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By MD Frank H. Netter

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Genetic Principles As already described, most cases of type I osteogenesis imperfecta are caused by partial or complete loss-of-function mutations in COL1A1. However, in approximately one-third of affected individuals, the disease is caused by a new mutation; in addition, there are many ways in which DNA sequence alterations can reduce gene expression. Consequently, there is a wide range of mutant alleles (ie, allelic heterogeneity), which represents a challenge for the development of molecular diagnostic tests.

Contiguous gene syndromes, described in Table 2–6, are generally rare, but they have played important roles in understanding the pathophysiology of aneuploid conditions. TABLE 26 Phenotype and karyotype of some contiguous gene syndromes. 3 absence of cortical gyri (lissencephaly) and corpus callosum Carriers for robertsonian translocations that involve chromosome 21 can produce several different types of unbalanced gametes (Figure 2–15). However, the empiric risk for such a carrier bearing an infant with Down syndrome is higher than for other aneuploid conditions, in part because embryos with other types of aneuploidies are likely to result in miscarriages early in development.

Gametic imprinting affects a handful of genes involved in fetal or placental growth, including insulin-like growth factor 2 (IGF2) and the type 2 IGF receptor (IGF2R); for example, the IGF2 gene is expressed only on the paternally derived chromosome, whereas in some individuals the IGF2R gene is expressed only on the maternally derived chromosome. The mechanisms responsible for gametic imprinting depend on biochemical modifications to the chromosome that occur during gametogenesis; these modifications do not affect the actual DNA sequence but are stably transmitted for a certain number of cell divisions (ie, they are epigenetic and contribute to the pathogenesis of certain types of cancer).

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