Kinetics of amino acid incorporation into serum proteins

1. The effect of varying body temperature on the rate of amino acid incorporation into serum protein does not give support to the idea that the rate of this process is adjusted in vivo to restore those protein molecules destroyed by thermal denaturation. The experimentally observed Q₁₀ was about 3.9. 2. When amino acids are injected into the blood of animals in a steady state of serum protein turnover, a period of time elapses before these amino acids can be found in the serum proteins. This has been called transit time. At a given temperature (31°) it is the same in rabbits, turtles, and Limulus (1 hour). In rabbits and turtles it has a Q₁₀ of 3.2. It appears to be specifically related to the process of synthesis (or release) of serum proteins. 3. It was not possible to affect the transit time or the incorporation rate by the administration of amino acid analogues.     

Exposure to the neonicotinoid imidacloprid disrupts sex allocation cue use during superparasitism in the parasitoid wasp Nasonia vitripennis

1. Neonicotinoid insecticides are potent neurotoxins of significant economic importance. However, it is clear that their use can adversely impact beneficial insects in the environment, even at low, sub‐lethal doses. 2. It has recently been shown that the neonicotinoid imidacloprid disrupts adaptive sex allocation in the parasitoid wasp Nasonia vitripennis (Walker) by limiting their ability to respond to the presence of other females on oviposition patches. In the present study, that work was extended to explore whether sex allocation when superparasitising – laying eggs on a host that has already been parasitised – is also disrupted by imidacloprid. 3. Under superparasitism, sex allocation theory predicts that females should vary their offspring sex ratio in relation to their relative clutch size. It was found that sex allocation under superparasitism in Nasonia is disrupted in a dose‐dependent manner, with exposed females producing more daughters. 4. Importantly, imidacloprid does not appear to influence the ability of females to estimate the number of eggs already present on a host, suggesting a disassociation between the sex ratio and clutch size cues. 5. The present work highlights the fitness costs to beneficial insects of exposure to neonicotinoids, but also provides clues as to how female Nasonia use information when allocating sex.     

Initiation of Mammalian Viral Protein Synthesis

CULTURED human cells (KB) infected with human adenovirus type 2 (Ad 2) provide a model system for protein synthesis in mammalian cells. Adenovirus messenger RNA molecules are transcribed from nuclear viral DNA and transported to the cytoplasm for translation¹. Late after infection (18 h) 9–10 viral mRNA species with sedimentation values of 7S to 32S are present in polysomes (Parsons, Gardner and Green, in preparation) and specify eight viral structural proteins which account for 80–90% of the polypeptides synthesized in vivo^2–4. We now describe an in vitro cell-free system, derived from KB cells infected with Ad 2, which synthesizes 8–9 viral polypeptides and can initiate protein synthesis with a special class of yeast methionyl-tRNA. In vivo and in vitro experiments suggest that methionine is the initiator amino-acid for most, if not all, adenovirus structural proteins.     

Mutant Ribosomal Protein with Defective RNA Binding Site

THE 30S ribosomal subunits of Escherichia coli contain twenty-one different proteins^1–4, which together with 16S RNA can reassemble in vitro to form functional 30S particles⁵. Five proteins can individually bind to specific sites on the 16S RNA^6–8 and these are S4, S7, S8, S15 and S20 (in the nomenclature recently adopted by several laboratories to report results with the E. coli system⁹). We report here the first identification of a mutation that affects a ribosomal protein-nucleic acid interaction.     

Surface Alterations of Cells Carrying RNA Tumour Virus Genetic Information

CELLS transformed by the DNA tumour viruses, polyoma virus and SV40, are agglutinated by lectins such as wheat germ agglutinin¹, concanavalin A (Con A)² and soybean agglutinin³. Agglutination in these cases presumably reflects changes in the cell surface related to the transformed properties of the cell; studies with a temperature-dependent mutant of polyoma virus has shown that cell surface changes are controlled by viral genes⁴. Here we describe experiments in which we investigated the agglutinability of cells transformed by RNA tumour viruses. One recent report had suggested that cells transformed by RNA tumour viruses were not specifically agglutinated⁵, whereas a second more recent report claimed the specific agglutination of cells transformed by RSV⁶. We find that transformed rat, mouse and cat cells that replicate the sarcoma-leukaemia virus complex of murine (MSV) and feline (FeSV) origin are strongly agglutinated by Con A, but mouse and human cells that replicate the murine and feline leukaemia virus components alone are not agglutinated. The ability to agglutinate is rapidly acquired by normal mouse cells on infection with the murine sarcoma virus at a rate that parallels virus replication. In contrast to the results obtained with cells producing virus, non-virus-producing transformed hamster and mouse cells that synthesize virus-specific RNA are either not agglutinated or are agglutinated to a lesser degree. These results suggest that the cell surface alterations responsible for agglutination are not necessarily associated with the transformed state of the cell, but rather with the possession of sarcoma virus-specific information.     

Inheritance of Pattern: Analysis from Phenotype to Gene

The form and pattern of multicellular organisms are developmentalphenotypes. They are long term processes rather than staticstructures. They involve myriad events at multiple locations.The efficient encoding of such phenotypes is analyzed here intwo stages. First, the complex developmental behavior is brokendown so it can be accounted for by cell or tissue rules. Themost effective rules have the instantaneous character foundin time-based differential equations. When integrated over timeand space, the rules produce the behavior. Second, the cytologicaland nuclear basis of the rules is sought. One thus studies acomplex phenotype in terms of its successive antecedent causes,refining understanding as one gets closer to the genome. The approach is applied here to phyllotactic (leaf placement)patterns. Leaves may be alternating in a plane, whorled, orin a helical arrangement. In all three cases a new leaf formsas an arc-like bulge at a site apical to a small number of neighboringleaves. The leaf-forming sites are irregularities in the patternof cellulose reinforcement in the surface of the apical dome.Two organ-level rules combine to produce new leaf sites. First,each established leaf develops a single reinforcement field,with gently curved reinforcement lines, on the region of thedome just above the leaf. Second, where parts of two or threesuch fields abut on the dome they combine to make the irregularityfor the next leaf. Hence a given reinforcement pattern on thedome produces a leaf; the action of the leaves in turn reestablishesthe reinforcement pattern. The cellular basis of generatinga reinforcement field appears to be a cytoskeletal responseto excessive stretch, brought on by rapid growth of adjacentleaf bases. The large scale patterns are thus traceable to cytoskeletalphenomena and from there to genes involving microtubular behavior.