Mito-protective autophagy is impaired in erythroid cells of aged mtDNA-mutator mice

Author:

Li-Harms XiuJie1,Milasta Sandra2,Lynch John3,Wright Christopher1,Joshi Aashish1,Iyengar Rekha1,Neale Geoffrey4,Wang Xi5,Wang Yong-Dong6,Prolla Tomas A.7,Thompson James E.8,Opferman Joseph T.5,Green Douglas R.2,Schuetz John3,Kundu Mondira1

Affiliation:

1. Department of Pathology,

2. Department of Immunology,

3. Department of Pharmaceutical Sciences,

4. Hartwell Center for Bioinformatics & Biotechnology,

5. Department of Cell and Molecular Biology, and

6. Department of Computational Biology, St. Jude Children’s Research Hospital, Memphis, TN;

7. Department of Genetics, University of Wisconsin-Madison, Madison, WI; and

8. Department of Medicine, Roswell Park Cancer Institute, Buffalo, NY

Abstract

Key Points Mitochondrial dysfunction in aged mtDNA-mutator mice is associated with activation of mechanistic target of rapamycin and suppression of autophagy in erythroid cells. Autophagy maintains mitochondrial function in erythroid progenitors of mtDNA-mutator mice, and disrupting it accelerates onset of anemia.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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