ArticleNature structural & molecular biology2024
Structural basis of the subcortical maternal complex and its implications in reproductive disorders.
Article in Nature structural & molecular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 23 citations in OpenAlex.
- Cytoplasmic lattices store developmentally poised degradative and cytoskeletal complexes in mammalian eggs.Nature structural & molecular biology · 2026Article
- In-situ cryo-ET of mouse embryos reveals cytoplasmic lattices contain ubiquitin-charged E2-E3 ligase assemblies.The EMBO journal · 2026Article
- Review
- Structure of the mouse cytoplasmic lattice.Nature · 2026Article
- Article
- Article
- Loss of the maternal effect gene NLRP2 impairs embryonic and extra-embryonic development, revealing a novel genetic cause of congenital anomalies†.Biology of reproduction · 2026Article
- NLRP14 modulates the activity of E3 ubiquitin ligases during the oocyte-to-embryo transition.Nature communications · 2026Article
- The cytoplasmic lattice in mammalian eggs sequesters ubiquitination machinery and tubulin in reserve.bioRxiv : the preprint server for biology · 2026Article
- TCL1A mediates DNA methylation defects in recurrent hydatidiform mole with NLRP7 pathogenic variants.Nature communications · 2026Article
- The maternal PADI6-UHRF1-UBE2D complex regulates ubiquitination during oocyte maturation and embryogenesis.Nature structural & molecular biology · 2026Article
- Genetic landscape of human oocyte/embryo defects.Cell genomics · 2026Article
- Genetic architecture and phenotypic diversity of oocyte and early embryo competence defects in female infertility.Nature medicine · 2026Article
- An Nlrp5-null mutation leads to attenuated de novo methylation in oocytes, accompanied by a significant reduction in DNMT3L.Molecular human reproduction · 2025Article
- ESHRE's key research priorities in infertility: maximizing impact on science, people and society†.Human reproduction (Oxford, England) · 2025Article
- The subcortical maternal complex safeguards mouse oocyte-to-embryo transition by preventing nuclear entry of SPIN1.Nature structural & molecular biology · 2025Article
- Maternal loss of mouse Nlrp2 alters the transcriptome and DNA methylome in GV oocytes and impairs zygotic genome activation in embryos.Clinical epigenetics · 2025Article
- Cryo-EM structure of the BLOC-3 complex provides insights into the pathogenesis of Hermansky-Pudlak syndrome.Nature communications · 2025Article
- Identification of a novel TLE6 mutation linked to embryonic arrest and limited rescue by mRNA supplementation.Frontiers in medicine · 2025Article
- Unraveling the mysteries of early embryonic arrest: genetic factors and molecular mechanisms.Journal of assisted reproduction and genetics · 2024Review
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The subcortical maternal complex (SCMC) plays a crucial role in early embryonic development. Malfunction of SCMC leads to reproductive diseases in women. However, the molecular function and assembly basis for SCMC remain elusive. Here we reconstituted mouse SCMC and solved the structure at atomic resolution using single-particle cryo-electron microscopy. The core complex of SCMC was formed by MATER, TLE6 and FLOPED, and MATER embraced TLE6 and FLOPED via its NACHT and LRR domains. Two core complexes further dimerize through interactions between two LRR domains of MATERs in vitro. FILIA integrates into SCMC by interacting with the carboxyl-terminal region of FLOPED. Zygotes from mice with Floped C-terminus truncation showed delayed development and resembled the phenotype of zygotes from Filia knockout mice. More importantly, the assembly of mouse SCMC was affected by corresponding clinical variants associated with female reproductive diseases and corresponded with a prediction based on the mouse SCMC structure. Our study paves the way for further investigations on SCMC functions during mammalian preimplantation embryonic development and reveals underlying causes of female reproductive diseases related to SCMC mutations, providing a new strategy for the diagnosis of female reproductive disorders.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.