Mitochondrial dynamics during spermatogenesis

Varuzhanyan, Grigor; Chan, David C.

doi:10.1242/jcs.235937

Cited by 63 publications

(61 citation statements)

References 132 publications

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“…We assumed that Cr (VI) might disturb the balance between mitochondrial fusion and fission. To this end, we performed a qPCR analysis for mitochondrial fusion-(Mfn1, Mfn2, and Opa1) and fission-related genes (Drp1; Varuzhanyan and Chan, 2020). The qPCR result showed significant downregulation of Mfn1, Mfn2, and Opa1 but upregulation of Drp1 at the mRNA level (Figure 3G).…”

Section: Cr (Vi) Induced Mitochondrial Dynamic Imbalance and Mitophagy In Sscs/ Progenitorsmentioning

confidence: 99%

Melatonin Attenuates Chromium (VI)-Induced Spermatogonial Stem Cell/Progenitor Mitophagy by Restoration of METTL3-Mediated RNA N6-Methyladenosine Modification

Yang

et al. 2021

Front. Cell Dev. Biol.

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Spermatogonial stem cells (SSCs) are the basis of spermatogenesis, and any damage to SSCs may result in spermatogenic disorder and male infertility. Chromium (Cr) (VI) is a proven toxin, mutagen, and carcinogen, perpetually detrimental to environmental organisms due to its intricate and enduring detoxification process in vivo. Despite this, the deleterious effects of Cr (VI) on SSCs and the underlying mechanisms remain poorly understood. In this study, we identified that Cr (VI) impaired male reproductive system in mouse testes and induced mitochondrial dynamic imbalance and mitophagy in SSCs/progenitors. Cr (VI) also downregulated the RNA N6-methyladenosine (m6A) modification levels in mitochondrial dynamic balance and mitophagy genes in SSCs/progenitors. Inspiringly, the toxic effects of Cr (VI) could be relieved by melatonin pretreatment. Melatonin alleviated Cr (VI)-induced damage to male reproductive system and autophagy in mouse testes. Melatonin also attenuated Cr (VI)-induced cell viability loss and reactive oxygen species (ROS) generation, as well as mitochondrial dynamic disorders and mitophagy in SSCs/progenitors. The protective roles of melatonin against Cr (VI)-induced mitophagy were exerted by restoration of METTL3-mediated RNA m6A modification and activation of mitochondrial fusion proteins MFN2 and OPA1, as well as inhibition of the mitophagy BNIP3/NIX receptor pathway. Thus, our study provides novel insights into the molecular mechanisms for RNA m6A modification underlying the gene regulatory network responsible for mitochondrial dynamic balance, and also lays new experimental groundwork for treatment of Cr (VI)-induced damage to male fertility.

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Section: Cr (Vi) Induced Mitochondrial Dynamic Imbalance and Mitophagy In Sscs/ Progenitorsmentioning

confidence: 99%

Melatonin Attenuates Chromium (VI)-Induced Spermatogonial Stem Cell/Progenitor Mitophagy by Restoration of METTL3-Mediated RNA N6-Methyladenosine Modification

Yang

et al. 2021

Front. Cell Dev. Biol.

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“…It is tempting to speculate further suggesting that enhanced permeability of VDAC3 to Ca 2+ may be related to its high expression level in the testes and sperm, where VDAC3 KO in mice leads to male infertility and sperm defects (59). Mitochondrial dynamics and energetics are being increasingly recognized to play an important role in spermatogenesis (60).…”

Section: Discussionmentioning

confidence: 99%

α-Synuclein emerges as a potent regulator of VDAC-facilitated calcium transport

et al. 2021

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When the Parkinson's disease (PD) related neuronal protein, alpha-synuclein (Syn), is added to the reconstituted mitochondrial voltage-dependent anion channel (VDAC), it reversibly and partially blocks VDAC conductance by its acidic C-terminal tail. Using single-molecule electrophysiology of reconstituted VDAC we now demonstrate that, at CaCl2 concentrations below 150 mM, Syn reverses the channel's selectivity from anionic to cationic. Importantly, we find that the decrease in channel conductance upon its blockage by Syn is hugely overcompensated by a favorable change in the electrostatic environment for calcium, making the blocked state orders-of-magnitude more selective for calcium and thus increasing its net flux. These findings reveal a new regulatory role of Syn, with clear implications for both normal calcium signaling and PD-associated mitochondrial dysfunction.under 17 USC 105 and is also made available for use under a CC0 license.

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Section: Discussionmentioning

confidence: 99%

α-Synuclein emerges as a potent regulator of VDAC-facilitated calcium transport

Rosencrans

Aguilella

Rostovtseva

et al. 2020

Preprint

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When the Parkinson’s disease (PD) related neuronal protein, alpha-synuclein (αSyn), is added to the reconstituted mitochondrial voltage-dependent anion channel (VDAC), it reversibly and partially blocks VDAC conductance by its acidic C-terminal tail. Using single-molecule electrophysiology of reconstituted VDAC we now demonstrate that, at CaCl2 concentrations below 150 mM, αSyn reverses the channel’s selectivity from anionic to cationic. Importantly, we find that the decrease in channel conductance upon its blockage by αSyn is hugely overcompensated by a favorable change in the electrostatic environment for calcium, making the blocked state orders-of-magnitude more selective for calcium and thus increasing its net flux. These findings reveal a new regulatory role of αSyn, with clear implications for both normal calcium signaling and PD-associated mitochondrial dysfunction.

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Mitochondrial dynamics during spermatogenesis

Cited by 63 publications

References 132 publications

Melatonin Attenuates Chromium (VI)-Induced Spermatogonial Stem Cell/Progenitor Mitophagy by Restoration of METTL3-Mediated RNA N6-Methyladenosine Modification

Melatonin Attenuates Chromium (VI)-Induced Spermatogonial Stem Cell/Progenitor Mitophagy by Restoration of METTL3-Mediated RNA N6-Methyladenosine Modification

α-Synuclein emerges as a potent regulator of VDAC-facilitated calcium transport

α-Synuclein emerges as a potent regulator of VDAC-facilitated calcium transport

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