Impaired mitophagy in Fanconi anemia is dependent on mitochondrial fission

摘要: // Pavithra Shyamsunder 1, 2, * , Milan Esner 3, Maunish Barvalia 4, 10 Yu Jun Wu 5 Tomas Loja 6 Huat Bay Boon Matilde E. Lleonart 7 Rama S Verma 2 Lumir Krejci 8, 9 Alex Lyakhovich 1 Cancer Science Institute of Singapore, National University Singapore Stem Cell and Molecular Biology Laboratory, Department Biotechnology, Indian Technology Madras, Chennai, India 3 Histology Embryology, Faculty Medicine, Masaryk University, Brno, Czech Republic 4 Yong Loo Lin School Anatomy, Central European Technology, Translational Research in Cells, Vall d´Hebron Institut de Recerca (VHIR), Barcelona, Spain 8 Biology, ICRC- FNUSA, International Clinical Center St. Anne’s Hospital Current Address: Microbiology Immunology, British Columbia, Life Sciences Institute, Vancouver, Canada These authors have contributed equally to this work Correspondence to: Lyakhovich, email: lyakhovich@gmail.com alex.lyakhovich@mail.muni.cz Krejci, lkrejci@chemi.muni.cz Keywords: mitophagy, impaired autophagy, Fanconi anemia, ROS, oxidative stress Received: June 04, 2016      Accepted: July 29, Published: August 09, 2016 ABSTRACT anemia (FA) is a rare genetic disorder associated with bone-marrow failure, genome instability cancer predisposition. Recently, we others demonstrated dysfunctional mitochondria morphological alterations FA cells accompanied by high reactive oxygen species (ROS) levels. Mitochondrial morphology regulated continuous fusion fission events the misbalance between these two often autophagy. Here, provide evidence autophagy FA. We demonstrate that increased number autophagic (presumably mitophagic) accumulate due an ability degrade them. Moreover, mitochondrial (OS) prerequisite condition for mitophagy blocking pathway may release machinery clear mitochondria.