Genetic loss of Ncor1 and Ncor2 results in ectopic Fgf8 expression and small somites.
NCOR1/2 corepressors, but not coactivators, are recruited to the Fgf8 RARE by RA.
Genomic deletion of Fgf8 RARE with CRISPR/Cas9 often results in small somite defect.
Nuclear receptor corepressors NCOR1 and NCOR2 mediate RA-dependent Fgf8 repression.