UMass Chan Medical School Faculty Publications


MED20 is essential for early embryogenesis and regulates NANOG expression

UMMS Affiliation

Division of Genes and Development, Department of Pediatrics; Rivera Lab

Publication Date


Document Type



Cell Biology | Developmental Biology | Nucleic Acids, Nucleotides, and Nucleosides | Physiological Processes | Reproductive and Urinary Physiology


Mediator is an evolutionarily conserved multi-subunit complex, bridging transcriptional activators and repressors to the general RNA polymerase II (Pol II) initiation machinery. Though the Mediator complex is crucial for the transcription of almost all Pol II promoters in eukaryotic organisms, the phenotypes of individual Mediator subunit mutants are each distinct. Here, we report for the first time, the essential role of subunit MED20 in early mammalian embryo development. Although Med20 mutant mouse embryos exhibit normal morphology at E3.5 blastocyst stage, they cannot be recovered at early post-gastrulation stages. Outgrowth assays show that mutant blastocysts cannot hatch from the zona pellucida, indicating impaired blastocyst function. Assessments of cell death and cell lineage specification reveal that apoptosis, inner cell mass, trophectoderm and primitive endoderm markers are normal in mutant blastocysts. However, the epiblast marker NANOG is ectopically expressed in the trophectoderm of Med20 mutants, indicative of defects in trophoblast specification. These results suggest that MED20 specifically, and the Mediator complex in general, are essential for the earliest steps of mammalian development and cell lineage specification.


Mediator Med20, Mouse embryo, Nanog, Trophectoderm, Cell lineage specification

DOI of Published Version



Cui W, Marcho C, Wang Y, Degani R, Golan M, Tremblay KD, Rivera-Pérez JA, Mager J. MED20 is essential for early embryogenesis and regulates NANOG expression. Reproduction. 2019 Mar;157(3):215-222. doi: 10.1530/REP-18-0508. PMID: 30571656; PMCID: PMC6545164. Link to article on publisher's site

Related Resources

Link to Article in PubMed

Journal/Book/Conference Title

Reproduction (Cambridge, England)

PubMed ID