Mechanisms for sperm mitochondrial removal in embryos.

Autor: de Melo KP; Department of Surgery, Division of Urology, Human Reproduction Section, Universidade Federal de São Paulo, São Paulo, Brazil., Camargo M; Department of Surgery, Division of Urology, Human Reproduction Section, Universidade Federal de São Paulo, São Paulo, Brazil. Electronic address: mcamargo@unifesp.br.
Jazyk: angličtina
Zdroj: Biochimica et biophysica acta. Molecular cell research [Biochim Biophys Acta Mol Cell Res] 2021 Feb; Vol. 1868 (2), pp. 118916. Date of Electronic Publication: 2020 Dec 01.
DOI: 10.1016/j.bbamcr.2020.118916
Abstrakt: Background: Different animal species have different characteristics regarding the transmission of mitochondrial DNA. While some species have biparental mitochondrial inheritance, others have developed pathways to remove paternal mtDNA. These pathways guarantee the uniparental mitochondrial inheritance, so far well known in mammals, avoiding heteroplasmy, which may have the potential to cause certain mitochondrial diseases in the offspring.
Scope of Review: This review aims to address the main mechanisms that involve mitochondrial degradation in different animal species, as well as to describe what is present in the literature on the mechanisms involved in mitochondrial inheritance.
Major Conclusions: Two theories are proposed to explain the uniparental inheritance of mtDNA: (i) active degradation, where mechanisms for paternal mitochondrial DNA elimination involve mitochondrial degradation pathway by autophagy and, in some species, may also involve the endocytic degradation pathway; and (ii) passive dilution, where the paternal mitochondria are diluted in the cells of the embryo according to cell division, until becoming undetectable.
General Significance: This work brings a wide review of the already published evidence on mitochondrial inheritance in the animal kingdom and the possible mechanisms to mtDNA transmission already described in literature.
(Copyright © 2020 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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