The genetics of phenotypic plasticity. IV. Chromosomal localization

The contributions of each chromosome to the traits thorax size and plasticity of thorax size as affected by temperature in Drosophila melanogaster were measured. A composite stock was created from lines previously subjected to selection on thorax size or plasticity of thorax size. A chromosome extraction was performed against a uniform background lacking genetic variation, provided by a stock of marked balancer flies. With regard to amount of plasticity, chromosome I and the balancer stock showed no plasticity, the composite stock showed the greatest plasticity, and chromosomes II and III were intermediate. Chromosome I showed significant genetic variation for thorax size at both 19° C and 25° C, but not for plasticity, while chromosome II showed significant genetic variation for plasticity, but not for thorax size. Chromosome III showed significant genetic variation for both thorax size and plasticity. We tested the predictions of three models of the genetic basis of phenotypic plasticity: overdominance, pleiotropy, and epistasis. The results support the epistasis model, in agreement with earlier work. The amount of developmental noise was correlated with phenotypic plasticity at 25° C, in agreement with earlier work. A negative correlation was found at 19° C for chromosome II, contrary to earlier work.     

Delineation of type-specific regions on the envelope glycoproteins of human T cell leukemia viruses.

Two different approaches were used to map the type-specific regions on human T cell leukemia virus (HTLV) envelope glycoproteins. 1) Antibody reactivities of polymerase chain reaction-confirmed HTLV-I or HTLV-II carriers' sera were analyzed by Western blot assay with seven recombinant proteins containing different regions of HTLV-I or HTLV-II envelope proteins. 2) Rabbit antibodies elicited by nine HTLV-I Env synthetic peptides were used to react with the native HTLV envelope glycoproteins in an antibody-dependent cellular cytotoxicity (ADCC) assay. The results of the Western blot analysis showed that RP-B2, which contains amino acid residues 166 to 213 from HTLV-II exterior glycoprotein, was specifically reactive with 90.6% (48 of 53) of the HTLV-II carriers' sera but not with any of the HTLV-I carriers' serum (0 of 71). In contrast, RP-B, which contains amino acid residues 166 to 229 from HTLV-I exterior glycoprotein, was reactive with 85.1% (114 of 134) of the HTLV-I carriers' sera but not with any HTLV-II carrier serum (0 of 62). Furthermore, anti-HTLV-I Env synthetic peptide antibody-mediated ADCC identified several distinguishing HTLV-I ADCC epitopes in the middle region (amino acid residues 177 to 257) of the HTLV-I exterior glycoprotein. Therefore, HTLV type-specific epitopes reside mainly in a 69-amino acid sequence bounded by two cysteine residues (amino acids 157 and 225 for HTLV-I and 153 and 221 for HTLV-II), in the middle region of the exterior envelope glycoproteins.     

Ultrastructural specialization of intestinal epithelium over Peyer's patches in the bonnet monkey, Macaca radiata.

The follicle associated epithelium (FAE) which separates the lymphoid follicle of Peyer's patch from the gut lumen is known to have specialized cells called M cells or "microfold" cells in man and certain animals. These cells are considered to be involved in antigen uptake and transport. Our light microscopic study of the small intestine of bonnet monkeys suggested the presence of such specialised cells in FAE. We have confirmed the presence of M cells in bonnet monkey FAE having ultrastructural features very similar to those of human M cells.     

A universal primer mixture for sequence determination at the 3′ ends of cDNAs

We have devised a universal primer which can be used to sequence the 3′-ends of cloned cDNAs containing a polyA tail. The primer consists of an equimolar mixture of three primers: 20 T nucleotides followed by either an A, C, or G nucleotide (5′→3′). With this primer mixture and the dideoxynucleotide chain termination method, we determined the 3′-terminal sequence of human β-actin cDNA in an Okayama-Berg vector, in four parallel sets of reactions containing either a single primer (T₂₀G, T₂₀C, or T₂₀A) or an equimolar mixture of all three primers. Priming with both T₂₀A and the triple mixture gave clearly readable results that agree with the known sequence of the human β-actin gene, and we have applied this method successfully to several other cDNAs in the Okayama-Berg expression vector. Use of this universal primer mixture facilitates determination of sequences at the 3′-ends of cDNAs while by-passing the polyA tail region.     

Late replication patterns in adult and embryonic mice carrying Searle's X-autosome translocation

Bromodeoxyuridine-dye technique analysis of X chromosome DNA synthesis in female adult and fetal mice carrying the balanced form of the T(X; 16) 16H translocation demonstrated that the structurally normal X chromosome was late replicating (and hence presumably inactive) in 93% of the adult cells and 99% of the 9-day embryo cells, with the X¹⁶ chromosome late replicating in the remaining cells. We conclude from these results that in T16H/+ females either there is preferential inactivation of the normal X chromosome or that, if inactivation is random, cell selection takes place before 9 days of development. Two 9-day female embryos with an unbalanced karyotype were also studied; both had two late-replicating chromosomes in most of their cells, one being the chromosome 16^X, the other a normal X chromosome. These results, together with the presence of a late-replicating X¹⁶ chromosome in T16H/+ adult and fetal mice, support the concept that more than one inactivation center is present on the X chromosome of the mouse because the X¹⁶ and the 16^x chromosomes can be late replicating.     

The myocardium and its vasculature: a histochemical comparison of the normal and chronically sympathectomized dog heart

Summary Using histochemical techniques, the reactivities of selected enzymes and other metabolic components were examined in the myocardium, coronary arteries, and coronary arterioles of normal, two-week-sympathectomized, and sham-operated canine hearts. There were no differences in the histochemistry of coronary arteries in any of the hearts, but important differences were noted in the myocardium and especially in the arterioles. The reactivities of the enzyme glucose-6-phosphate dehydrogenase and the nucleic acids were increased in arterioles of the sympathectomized heart, possibly indicating an increased protein synthesis. The reactivities of succinate dehydrogenase, NAD-isocitrate dehydrogenase, and cytochrome oxidase were reduced in myocardium and arterioles of sympathectomized hearts as well as in arterioles of sham-operated hearts; the changes were greater in the sympathectomized arterioles where there was also observed an increase in reactivity of lactate dehydrogenase. These findings suggest a depression in aerobic metabolic capacity and, in the case of the sympathectomized arteriole, imply a possible shift in adaptation from aerobic to anaerobic metabolism.