Galactosemia is a rare disorder that is caused by a mutation in the GALT gene and affects the body's ability to break down galactose. Below is a gel showing the results of RT-PCR to amplify the full length of the GALT gene transcripts from a person who does not have galactosemia (lane N) and five patients who do have galactosemia (lanes A–E). Products were loaded in the wells at the top of the gel. Assume band intensity is indicative of mRNA levels in each sample, and ignore nonsense-mediated decay for this question. Maya has an ATG to CTG mutation in the translational start codon for the GALT gene. Which lane in the gel could represent Maya’s mRNA? Explain your answer.
Added by Rebecca F.
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RT-PCR measures mRNA levels, not protein function, so Maya’s GALT mRNA level would be expected to be similar to normal if only the start codon is mutated. Show more…
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Select the statements that best explain Makali's GALT activity levels: Makali may produce no GALT enzyme. Makali may have normal amounts of GALT, but the enzyme may be mutated. Makali may produce only small amounts of non-mutated (wild-type) GALT enzyme. Makali may have a mutation in the gene that encodes galactokinase.
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In humans, the disease galactosemia causes mental retardation at an early age. Lactose (milk sugar) is broken down to galactose plus glucose. Normally, galactose is broken down further by the enzyme galactose- phate uridyltransferase (GALT). However, in patients with galactosemia, GALT is inactive, leading to a buildup of high levels of galactose, which, in the brain, causes mental retardation. How would you provide a secondary cure for galactosemia? Would you expect this disease phenotype to be dominant or recessive?
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