Author response: Elimination of paternal mitochondria in mouse embryos occurs through autophagic degradation dependent on PARKIN and MUL1

Rojansky, Rebecca; Cha, Moon-Yong; Chan, David C.

doi:10.7554/elife.17896.016

Cited by 6 publications

(1 citation statement)

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“…The oocyte is quiescent with low ATP production, thus minimizing the number of mitochondrial DNA mutations (Babayev and Seli, 2015). Following fertilization, any paternal mtDNA arriving from the sperm is eliminated via mitophagy (Rojansky et al, 2016). In postimplantation embryos, the maternal mitochondria undergo structural changes that include elongation and the formation of organized cristae, presumably in response to the increased energy demands of cellular differentiation and development (Schatten et al, 2014;Prigione et al, 2015;Lima et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Nuclear encoded mitochondrial ribosomal proteins are required to initiate gastrulation

et al. 2020

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Mitochondria are essential for energy production and although they have their own genome, many nuclear-encoded mitochondrial ribosomal proteins (MRPs) are required for proper function of the organelle. Although mutations in MRPs have been associated with human diseases, little is known about their role during development. Presented here are the null phenotypes for 21 nuclear-encoded mitochondrial proteins and in-depth characterization of mouse embryos mutant for the Mrp genes Mrpl3, Mrpl22, Mrpl44, Mrps18c and Mrps22. Loss of each MRP results in successful implantation and egg-cylinder formation, followed by severe developmental delay and failure to initiate gastrulation by embryonic day 7.5. The robust and similar single knockout phenotypes are somewhat surprising given there are over 70 MRPs and suggest little functional redundancy. Metabolic analysis reveals that Mrp knockout embryos produce significantly less ATP than controls, indicating compromised mitochondrial function. Histological and immunofluorescence analyses indicate abnormal organelle morphology and stalling at the G2/M checkpoint in Mrp null cells. The nearly identical pregastrulation phenotype observed for many different nuclear-encoded mitochondrial protein knockouts hints that distinct energy systems are crucial at specific time points during mammalian development. This article has an associated 'The people behind the papers' interview.

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Section: Introductionmentioning

confidence: 99%

Nuclear encoded mitochondrial ribosomal proteins are required to initiate gastrulation

et al. 2020

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Porcine model for the study of sperm capacitation, fertilization and male fertility

et al. 2020

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A Glimmer of Hope: Maintain Mitochondrial Homeostasis to Mitigate Alzheimer’s Disease

Kui

Demetrios

et al. 2020

Aging and disease

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Mitochondria are classically known to be cellular energy producers. Given the high-energy demanding nature of neurons in the brain, it is essential that the mitochondrial pool remains healthy and provides a continuous and efficient supply of energy. However, mitochondrial dysfunction is inevitable in aging and neurodegenerative diseases. In Alzheimer's disease (AD), neurons experience unbalanced homeostasis like damaged mitochondrial biogenesis and defective mitophagy, with the latter promoting the disease-defining amyloid β (Aβ) and p-Tau pathologies impaired mitophagy contributes to inflammation and the aggregation of Aβ and p-Tau-containing neurotoxic proteins. Interventions that restore defective mitophagy may, therefore, alleviate AD symptoms, pointing out the possibility of a novel therapy. This review aims to illustrate mitochondrial biology with a focus on mitophagy and propose strategies to treat AD while maintaining mitochondrial homeostasis.

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Author response: Elimination of paternal mitochondria in mouse embryos occurs through autophagic degradation dependent on PARKIN and MUL1

Cited by 6 publications

References 0 publications

Nuclear encoded mitochondrial ribosomal proteins are required to initiate gastrulation

Nuclear encoded mitochondrial ribosomal proteins are required to initiate gastrulation

Porcine model for the study of sperm capacitation, fertilization and male fertility

A Glimmer of Hope: Maintain Mitochondrial Homeostasis to Mitigate Alzheimer’s Disease

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