Isografts of heterotypic recombinants of embryonic mammary epithelium with salivary mesenchyme undergo development morphogenetically resembling that of salivary gland. However, cytodifferentiation of the epithelium is like that of mammary gland. In lactating hosts these isografts respond to endogenous hormonal stimulation and synthesize a milk protein, alpha-lactalbumin.

No abstract

1983. A chromosomal inversion polymorphism in Scandinavian populations of the seaweed fly, Coelopa frigida. -Hereditas 99: 135-145. Lund, Sweden. ISSN 0018-0661. Received November 29, 1982 British populations of the seaweed fly Coelopa frigida are polymorphic for the large a@ inversion on chromosome I (BUTLIN et al., Heredity48: 45-55). Flies from Norway, Swedenand Denmark are shown to possess the same inversion polymorphism, and to exhibit similar though not identical polymorphisms at two enzyme-determining loci associated with this inversion. There is a cline in inversion frequencies from the North Sea, through the Skagerrak and Kattegat, into the Raltic Sea. This cline correlates with salinities, the algal composition of seaweed beds in which Coelopa breeds: and with the presence of the sibling species C. pilipes.It is suggested that heterokaryotypic advantage is the major selective force maintaining this polymorphism, and that genotype-related differences in generation times, and the longevity of seaweed beds, may constitute lesser forces acting on the inversion frequencies.

By testing recombinants between "high tumor" (inducing a high incidence of tumors) and "low tumor" (inducing a low incidence of tumors) strains of polyomavirus, we have previously shown that the key determinant(s) for induction of a high tumor profile resides in coding regions of the high tumor strain (R.

We determined the DNA sequences of the noncoding regions of two polyomavirus strains that differ profoundly in their abilities to induce tumors in mice. Differences between strains were found, both on the late side of the replication origin in the region containing known enhancer elements and on the early side of the origin, affecting the number and location of large-T-antigen-binding sites. By constructing and analyzing recombinant viruses between these highand low-tumor strains, we attempted to localize determinants which affect the frequency and histotype of tumors. Seven recombinants were constructed and propagated in vitro, and the tumor profile of each was established by inoculation into newborn C3H mice. Recombinants containing noncoding sequences from the high-tumor strain and coding sequences from the low-tumor strain behaved like the latter, inducing tumors at a low frequency and strictly of mesenchymal origin. Reciprocal recombinants with noncoding sequences of the low-tumor strain linked to structural determinants from the high-tumor strain induced several types of epithelial tumors typical of the high-tumor strain but at reduced frequency, in addition to mesenchymal tumors. A high frequency and full diversity of epithelial tumors required, in addition to structural regions from the high-tumor strain, noncoding sequences on the early side of the origin also present in this strain. A high-tumor profile thus resulted from the combined effects of structural and regulatory determinants in the high-tumor strain, with the former affecting primarily the tissue tropism and the latter affecting the frequency of tumors. No differential effects of the enhancer regions from the late side of the origin in the two virus strains were seen in this study.