Maternal spindle transfer overcomes embryo developmental arrest caused by ooplasmic defects in mice

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  • dc.contributor.author Costa Borges, Nuno Luis
  • dc.contributor.author Spath, Katharina
  • dc.contributor.author Miguel Escalada, Irene
  • dc.contributor.author Mestres, Enric
  • dc.contributor.author Balmaseda, Rosa
  • dc.contributor.author Serafín, Anna
  • dc.contributor.author Garcia Jiménez, Maria
  • dc.contributor.author Vanrell, Ivette
  • dc.contributor.author González, Jesús
  • dc.contributor.author Rink, Klaus
  • dc.contributor.author Wells, Dagan
  • dc.contributor.author Calderón, Gloria
  • dc.date.accessioned 2020-05-14T06:49:13Z
  • dc.date.available 2020-05-14T06:49:13Z
  • dc.date.issued 2020
  • dc.description.abstract The developmental potential of early embryos is mainly dictated by the quality of the oocyte. Here, we explore the utility of the maternal spindle transfer (MST) technique as a reproductive approach to enhance oocyte developmental competence. Our proof-of-concept experiments show that replacement of the entire cytoplasm of oocytes from a sensitive mouse strain overcomes massive embryo developmental arrest characteristic of non-manipulated oocytes. Genetic analysis confirmed minimal carryover of mtDNA following MST. Resulting mice showed low heteroplasmy levels in multiple organs at adult age, normal histology and fertility. Mice were followed for 5 generations (F5), revealing that heteroplasmy was reduced in F2 mice and was undetectable in the subsequent generations. This pre-clinical model demonstrates the high efficiency and potential of the MST technique, not only to prevent the transmission of mtDNA mutations, but also as a new potential treatment for patients with certain forms of infertility refractory to current clinical strategies.
  • dc.format.mimetype application/pdf
  • dc.identifier.citation Costa-Borges N, Spath K, Miguel-Escalada I, Mestres E, Balmaseda R, Serafín A, Garcia-Jiménez M, Vanrell I, González J, Rink K, Wells D, Calderón G. Maternal spindle transfer overcomes embryo developmental arrest caused by ooplasmic defects in mice. Elife. 2020 Apr 29;9:e48591. DOI: 10.7554/eLife.48591
  • dc.identifier.doi http://dx.doi.org/10.7554/eLife.48591
  • dc.identifier.issn 2050-084X
  • dc.identifier.uri http://hdl.handle.net/10230/44541
  • dc.language.iso eng
  • dc.publisher eLife
  • dc.relation.ispartof Elife. 2020 Apr 29;9:e48591
  • dc.rights © 2020, Costa-Borges et al. This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use and redistribution provided that the original author and source are credited.
  • dc.rights.accessRights info:eu-repo/semantics/openAccess
  • dc.rights.uri http://creativecommons.org/licenses/by/4.0/
  • dc.subject.keyword Cell biology
  • dc.subject.keyword Developmental biology
  • dc.subject.keyword Mouse
  • dc.title Maternal spindle transfer overcomes embryo developmental arrest caused by ooplasmic defects in mice
  • dc.type info:eu-repo/semantics/article
  • dc.type.version info:eu-repo/semantics/publishedVersion