The Multifaceted Regulation of Mitochondrial Dynamics During Mitosis

Abstract

Mitosis ensures genome integrity by mediating precise segregation of the duplicated genetic material. Segregation of subcellular organelles during mitosis also needs to be tightly coordinated in order to warrant their proper inheritance and cellular homeostasis. The inheritance of mitochondria, a powerhouse of the cell, is tightly regulated in order to meet the high energy demand to fuel the mitotic machinery. Mitochondria are highly dynamic organelles, which undergo events of fission, fusion and transport during different cell cycle stages. Importantly, during mitosis several kinases phosphorylate the key mitochondrial factors and drive fragmentation of mitochondria to allow for their efficient distribution and inheritance to two daughter cells. Recent evidence suggests that mitochondrial fission can also actively contribute to the regulation of mitotic progression. This review aims at summarizing established and emerging concepts about the complex regulatory networks which couple crucial mitotic factors and events to mitochondrial dynamics and which could be implicated in human disease.

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“…TTK is an important member of a number of mitotic stages in a wide range of eukaryotic cells ( Wang et al, 2018 , Pangou and Sumara, 2021 ). It is a major kinase implicated in the localisation of kinetochores and the spindle assembly checkpoint ( Liu et al, 2020 , Pachis and Kops, 2018 ).…”

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“…The fusion is operated by the dynamin-like GTPases mitofusins 1 and 2 (Mfn1 and Mfn2) at the outer membrane, and optic atrophy 1 (Opa1) localized on the inner membrane. If the cell lacks Mfn1 and Mfn2, no outer membrane fusion occurs [ 7 , 8 , 10 , 11 ]. Mice models demonstrated that targeted deletion of either Mfn1 or Mfn2 leads to phenotype consistent with female reproductive aging (e.g., apoptotic cell loss resulting in accelerated follicular depletion).…”

“…The fission process is mediated by the dynamin-related protein 1 (DRP1) recruited from the cytosol to the outer mitochondrial membrane. Its assembly on the mitochondrial surface causes constriction of the mitochondria and eventual division of the organelle into two separate entities [ 7 , 8 , 10 , 11 ]. There are four DRP1 receptors at the mitochondrial outer membrane: Fis1 (Anti-Mitochondrial fission 1 protein), Mff (Mitochondrial fission factor), Mid49 (Mitochondrial dynamics protein of 49 kDa), and Mid51 (Mitochondrial dynamics protein of 51 kDa), from which the latter three play the major role in fission.…”

Le transport mitochondrial

“…Un déséquilibre de répartition des mitochondries entre les cellules filles pourrait être source de différences dans le métabolisme bioénergétique au sein de la tumeur, et, à terme, induire une hétérogénéité intra-tumorale. La ségrégation des mitochondries au cours de la division cellulaire met en jeu une régulation de leur dynamique [27] et des mécanismes successifs de diffusion passive [28,29] et de transport actif, impliquant une coordination des réseaux de microtubules et d'actine [14,30,31] (Figure 3). Alors qu'en début de mitose, les mitochondries se redistribuent de façon passive et aléatoire au niveau du cortex cellulaire, à partir de l'anaphase, un transport antérograde mitochondrial se met La RRM est un processus au cours duquel les mitochondries endommagées par le stress sont acheminées, par un transport rétrograde, vers le noyau de la cellule avec lequel elles pourront physiquement s'associer et « rétro-communiquer » [45].…”