4 research outputs found

    Low nonpaternity rate in an old Afrikaner family

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    Extrapair paternity is a crucial parameter for evolutionary explanations of reproductive behavior. Early studies and human testis size suggest that human males secure/suffer frequent extrapair paternity. If these high rates are indeed true, it brings into question studies that use genealogies to infer human life history and the history of diseases since the recorded genealogies do not reflect paths of genetic inheritance. We measure the rate of nonpaternity in an old Afrikaner family in South Africa by comparing Y-chromosome short tandem repeats to the genealogy of males. In this population, the nonpaternity rate was 0.73%. This low rate is observed in other studies that matched genealogies to genetic markers and more recent studies that also find estimates below 1%. It may be that imposed religious morals have led to reduced extrapair activities in some historic populations. We also found that the mutation rate is high for this family, but is unrelated to age at conception.http://www.ehbonline.orghb2016Genetic

    Nucleotide sequence analysis to identify a one-step mutation in a STR DNA profile during paternity testing at locus D7S820

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    During routine paternity testing with AmpFℓSTR Identifiler Plus Kit, the kit failed to amplify the child’s allele at locus D7S820 leading to parent-child inconsistency with a single-step mutation. The aim was to identify possible causes of this mismatch. New singleplex primers were designed and the samples were amplified, cloned and sequenced using pJET1.2/blunt cloning vector forward and reverse sequencing primers. The amplicons were ascertained using CLC Bio Main Workbench. We confirmed the presence of allele dropout at the child’s locus. We describe a single nucleotide polymorphism (SNP), from cytosine (C) to thymine (T) in the kit primer binding site region of the alleged father’s profile. The child’s profile changed from homozygous to heterozygous showing that the commercial kit failed to amplify the allele and this was concluded to be most likely due to polymerase slippage
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