A pair of transporters controls mitochondrial Zn2+ levels to maintain mitochondrial homeostasis

Ma, Tengfei; Zhao, Ludan; Zhang, Jie; Tang, Ruofeng; Wang, Xin; Liu, Nan; Zhang, Qian; Li, Meijiao; Qian, Shan; Yang, Yang; Yin, Qiuyuan; Yang, Limei; Gan, Qiwen; Yang, Chonglin

doi:10.1007/s13238-021-00881-4

Cited by 41 publications

(31 citation statements)

References 58 publications

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“…Moreover, SLC-25A25/SCaMC-2 was identified as an important regulator of mitochondrial Zn 2+ import, the losing of which suppresses functional and structural defects caused by a loss of SLC-30A9. It was shown that mitochondria mostly import Zn 2+ from the endoplasmic reticulum Zn 2+ pool [29]. Similarly, the role of SLC-30A9 in Zn 2+ export from mitochondria was also confirmed in humans, where loss of SLC-30A9 leads to excessive Zn 2+ accumulation in mitochondria, severe mitochondrial swelling, increased ROS production and dysregulated metabolic function.…”

Section: Zn 2+ In Mitochondrial Homeostasismentioning

confidence: 78%

Interplay between Zn2+ Homeostasis and Mitochondrial Functions in Cardiovascular Diseases and Heart Ageing

Dabravolski

Sadykhov

Kartuesov

et al. 2022

IJMS

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Zinc plays an important role in cardiomyocytes, where in exists in bound and histochemically reactive labile Zn2+ forms. Although Zn2+ concentration is under tight control through several Zn2+-transporters, its concentration and intracellular distribution may vary during normal cardiac function and pathological conditions, when the protein levels and efficacy of Zn2+ transporters can lead to zinc re-distribution among organelles in cardiomyocytes. Such dysregulation of cellular Zn2+ homeostasis leads to mitochondrial and ER stresses, and interrupts normal ER/mitochondria cross-talk and mitophagy, which subsequently, result in increased ROS production and dysregulated metabolic function. Besides cardiac structural and functional defects, insufficient Zn2+ supply was associated with heart development abnormalities, induction and progression of cardiovascular diseases, resulting in accelerated cardiac ageing. In the present review, we summarize the recently identified connections between cellular and mitochondrial Zn2+ homeostasis, ER stress and mitophagy in heart development, excitation–contraction coupling, heart failure and ischemia/reperfusion injury. Additionally, we discuss the role of Zn2+ in accelerated heart ageing and ageing-associated rise of mitochondrial ROS and cardiomyocyte dysfunction.

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Section: Zn 2+ In Mitochondrial Homeostasismentioning

confidence: 78%

Interplay between Zn2+ Homeostasis and Mitochondrial Functions in Cardiovascular Diseases and Heart Ageing

Dabravolski

Sadykhov

Kartuesov

et al. 2022

IJMS

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“…In addition, the target site of the steroid 1,3,4-oxadiazole was demonstrated to be the mitochondria and nucleus in the midgut tissues of Eriosoma lanigerum [ 49 ]. Mitochondria are the powerhouses of the cell and mitochondrial dysfunction is related to oxidative homeostasis and lipid and energy metabolism [ 50 , 64 ]. For example, zebrafish exposed to triazoles had impaired mitochondrial oxidative phosphorylation and oxidative stress as well as dysregulation of lipid metabolism, which resulted in developmental disorders and movement disorders [ 64 ].…”

Section: Discussionmentioning

confidence: 99%

“…Sample preparation was the same as that described above. A previous method was modified as appropriate [ 47 , 48 , 49 , 50 ]. Samples were fixed overnight at 4 °C using 2.5% glutaraldehyde in 0.1 M PB (pH 7.4).…”

Section: Methodsmentioning

confidence: 99%

The Insecticidal Efficacy and Physiological Action Mechanism of a Novel Agent GC16 against Tetranychus pueraricola (Acari: Tetranychidae)

Xie

et al. 2022

Insects

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Chemical control plays a crucial role in pest management but has to face challenges due to insect resistance. It is important to discover alternatives to traditional pesticides. The spider mite Tetranychus pueraricola (Ehara & Gotoh) (Acari: Tetranychidae) is a major agricultural pest that causes severe damage to many crops. GC16 is a new agent that consists of a mixture of Calcium chloride (CaCl2) and lecithin. To explore the acaricidal effects and mode of action of GC16 against T. pueraricola, bioassays, cryogenic scanning electron microscopy (cryo-SEM) and transmission electron microscopy (TEM) were performed. GC16 had lethal effects on the eggs, larvae, nymphs, and adults of T. pueraricola, caused the mites to dehydrate and inactivate, and inhibited the development of eggs. GC16 displayed contact toxicity rather than stomach toxicity through the synergistic effects of CaCl2 with lecithin. Cryo-SEM analysis revealed that GC16 damaged T. pueraricola by disordering the array of the cuticle layer crest. Mitochondrial abnormalities were detected by TEM in mites treated by GC16. Overall, GC16 had the controlling efficacy on T. pueraricola by cuticle penetration and mitochondria dysfunction and had no effects on Picromerus lewisi and Harmonia axyridis, indicating that GC16 is likely a new eco-friendly acaricide.

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“…Further still the zinc transporters Zip7 and ZnT7 have also been shown to have dual localization in mitochondria and ER and expression of Zip7 and ZnT7 contribute to cellular zinc exchange between the organelles in certain cell types ( Tuncay et al, 2019 ). Finally Znt9 (SLC30A9) was identified as a zinc exporter in mitochondria ( Deng et al, 2021 ) and SLC25A25 has been implicated in at least regulating uptake of zinc as deletion can reverse phenotypes induced by SLC30A9 deletion ( Ma et al, 2022 ). Perhaps redundancy is the reason for the failure of the yeast genetic screens to yield a single candidate.…”

Section: Metals In Mitochondriamentioning

confidence: 99%

Prime Real Estate: Metals, Cofactors and MICOS

Medlock

Hixon

Bhuiyan

et al. 2022

Front. Cell Dev. Biol.

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Metals are key elements for the survival and normal development of humans but can also be toxic to cells when mishandled. In fact, even mild disruption of metal homeostasis causes a wide array of disorders. Many of the metals essential to normal physiology are required in mitochondria for enzymatic activities and for the formation of essential cofactors. Copper is required as a cofactor in the terminal electron transport chain complex cytochrome c oxidase, iron is required for the for the formation of iron-sulfur (Fe-S) clusters and heme, manganese is required for the prevention of oxidative stress production, and these are only a few examples of the critical roles that mitochondrial metals play. Even though the targets of these metals are known, we are still identifying transporters, investigating the roles of known transporters, and defining regulators of the transport process. Mitochondria are dynamic organelles whose content, structure and localization within the cell vary in different tissues and organisms. Our knowledge of the impact that alterations in mitochondrial physiology have on metal content and utilization in these organelles is very limited. The rates of fission and fusion, the ultrastructure of the organelle, and rates of mitophagy can all affect metal homeostasis and cofactor assembly. This review will focus of the emerging areas of overlap between metal homeostasis, cofactor assembly and the mitochondrial contact site and cristae organizing system (MICOS) that mediates multiple aspects of mitochondrial physiology. Importantly the MICOS complexes may allow for localization and organization of complexes not only involved in cristae formation and contact between the inner and outer mitochondrial membranes but also acts as hub for metal-related proteins to work in concert in cofactor assembly and homeostasis.

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A pair of transporters controls mitochondrial Zn2+ levels to maintain mitochondrial homeostasis

Cited by 41 publications

References 58 publications

Interplay between Zn2+ Homeostasis and Mitochondrial Functions in Cardiovascular Diseases and Heart Ageing

Interplay between Zn2+ Homeostasis and Mitochondrial Functions in Cardiovascular Diseases and Heart Ageing

The Insecticidal Efficacy and Physiological Action Mechanism of a Novel Agent GC16 against Tetranychus pueraricola (Acari: Tetranychidae)

Prime Real Estate: Metals, Cofactors and MICOS

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