a glutathione peroxidase, intracellular peptidases and the tor complexes regulate peptide transporter pept-1 in c. elegans谷胱甘肽过氧化物酶,胞内肽酶,tor复合物调节肽转运pept-1秀丽隐杆线虫.pdfVIP

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a glutathione peroxidase, intracellular peptidases and the tor complexes regulate peptide transporter pept-1 in c. elegans谷胱甘肽过氧化物酶,胞内肽酶,tor复合物调节肽转运pept-1秀丽隐杆线虫.pdf

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a glutathione peroxidase, intracellular peptidases and the tor complexes regulate peptide transporter pept-1 in c. elegans谷胱甘肽过氧化物酶,胞内肽酶,tor复合物调节肽转运pept-1秀丽隐杆线虫

A Glutathione Peroxidase, Intracellular Peptidases and the TOR Complexes Regulate Peptide Transporter PEPT-1 in C. elegans Jacqueline Benner, Hannelore Daniel, Britta Spanier* ¨ ¨ ZIEL Research Center of Nutrition and Food Sciences, Abteilung Biochemie, Technische Universitat Munchen, Freising, Germany Abstract + The intestinal peptide transporter PEPT-1 in Caenorhabditis elegans is a rheogenic H -dependent carrier responsible for the absorption of di- and tripeptides. Transporter-deficient pept-1(lg601) worms are characterized by impairments in growth, development and reproduction and develop a severe obesity like phenotype. The transport function of PEPT-1 as well as the influx of free fatty acids was shown to be dependent on the membrane potential and on the intracellular pH homeostasis, both of which are regulated by the sodium-proton exchanger NHX-2. Since many membrane proteins commonly function as complexes, there could be proteins that possibly modulate PEPT-1 expression and function. A systematic RNAi screening of 162 genes that are exclusively expressed in the intestine combined with a functional transport assay revealed four genes with homologues existing in mammals as predicted PEPT-1 modulators. While silencing of a glutathione peroxidase surprisingly caused an increase in PEPT-1 transport function, silencing of the ER to Golgi cargo transport protein and of two cytosolic peptidases reduced PEPT-1 transport activity and this even corresponded with lower PEPT-1 protein levels. These modifications of PEPT-1 function by gene silencing of homologous