Amplified gene for the epidermal growth factor receptor in a human glioblastoma cell line encodes an enzymatically inactive protein.

The gene encoding the receptor for epidermal growth factor was amplified two- to fivefold in the human glioblastoma cell line SF268. The amplified gene gave rise to abundant quantities of receptor that bound EGF with a high affinity (Kd, 0.35 nM). The binding of ligand failed to elicit cellular DNA synthesis, however, and the receptor was enzymatically inactive. We presume that the amplified receptor gene carries a mutation(s) that affects several aspects of the receptor's function. Characterization of the mutation(s) may illuminate how structure dictates function in the receptor protein.     

Differences in the fatty acid composition of soybean seed produced in northern and southern areas of the U.S.A.

The fatty acid composition of soybean (Glycine max) seeds was sensitive to the influence of both genotype and environment. To quantify their relative environmental sensitivities, four soybean cultivars, Wells, Wayne, Cutler and Union, plus two experimental lines, 9656 and 9686, developed for lower concentrations of linolenate, were grown in Indiana (northern area) and Mississippi (southern area) in 1981. Seeds produced in the two environments were analysed for total oil content and for fatty acid composition. Seeds produced in the southern area were slightly higher (20% vs 16%) in oil content, but weighed significantly less than those produced in the north. The oil content per seed of seeds produced in the south was only 51% of the oil content of seeds produced in the north. Seeds produced in the south were significantly lower in both myristate and linolenate, but significantly higher in oleate than seeds produced in the north. Genotype by environment interactions for many oil quality measurements were largely attributable to the responses of the lines 9656 and 9686. These results indicate that higher environmental temperature reduced the linolenate concentration of soybean oil.     

Identification and sequencing the juvenile spermatogonial depletion critical interval on mouse chromosome 1 reveals the presence of eight candidate genes.

In mice, the recessive, non-pleiotropic, juvenile spermatogonial depletion (jsd) mutation results in a single wave of spermatogenesis, followed by failure of type A spermatogonial stem cells to differentiate, rendering adult males sterile. As part of an effort to identify the gene underlying this mutation, we report here the construction of a high-resolution genetic map involving more than 1000 meioses and 24 polymorphic loci. Our data define a critical jsd interval of approximately 0.4 cM at 49 cM on mouse chromosome 1, between D1Mit215 and 257SP6. We have constructed a physical map spanning the region comprising 24 overlapping BACs. Eighteen of these BACs have been fully sequenced, or are in draft form, allowing us to annotate approximately 2.5 Mb of DNA surrounding the jsd locus. The critical 0.4 cM jsd interval corresponds to a physical distance of approximately 1.5 Mb. Eight genes have been identified in this interval, two of which appear to be possible candidates for the jsd mutation.     

Assessment of type A behavior in children: a comparison of two instruments

The agreement of classifications yielded from two instruments used to assess children's Type A-Type B behavior, the Matthews Youth Test for Health (MYTH) and Hunter-Wolf (HWolf), was evaluated with a sample of rural children from the southern United States. Fifth grade children (N = 276) served as subjects. MYTH and HWolf scores were found to be only weakly correlated and the agreement of Type A-Type B classifications occurred at a rate only slightly above chance. To assess the psychometric properties of the instruments, both were subjected to factor analysis and reliability/internal consistency estimates were obtained and compared with previous results. A factor structure remarkably similar to that of previous reports was found for the MYTH but not the HWolf. The results closely parallel those of another recent report and provide further support for the recommendation that these instruments should not be considered interchangeable measures of Type A behavior and that when multiple measures cannot be employed for research, the investigator should use the MYTH. Caution is indicated in interpreting scores of either measure, however, since neither has yet been shown to relate to later development of coronary heart disease.