title: Transient overexpression of Werner protein rescues starvation induced autophagy in Werner syndrome cells.
abstract: Reduced autophagy may be associated with normal and pathological aging. Here we report a link between autophagy and Werner protein (WRNp), mutated in Werner syndrome, the human premature aging Werner syndrome (WS). WRN mutant fibroblast AG11395 and AG05229 respond weakly to starvation induced autophagy compared to normal cells. While the fusion of phagosomes with lysosome is normal, WS cells contain fewer autophagy vacuoles. Cellular starvation autophagy in WS cells is restored after transfection with full length WRN. Further, siRNA mediated silencing of WRN in the normal fibroblast cell line WI-38 results in decreased autophagy and altered expression of autophagy related proteins. Thus, our observations suggest that WRN may have a role in controlling autophagy and hereby cellular maintenance.
authors.affiliation: Department of Life Science and Biotechnology, Jadavpur University, Kolkata 700032, India.
authors.forename: Jyotirindra
authors.initials: J
authors.lastname: Maity
authors.affiliation: Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, United States.
authors.forename: Vilhelm A
authors.initials: VA
authors.lastname: Bohr
authors.affiliation: CSIR-Indian Institute of Chemical Biology, Kolkata 700032, India.
authors.forename: Aparna
authors.initials: A
authors.lastname: Laskar
authors.affiliation: Department of Life Science and Biotechnology, Jadavpur University, Kolkata 700032, India. Electronic address: pkarmakar_28@yahoo.co.in.
authors.forename: Parimal
authors.initials: P
authors.lastname: Karmakar
mesh_terms: D000328:Adult; D001343:Autophagy / Q000187:drug effects / Q000235:genetics*; D015153:Blotting, Western; D002460:Cell Line; D002478:Cells, Cultured; D003470:Culture Media / Q000737:chemistry / Q000494:pharmacology; D005090:Exodeoxyribonucleases / Q000235:genetics* / Q000378:metabolism; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D015870:Gene Expression; D049452:Green Fluorescent Proteins / Q000235:genetics / Q000378:metabolism; D006801:Humans; D008297:Male; D046529:Microscopy, Electron, Transmission; D008856:Microscopy, Fluorescence; D008869:Microtubule-Associated Proteins / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D034622:RNA Interference; D053484:RecQ Helicases / Q000235:genetics* / Q000378:metabolism; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D014162:Transfection; D014898:Werner Syndrome / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D000071657:Werner Syndrome Helicase
chemical_list: D003470:Culture Media; C477012:MAP1LC3A protein, human; D008869:Microtubule-Associated Proteins; D049452:Green Fluorescent Proteins; C546842:MTOR protein, human; D058570:TOR Serine-Threonine Kinases; D005090:Exodeoxyribonucleases; D053484:RecQ Helicases; C098785:WRN protein, human; D000071657:Werner Syndrome Helicase
keywords: Aging; Autophagy; Beclin-1; RecQ helicase; Werner protein; Werner syndrome