T-cell-restricted intracellular antigen 1 facilitates mitochondrial fragmentation by enhancing the expression of mitochondrial fission factor
Authors: Jung Woo Eun
Wook Kim
So Jung Park
Eun Kyung Lee
Chongtae Kim
Suk Woo Nam
Dong-Hyung Cho
Heejin Lee
Hyosun Tak
Eunbyul Ji
Kyungbun Lee
Jihye Kim
Hoin Kang
Journal: Cell death and differentiation (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Mitochondrial morphology; mitochondrial dynamics; T-cell intracellular antigen protein-1 (TIA-1); mitochondrial fission; mitochondrial elongation
Affiliations: Department of Biochemistry, The Catholic University of Korea College of Medicine, Seoul, South Korea., Department of Pathology, The Catholic University of Korea College of Medicine, Seoul, South Korea., Department of Molecular Science and Technology, Ajou University, Suwon, South Korea., Department of East-West Medical Science, Graduate School of East-West Medical Science, Kyung Hee University, Yongin, South Korea., Department of Pathology, Seoul National University College of Medicine, Seoul, South Korea., Cancer Evolution Research Center, The Catholic University of Korea College of Medicine, Seoul, South Korea., Institute for Aging and Metabolic Disease, The Catholic University of Korea College of Medicine, Seoul, South Korea.

Abstract:  Mitochondrial morphology is dynamically regulated by the formation of small fragmented units or interconnected mitochondrial networks, and this dynamic morphological change is a pivotal process in normal mitochondrial function. In the present study, we identified a novel regulator responsible for the regulation of mitochondrial dynamics. An assay using CHANG liver cells stably expressing mitochondrial-targeted yellow fluorescent protein (mtYFP) and a group of siRNAs revealed that T-cell intracellular antigen protein-1 (TIA-1) affects mitochondrial morphology by enhancing mitochondrial fission. The function of TIA-1 in mitochondrial dynamics was investigated through various biological approaches and expression analysis in human specimen. Downregulation of TIA-1-enhanced mitochondrial elongation, whereas ectopic expression of TIA-1 resulted in mitochondria fragmentation. In addition, TIA-1 increased mitochondrial activity, including the rate of ATP synthesis and oxygen consumption. Further, we identified mitochondrial fission factor (MFF) as a direct target of TIA-1, and showed that TIA-1 promotes mitochondrial fragmentation by enhancing MFF translation. TIA-1 null cells had a decreased level of MFF and less mitochondrial Drp1, a critical factor for mitochondrial fragmentation, thereby enhancing mitochondrial elongation. Taken together, our results indicate that TIA-1 is a novel factor that facilitates mitochondrial dynamics by enhancing MFF expression and contributes to mitochondrial dysfunction. 

Retracted: No

PubPeer comments:
 Figure 2B. The fluorescence images with different brightness in the white boxes are duplicated. Arrows in these images indicate identical cells. ![file] , 
 As the corresponding author, I regret that incorrect images appear in Figure 2B during data re-arrangement. Unfortunately, there seems to have been an unintended mistake in the process of creating the revised version of manuscript. Please see the schematic drawing below. Several images per each group (siCtrl mock and siTIA-1 oligomycin) were obtained, but during re-arrangement of figure, u2018image Au2019 in u2018siTIA-1 oligomycinu2019 group was mis-labeled and displayed as a u2018siCtrl mocku2019. Images of A and D were independently obtained from the same slide of siTIA-1 oligomycin-treated cells, but partially overlapped (white box). The different intensity between them is likely due to photobleaching in fluorescence microscopy. The image was not duplicated, manipulated, and cropped. We have all original raw data files and will provide them to Editor during the correction process. Even if it was not intentional, this is clearly our mistake. We are communicating with Editorial office for the correction and will post the decision soon. Thank you for your interest in our publication and giving a chance to correct our mistake. And we apologize for the inconvenience. ![file] ![file] ,