation

**Core Concept:**
Frederick's Ataxia is a genetic disorder caused by mutations in the FXN gene, located on chromosome 9. This gene encodes for the protein frataxin, which is essential for maintaining mitochondrial function and iron homeostasis in the cell. The disease is characterized by progressive loss of balance and gait instability.

**Why the Correct Answer is Right:**
Frederick's Ataxia is caused by a recessive mutation, meaning that both copies of the FXN gene (one inherited from each parent) must carry the mutated allele for the disease to be expressed. In contrast, dominant mutations only require one mutated copy for the disease to manifest.

**Why Each Wrong Option is Incorrect:**
A. Dominant mutations typically involve a single mutated allele, making option A incorrect in this context.
C. De novo mutations are new mutations that occur spontaneously in a person, unlike Frederick's Ataxia which is inherited. Therefore, option C is incorrect.
D. X-linked mutations are associated with genes located on the X chromosome, whereas the FXN gene is located on chromosome 9, making option D incorrect.

**Why Frederick's Ataxia is Recessive:**
Frederick's Ataxia is inherited in an autosomal recessive pattern, meaning that it can be passed down through generations. Parents who are carriers of the mutated allele typically display no symptoms but may pass on the mutated allele to their offspring. If both parents are carriers, there is a 25% chance with each pregnancy that their child will have the disease, a 50% chance that the child will be a carrier, and a 25% chance that the child will inherit two normal copies of the FXN gene and be unaffected.

**Clinical Pearl:**
Recognizing the pattern of inheritance and understanding the molecular basis of the disease can help clinicians counsel families at risk for carrying the mutated allele and anticipate the likelihood of affected offspring. This knowledge is crucial for anticipating the disease in future generations and implementing appropriate genetic counseling.