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We study two models describing infinite random mating age-structured populations. Under model I, the number of matings at any time is proportional to the number of mature females at that time, and the fecundity of a mating is assumed to be a product of factors that depend upon the ages of the mates, but not upon sex. Under model II, individuals can mate only with others of the same age group, and the number of matings of individuals of an age group is, at any time, proportional to the number of females of that age group. If model II holds, or the special case of model I in which the fecundity of all matings is the same, it is possible to show that, in the long run, allele frequencies converge and the gametic disequilibrium approaches zero at a geometric rate. A heuristic argument and a numerical example suggest that these things are also more generally true for model I. A good approximation to the time that it takes to reduce the gametic disequilibrium by a fraction equal to the recombination rate turns out to be the measure of the generation interval in Leslie's theory of population growth.  相似文献   
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Imprinted genes are epigenetically modified in a parent‐of‐origin dependent manner and as a consequence are differentially expressed, with one allele typically expressed while the other is repressed. In canine, the insulin like growth factor 2 receptor gene (IGF2R) is imprinted with predominant expression of the maternally inherited allele. Because imprinted genes usually occur in clusters, we examined the allelic expression pattern of the gene encoding the canine Mas receptor (MAS1), which is located upstream of IGF2R on canine chromosome 1 and is highly conserved in mammals. In this report we describe monoallelic expression of canine MAS1 in the neonatal umbilical cord of several individuals and we identify the expressed allele as maternally inherited. These data suggest that canine MAS1 is an imprinted gene.  相似文献   
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We describe the histopathological, immunohistochemical, and molecular characterization of a lymphoma arising in a 7-year-old cat following experimental infection with feline immunodeficiency virus (FIV). The tumor was high grade and of B-cell lineage. The transformed cell had an immature phenotype (CD79a+, CD79b, CD21, immunoglobulin heavy and light chain negative), confirmed by antigen receptor gene analysis, which showed germ line configuration. Single-copy, clonally integrated FIV provirus was detected in tumor genomic DNA. FIV p24 antigen was not detected in tumor cells by immunostaining. This study provides the first evidence that the feline lentivirus may play a direct role in cell transformation under certain circumstances.  相似文献   
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