MAPRE2 regulates the first meiotic progression in mouse oocytes.

Microtubule plus-end tracking proteins (+TIPs) associate with growing microtubule plus ends and control microtubule dynamics and interactions with different cellular structures during cell division, cell migration and morphogenesis. Microtubule-associated RP/EB family member 2 (MAPRE2/EB2) is a highly conserved core component of +TIPs networks, but whether this molecule is required for mammalian meiotic progression is unknown. In this study, we investigated the expression and function of MAPRE2 during oocyte maturation. Our results showed that MAPRE2 was consistently expressed from germinal vesicle (GV) to metaphase II (MII) stages and that MAPRE2 was distributed in the cytoplasm of oocytes at GV stage and along the spindle at metaphase I (MI) and MII stages. Small interfering RNA-mediated knockdown of Mapre2 severely impaired microtubule stability, kinetochore-microtubule attachment, and chromosome alignment and subsequently caused spindle assembly checkpoint (SAC) activation and cyclin B1 nondegradation, leading to failure of chromosome segregation and first polar body extrusion. This study demonstrates for the first time that MAPRE2 plays an important role during mouse oocyte meiosis.

(Benzyl phenyl sulfoxide-κO)-chlorido-triphenyl-tin(IV).

The Sn(IV) atom in the title compound, [Sn(C(6)H(5))(3)Cl(C(13)H(12)OS)], is situated within a distorted C(3)ClO trigonal-bipyramidal coordination geometry with a mean Sn-C distance of 2.136 (6) Šand with an Sn-O distance of 2.393 (4) Å. The Sn(IV) atom lies 0.171 (3) Šout of the equatorial C(3) plane in the direction of the axially bound Cl atom.

Reduction of mtDNA heteroplasmy in mitochondrial replacement therapy by inducing forced mitophagy.

Mitochondrial replacement therapy (MRT) has been used to prevent maternal transmission of disease-causing mutations in mitochondrial DNA (mtDNA). However, because MRT requires nuclear transfer, it carries the risk of mtDNA carryover and hence of the reversion of mtDNA to pathogenic levels owing to selective replication and genetic drift. Here we show in HeLa cells, mouse embryos and human embryos that mtDNA heteroplasmy can be reduced by pre-labelling the mitochondrial outer membrane of a donor zygote via microinjection with an mRNA coding for a transmembrane peptide fused to an autophagy receptor, to induce the degradation of the labelled mitochondria via forced mitophagy. Forced mitophagy reduced mtDNA carryover in newly reconstructed embryos after MRT, and had negligible effects on the growth curve, reproduction, exercise capacity and other behavioural characteristics of the offspring mice. The induction of forced mitophagy to degrade undesired donor mtDNA may increase the clinical feasibility of MRT and could be extended to other nuclear transfer techniques.

(Benzyl phenyl sulfoxide-κO)dichloridodiphenyl-tin(IV).

The Sn(IV) atom in the title compound, [Sn(C(6)H(5))(2)Cl(2)(C(13)H(12)OS)], displays a distorted C(2)Cl(2)O trigonal-bipyramidal coordination environment, with a mean Sn-C distance of 2.121 (9) Šand with Sn-O = 2.331 (2) Å. The Sn(IV) atom is displaced by 0.169 (2) Šfrom the equatorial C(2)Cl plane towards the direction of the second axially bonded Cl atom.