Differential expression of transforming growth factor-beta 1 (TGF-beta 1) receptors in murine myeloid cell lines transformed with oncogenes. Correlation with differential growth inhibition by TGF-beta 1.

Transforming growth factor-beta 1 (TGF-beta 1) is a pleiotropic polypeptide hormone known to play an important role as a modulator of hematopoietic processes in human and murine cells. One of the characteristics of TGF-beta 1 is the ability to inhibit the growth of several cell types, including cells of the myeloid lineage. To study the mechanism by which TGF-beta 1 inhibits the growth of myeloid cells, we have used three murine myeloid cell lines, the parental interleukin-3-dependent 32D-123 cell line and two retrovirally infected interleukin-3-independent cell lines (32D-abl, 32D-src), all of which are growth inhibited by TGF-beta 1. Each of these oncogene-transfected cells expresses a greater number of TGF-beta 1 receptors than the parental cell line and responds to TGF-beta 1 with increased sensitivity; 32D and 32D-src cells are 2- and 58-fold more sensitive to TGF-beta 1 inhibition than the parental cell line (ED50 = 35 pM). Both 32D-abl- and 32D-src-transformed cell lines expressed higher levels of the 65- and 85-kDa TGF-beta 1 receptor species than did the parental cells. We observed a correlation between the greater sensitivity of 32D-src cells to TGF-beta 1 and the more rapid down-modulation and reappearance of cell surface TGF-beta 1 receptors on 32D-src cells. Thus, the level of TGF-beta 1 receptor expression and rate of reexpression both have a crucial regulatory effect on the functional activity of the TGF-beta 1 ligand.     

Insulin acutely regulates Munc18-c subcellular trafficking: altered response in insulin-resistant 3T3-L1 adipocytes.

Preincubation of 3T3-L1 adipocytes in high glucose or glucosamine decreases acute insulin (100 nm)-stimulated glucose transport provided that insulin (0.6 nm) is included during preincubation. GLUT4 expression is unchanged (Nelson, B. A., Robinson, K. A., and Buse, M. G. (2000) Diabetes 49, 981-991). Munc18-c, a Syntaxin 4-binding protein, is a proposed regulator of the docking/fusion of GLUT4-containing vesicles with the plasma membrane. We examined the subcellular distribution of Munc18-c in response to acute (15-min) insulin (100 nm) stimulation after preincubation in 5 or 25 mm glucose +/- 0.6 nm insulin. Immunoblotting detected Munc18-c mainly in the Triton X-100-soluble plasma membrane (TS-PM) and the Triton X-100-insoluble low density microsomal (TI-LDM) fraction. Under each condition except high glucose + insulin preincubation, acute insulin increased Munc18-c (50-200%) in TS-PM and decreased Munc18-c (60%) in TI-LDM. Munc18-c traffic was time-dependent with a lag time of 3 min compared with GLUT4. Preincubation with high glucose + 0.6 nm insulin significantly impaired acute insulin-stimulated Munc18-c trafficking and decreased basal Munc18-c in the TI-LDM. Preincubation with glucosamine + insulin had similar effects. Total cellular Munc18-c remained unchanged. In conclusion, acute insulin stimulation promotes the translocation of Munc18-c, apparently from a TI-LDM-associated compartment to the TS-PM. Chronically increased glucose flux or exposure to glucosamine disrupts this process, which may negatively impact the fusion of GLUT4-containing vesicles with the plasma membrane.     

Analysis of a <Emphasis Type="Italic">c</Emphasis><Subscript>0</Subscript><Emphasis Type="Italic">t-1</Emphasis> library enables the targeted identification of minisatellite and satellite families in <Emphasis Type="Italic">Beta vulgaris</Emphasis>

Background  

Repetitive DNA is a major fraction of eukaryotic genomes and occurs particularly often in plants. Currently, the sequencing of the sugar beet (Beta vulgaris) genome is under way and knowledge of repetitive DNA sequences is critical for the genome annotation. We generated a c ₀ t-1 library, representing highly to moderately repetitive sequences, for the characterization of the major B. vulgaris repeat families. While highly abundant satellites are well-described, minisatellites are only poorly investigated in plants. Therefore, we focused on the identification and characterization of these tandemly repeated sequences.     

Can Text Messages Increase Empathy and Prosocial Behavior? The Development and Initial Validation of Text to Connect

To what extent can simple mental exercises cause shifts in empathic habits? Can we use mobile technology to make people more empathic? It may depend on how empathy is measured. Scholars have identified a number of different facets and correlates of empathy. This study is among the first to take a comprehensive, multidimensional approach to empathy to determine how empathy training could affect these different facets and correlates. In doing so, we can learn more about empathy and its multifaceted nature. Participants (N = 90) were randomly assigned to receive either an empathy-building text message program (Text to Connect) or one of two control conditions (active versus passive). Respondents completed measures of dispositional empathy (i.e. self-perceptions of being an empathic person), affective empathy (i.e. motivations to help, immediate feelings of empathic concern), and prosocial behavior (i.e. self-reports and observer-reports) at baseline, and then again after the 14 day intervention period. We found that empathy-building messages increased affective indicators of empathy and prosocial behaviors, but actually decreased self-perceptions of empathy, relative to control messages. Although the brief text messaging intervention did not consistently impact empathy-related personality traits, it holds promise for the use of mobile technology for changing empathic motivations and behaviors.     

The isolation and genetic characterization of X-linked mutations that affect pyrimidine metabolism in Drosophila melanogaster

Summary This paper focuses on the number of X-linked genes which play a role in pyrimidine metabolism. A series of mutation screens have been carried out for the following types of mutants: (a) mutants which reduce pyrimidine synthesis, (b) mutants which reduce pyrimidine catabolism, and (c) mutants which are unable to utilize dietary pyrimidines and depend upon de novo synthesis for survival. The genetic characterization of the 95 X-linked mutants obtained indicates that there are very few X-linked genes which play a direct role in pyrimidine metabolism.