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      False homozygous deletions of SMN1 exon 7 using Dra I PCR-RFLP caused by a novel mutation in spinal muscular atrophy.

      Genetic testing and molecular biomarkers
      Base Sequence, Deoxyribonucleases, Type II Site-Specific, metabolism, Exons, genetics, False Positive Reactions, Homozygote, Humans, Infant, Male, Molecular Sequence Data, Muscular Atrophy, Spinal, diagnosis, Nucleic Acid Amplification Techniques, Polymerase Chain Reaction, methods, Polymorphism, Restriction Fragment Length, Sequence Analysis, DNA, Sequence Deletion, Survival of Motor Neuron 1 Protein

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          Abstract

          Spinal muscular atrophy (SMA) is an autosomal recessive neuromuscular disorder, and about 95% of SMA patients are homozygous for deletions in the SMN1 gene. Herein, classical polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) using DraI yielded false homozygous deletions of SMN1 exon 7 in a patient with SMA, but multiple ligation-dependent probe amplification analysis revealed one remaining copy of SMN1 exon 7. Sequencing showed that this false deletion in the PCR-RFLP resulted from a novel mutation of one SMN1 copy that was not deleted (c.863G > T, p.R288M). This novel sequence variant introduced a mismatch that interfered with primer binding. These findings demonstrate that comprehensive analysis using PCR-RFLP, multiple ligation-dependent probe amplification, and sequencing can reliably and correctly diagnose SMA.

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