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Where would a predicted silent mutation have to be situated to actually result in a loss-of-function mutation (and potentially lead to the onset of disease)?
A. Intron-exon junction/splice site
B. Translational start site
C. Stop codon
D. Anywhere within the exonic sequences
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mode of action of wbcs types
how to determine that the phenotype of a wild type is due to the action of one or two genes?
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