ABSTRACT
The efficacy of decompression treatment as a non-destructive method to control larvae of the powderpost beetle, Lyctus africanus Lesne, was evaluated in the laboratory using various combinations of two pressure levels, 1.1 kPa and 40 kPa, and three temperature levels, 20, 25, and 40 °C. Larval mortality generally depended on weight reduction while decreases in the oxygen level had relatively little effect. The lower pressure, 1.1 kPa, significantly affected mortality, and no larvae survived after 12 h of this pressure treatment, at 25 °C. The average body weight was reduced with treatment time and temperature, and the reduction rate at 25 °C was higher than that at the lower temperature, 20 °C. Effects on larvae of the higher pressure treatment, 40 kPa, with a CO2 gas purge, were tested to determine the feasibility of decompression treatment in the manufacturing process. Although higher pressure resulted in low mortality, the body weight was dramatically decreased using the CO2 purge. These results present important information on the possibility of using decompression treatment for wood products.
ABSTRACT
Cellular signaling mediated by the EGF receptor (EGFR) plays a key role in controlling proliferation and differentiation of cortical progenitor cells (CPCs). However, regulatory mechanisms of EGFR signaling in CPCs remain largely unknown. Here we demonstrate that necdin, a MAGE (melanoma antigen) family protein, interacts with EGFR in primary CPCs and represses its downstream signaling linked to astrocyte differentiation. EGFR was autophosphorylated and interacted with necdin in EGF-stimulated CPCs. Necdin bound to autophosphorylated EGFR via its tyrosine kinase domain. EGF-induced phosphorylation of ERK was enhanced in necdin-null CPCs, where the interaction between EGFR and the adaptor protein Grb2 was strengthened, suggesting that endogenous necdin suppresses the EGFR/ERK signaling pathway in CPCs. In necdin-null CPCs, astrocyte differentiation induced by the gliogenic cytokine cardiotrophin-1 was significantly accelerated in the presence of EGF, and inhibition of EGFR/ERK signaling abolished the acceleration. Furthermore, necdin strongly suppressed astrocyte differentiation induced by overexpression of EGFR or its ligand binding-defective mutant equivalent to a glioblastoma-associated EGFR variant. These results suggest that necdin acts as an intrinsic suppressor of the EGFR/ERK signaling pathway in EGF-responsive CPCs to restrain astroglial development in a cell-autonomous manner.
Subject(s)
Astrocytes/metabolism , Cerebral Cortex/embryology , ErbB Receptors/metabolism , MAP Kinase Signaling System , Nerve Tissue Proteins/metabolism , Neural Stem Cells/metabolism , Nuclear Proteins/metabolism , Animals , Astrocytes/cytology , Astrocytes/enzymology , Cell Differentiation , Cell Proliferation , Cells, Cultured , Cerebral Cortex/cytology , Cerebral Cortex/enzymology , Cerebral Cortex/metabolism , ErbB Receptors/chemistry , Extracellular Signal-Regulated MAP Kinases/metabolism , Fibroblast Growth Factor 2/pharmacology , GRB2 Adaptor Protein/antagonists & inhibitors , GRB2 Adaptor Protein/metabolism , Mice , Neural Stem Cells/cytology , Neural Stem Cells/drug effects , Neural Stem Cells/enzymology , Protein DomainsABSTRACT
Sulfation represents an essential modification for various molecules and regulates many biological processes. The sulfation of glycans requires a specific transporter for 3'-phosphoadenosine 5'-phosphosulfate (PAPS) on the Golgi apparatus. This study investigated the expression of PAPS transporter genes in colorectal carcinomas and the significance of Golgi-specific sulfation in the proliferation of colorectal carcinoma cells. The relative amount of PAPST1 transcripts was found to be higher than those of PAPST2 in colorectal cancerous tissues. Immunohistochemically, the enhanced expression of PAPST1 was observed in fibroblasts in the vicinity of invasive cancer cells, whereas the expression of PAPST2 was decreased in the epithelial cells. RNA interference of either of the two PAPS transporter genes reduced the extent of sulfation of cellular proteins and cellular proliferation of DLD-1 human colorectal carcinoma cells. Silencing the PAPS transporter genes reduced fibroblast growth factor signaling in DLD-1 cells. These findings indicate that PAPS transporters play a role in the proliferation of colorectal carcinoma cells themselves and take part in a desmoplastic reaction to support cancer growth by controlling their sulfation status.
