Cell envelope phospholipid changes in a moderate halophile during phenotypic adaptation to altered salinity and osmotic stress

Abstract The increased content of negatively-charged phospholipids in membranes of Vibrio costicola grown at high salinities is mediated by increased phospholipid synthesis of phosphatidylglycerol relative to phosphatidylethanolamine. This phenomenon provides a system for investigating the factors involved in triggering and controlling haloadaptation in this moderately halophilic bacterium. We review recent experiments, which show that when subjected to sudden increases in external salinity, V. costicola senses both the absolute NaCl concentration and the magnitude of the salt shift. We show that the latter is sensed at least in part via osmotic pressure effects, since shift-up into sucrose-containing media triggers comparable changes in growth and in phospholipid composition and synthesis.     

Effects of secretin and gastric inhibitory polypeptide on human pancreatic growth hormone-releasing factor(1-40)-stimulated growth hormone levels in the rat

Synthetic human pancreatic growth hormone-releasing factor containing 40 amino acids ([hpGRF (1-40)]-OH) significantly stimulated plasma growth hormone (GH) levels in both sodium pentobarbital and urethane anesthetized rats. Synthetic secretin, gastric inhibitory polypeptide (GIP), and glucagon significantly decreased plasma GH levels while synthetic vasoactive intestinal peptide (VIP) had no effect. Secretin and GIP also altered the in vivo plasma GH response to [hpGRF(1-40)]-OH. Whether this effect is the result of an interaction at the pituitary level or is due to an extra-pituitary effect of secretin and GIP awaits further study.     

Skeletal growth in a medieval population from Sudanese Nubia

Long bone growth is analyzed for 180 children from a Medieval population at Kulubnarti in Sudanese Nubia (550–1450 A.D.). A regional interpopulation comparison is made with growth data from Wadi Halfa in Lower Nubia, and an intrapopulation analysis is undertaken to assess diachronic changes in growth at Kulubnarti. Changes in growth patterns are interpreted in the context of mortality and morbidity profiles and relationships between the three variables are discussed. It is suggested that changes in the sociopolitical environment may have been responsible in part for altering levels of biological stress and impacting growth.     

Identification of tyrosine-phosphorylated colony-stimulating factor 1 (CSF-1) receptor and a 56-kilodalton protein phosphorylated in intact human cells in response to CSF-1

Colony-stimulating factor 1 (CSF-1) selectively supports the survival, proliferation, and maturation of hemopoietic cells of the monocyte/macrophage lineage. Although the cellular receptor for CSF-1, (the c-fms protein) is a protein-tyrosine kinase activated by the binding of CFS-1, the role of phosphorylation of cellular proteins in CSF-1 signal transduction is poorly understood. Therefore, we examined the CSF-1-stimulated phosphorylation of cellular proteins in human BeWo choriocarcinoma cell line (known to express the c-fms protein). BeWo cells were metabolically labeled with 32Pi, stimulated with recombinant human CSF-1, and extracted with detergent. Phosphotyrosyl proteins were isolated from detergent extracts by affinity chromatography on a highly specific antibody to phosphotyrosine. Rapid phosphorylation of 170-kd protein, followed closely by the phosphorylation of a 56-kd protein, was observed in response to CSF-1. The 170-kd phosphotyrosyl protein bound to wheat germ agglutinin and was secondarily immunoprecipitated with a specific anti-fms serum, consistent with its identity as the CSF-1 receptor. Although purified human macrophages that proliferate in culture in response to CSF-1 are not generally accessible, CSF-1 did stimulate the phosphorylation of a 56-kd protein in intact mononuclear leukocytes from human peripheral blood. Thus, the BeWo cell line may represent a good model for the study of CSF-1-stimulated cellular protein phosphorylation.     

Seasonal changes in growth and standard metabolic rate of juvenile perch, Perca fluviatilis L.

The maximum growth rate of juvenile perch, PercaJuviatilis L., at different constant temperatures and in naturally changing day-lengths was studied in the laboratory. Standard metabolic rate was studied in starvation experiments at constant temperatures under short- and long-day conditions. Growth occurred in temperatures above 8 to 10°C. In winter, from mid-October until mid-April, maximal growth was considerably reduced and was relatively slow but constant. The standard metabolic rate was reduced c . 50% under short-day conditions. The seasonal change in metabolic rates, presumably controlled by an endogenous rhythm, was considered to be an adaptation to low food availability during the short winter days.     

Otolith microstructure indicating growth and mortality among plaice, Pleuronectes platessa L., post-larval sub-cohorts

Growth and mortality of post-metamorphosed plaice were studied by means of daily increments in the sagittal otoliths. The Gompertz model was the best fit to length-at-age data and there were no significant differences between length-at-age and back-calculated lengths. The microstructure pattern of the otoliths at metamorphosis was also used to estimate hatching and settlement distributions. Differential growth and mortality occurred among sub-cohorts; growth rates and mortality were higher in fish that settled earlier. In 1986, the best survival was for a sub-cohort settling in late May to early June. In contrast, in the warmer season of 1987, survival was highest for the second and third sub-cohorts settling in late April and mid May.     

Plant hormone response mutants

A variety of plant hormone response mutants has now been described, and is surveyed in this article. In addition to hormone-insensitive mutant phenotypes with defects in hormone-related features, there exist mutants apparently constitutive for the gibberellin responses, and also a mutant hyper-responsive to gibberellin. Although there is still little biochemical evidence on the nature of these mutants, the emerging picture of their genetic dominance relationships has given rise to tentative suggestions of the involvement of represser functions in hormonal control systems.     

Density-induced down regulation of epidermal growth factor receptors

Summary Previous studies have shown that cell density can regulate the binding of several growth factors. To determine whether cell density exerts a uniform effect on the expression of epidermal growth factor (EGF) receptors, seven cell lines were examined in detail. For each cell line, EGF binding was found to decrease as cell density increases. Scatchard analysis of the binding data reveals that decreases in EGF binding are due to reductions in the number of cell surface EGF receptors. The only apparent exception is the effect of cell density on the binding of EGF to A-431 cells. For these cells, increases in cell density lead to two effects: decreases in the number of high affinity EGF receptors and increases in the total number of EGF receptors. In addition to the effects of cell density on EGF receptors, it was determined that increases in cell density can coordinately down-regulate receptors for as many as four different growth factors. Overall, the findings described in this report for EGF and those previously described for transforming growth factor type-β (TGF-β) and fibroblast growth factor (FGF) demonstrate the existence of a common mechanism for down-regulating growth factor receptors. This work was supported by grants from the Nebraska Department of Health (89-51), the National Cancer Institute (Laboratory Research Center Support Grant, CA36727), and the American Cancer Society (Core Grant ACS SIG-16). EDITOR'S STATEMENT The paper by Rizzino et al. demonstrates that receptor number decreases as a function of cell density. This may represent a mechanism by which cell proliferation is reduced as cell density increases.