Remodeling of mitochondrial morphology and function: an emerging hallmark of cellular reprogramming
Authors:Anuj Rastogi1, Piyush Joshi2,3, Ela Contreras1 and Vivian Gama1,2,3,4
1 Department of Cell & Developmental Biology, Vanderbilt University, Nashville, TN 37240.
2 Neuroscience Program, Vanderbilt University Medical Center, Nashville, TN 37240.
3 Vanderbilt Brain Institute, Vanderbilt University Medical Center, Nashville, TN 37240.
4 Vanderbilt Center for Stem Cell Biology, Vanderbilt University, Nashville, TN 37240.
Keywords:
BCL-2 family, mitochondria, mitochondrial dynamics, apoptosis.
Abbreviatons:
BAK – BCL-2 antagonist killer,
BAX – BCL-2 associated X,
BCL-2 – B-Cell Lymphoma-2,
BID – BCL-2 interacting domain death agonist,
DRP – dynamin-related GTPase protein,
ER – endoplasmic reticulum,
ESC – embryonic stem cell,
hPSC – human PSC,
iPSC – induced PSC,
OXPHOS – oxidative phosphorylation,
PSC - pluripotent stem cell,
ROCK - Rho kinase,
ROS – reactive oxygen species,
SAM – S-adenosylmethionine,
TCA – tricarboxylic acid.
Corresponding Author(s):
Conflict of interest statement:
Authors declare no conflict of interest.
Please cite this article as:
Anuj Rastogi, Ela Contreras, Piyush Joshi and Vivian Gama (2019). Remodeling of mitochondrial morphology and function: an emerging hallmark of cellular reprogramming. Cell Stress 3(6): 181-194. doi: 10.15698/cst2019.06.189
© 2019 Rastogi et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduc-tion in any medium, provided the original author and source are acknowledged.
Abstract:
Research in the stem cell field has traditionally focused on understanding key transcriptional factors that provide pluripotent cell identity. However, much less is known about other critical non-transcriptional signaling networks that govern stem cell identity. Although we continue to gain critical insights into the mechanisms underlying mitochondrial morphology and function during cellular reprogramming – the process of reverting the fate of a differentiated cell into a stem cell, many uncertainties remain. Recent studies suggest an emerging landscape in which mitochondrial morphology and function have an active role in maintaining and regulating changes in cell identity. In this review, we will focus on these emerging concepts as crucial modulators of cellular reprogramming. Recognition of the widespread applicability of these concepts will increase our understanding of the mitochondrial mechanisms involved in cell identity, cell fate and disease.