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Two-dimensional protein patterns from whole mouse embryos with different trisomies (Ts) (Ts1, -12, -14, -19) and from different organs (normal or malformed) and developmental stages of Ts12 embryos were analyzed by comparison with control patterns. Quantitatively altered proteins were found, and a portion of these (21/approximately equal to 1,000, average) was attributable to the Ts conditions. Most of these variants were found always (regularly) in Ts embryos. They could be divided into two groups: group I shows characteristics (chromosome specific, density increased by a factor close to 1.5 +/- 0.12) compatible with proteins directly affected by the Ts; and group II (chromosome nonspecific, density decreased, seldom increased) results most likely from indirect effects. The incidence of group II variants (about 13/approximately equal to 1,000, average) was considerably greater than that of the group I variants (about 3/approximately equal to 1,000). The frequency of both types of variants, however, was far lower than was expected by a rough estimation. Apparently, a relatively small number of changes, rather than a complex, escalating effect, was induced at the protein level by the Ts. Some observations suggest that this is due to a stable regulation of protein concentrations. The proportion in which quantitative changes of different types occurred in the protein patterns did not correlate with the degree of developmental impairments (malformation, retardation, early death) of the embryos. The generalized occurrence of protein changes on the cellular level might explain the restricted viability of Ts mouse embryos.

Analysis of two-dimensional protein patterns from mouse embryos with different trisomies.