01974nas a2200313   4500000000100000008004100001260000900042653001300051653002300064653003500087653001100122653002100133653002000154653002000174653002200194653001700216653001100233653001200244653000900256653001900265100001500284700001800299700001600317245003700333300001100370490000600381520125900387022001401646       1984                            d  c198410aBiometry10aChromosome Mapping10aChromosomes, Human, 6-12 and X10aFemale10aGenes, Recessive10aGenetic Linkage10aGenetic Markers10aGenetics, Medical10aHLA Antigens10aHumans10aleprosy10aMale10aNuclear Family1 aBadner J A1 aChakravarti A1 aWagener D K00aA test of nonrandom segregation.  a329-400 v13 a<p>Within a family, associations between a disease and a marker locus are often inferred when affected offspring share marker alleles more often than is expected by chance. Generally, this is due to nonrandom parental transmission of marker alleles and specifically could be due to linkage, epistatic gene action, or segregation distortion at the marker locus. In this paper, we discuss the statistical properties of a general test of nonrandom segregation of a marker gene. The exact probability distribution of the test under the null hypothesis of random segregation is derived, as is the distribution under the alternative hypothesis of genetic linkage. We compute the mean and variance of these distributions as a means of judging the adequacy of random segregation to explain disease-marker data but also provide a method for computing the exact significance value under the null hypothesis. These methods have been utilized for studying HLA segregation in families with tuberculoid leprosy. On the assumption that this type of leprosy is autosomal recessive, we find evidence that a gene controlling susceptibility to infection by Mycobacterium leprae resides on human chromosome 6, approximately 13 map units away from the HLA locus in males.</p>  a0741-0395