Mitochondrial dynamics during cell cycling

Abstract

Mitochondria are the cell's power plant that must be in a proper functional state in order to produce the energy necessary for basic cellular functions, such as proliferation. Mitochondria are 'dynamic' in that they are constantly undergoing fission and fusion to remain in a functional state throughout the cell cycle, as well as during other vital processes such as energy supply, cellular respiration and programmed cell death. The mitochondrial fission/fusion machinery is involved in generating young mitochondria, while eliminating old, damaged and non-repairable ones. As a result, the organelles change in shape, size and number throughout the cell cycle. Such precise and accurate balance is maintained by the cytoskeletal transporting system via microtubules, which deliver the mitochondrion from one location to another. During the gap phases G and G, mitochondria form an interconnected network, whereas in mitosis and S-phase fragmentation of the mitochondrial network will take place. However, such balance is lost during neoplastic transformation and autoimmune disorders. Several proteins, such as Drp1, Fis1, Kif-family proteins, Opa1, Bax and mitofusins change in activity and might link the mitochondrial fission/fusion events with processes such as alteration of mitochondrial membrane potential, apoptosis, necrosis, cell cycle arrest, and malignant growth. All this indicates how vital proper functioning of mitochondria is in maintaining cell integrity and preventing carcinogenesis.

Melatonin: A Mitochondrial Targeting Molecule Involving Mitochondrial Protection and Dynamics

“…All these maintain mitochondrial and cellular functions. Collectively, these processes are referred to as mitochondrial dynamics [176,177]. The daily oscillations of mitochondria are believed to be dependent on the clock proteins Period1 and Period2 (PER1/2) since they are blunted in mice lacking these proteins [178].…”

Rotaviral nonstructural protein 4 triggers dynamin-related protein 1-dependent mitochondrial fragmentation during infection

“…(Liesa & Shirihai, 2013;Mishra & Chan, 2016;Nasrallah & Horvath, 2014), cell cycle progression (Horbay & Bilyy, 2016;Mishra & Chan, 2014), aging (Sato, Nakada, & Hayashi, 2006;Sebastián, Palacín, & Zorzano, 2017;Seo et al, 2010), innate immunity (Mills, Kelly, & O'Neill, 2017;Pourcelot & Arnoult, 2014), cell death, and survival (Otera & Mihara, 2012;Sheridan & Martin, 2010;Suen, Norris, & Youle, 2008). In addition to its positive role in mitochondrial fission, Drp1 also resulted in mitochondrial translocation of E3-ubiquitin ligase Parkin leading to degradation of mitochondrial fusion protein Mitofusin 1.…”

Hepatic stimulator substance resists hepatic ischemia/reperfusion injury by regulating Drp1 translocation and activation

“…Mitochondrial fission is also regulated by posttranslational modifications of Drp1, such as phosphorylation . Phosphorylation of Drp1 at Ser‐616 by the cyclin‐dependent kinase 1 (CDK1)/cyclin B complex stimulates Drp1 activition and results in mitochondrial fragmentation . As studies have shown that Ca 2+ /calmodulin‐dependent protein kinases Iα and II promote phosphorylation of Drp1 at Ser‐600/616 and increase Drp1 translocation to mitochondria, respectively, whether CDK1/cyclin B‐mediated phosphorylation at Ser‐616 could also promote Drp1 translocation to mitochondria warranted further study.…”