Extended Data Fig. 2: Transcriptional adaptation is independent of the loss of protein function.
From: Genetic compensation triggered by mutant mRNA degradation
a, qPCR analysis of epas1a, epas1b, vegfab, emilin3a and alcamb mRNA expression levels in wild-type and hif1ab, vegfaa, egfl7 and alcama mutant embryos injected (inj.) with eGFP mRNA (control; ctrl) or wild-type hif1ab, vegfaa, egfl7 or alcama mRNA. b, qPCR analysis of vclb, epas1a, epas1b and emilin3a mRNA expression levels in vcla, hif1ab and egfl7 wild-type, heterozygous and mutant zebrafish. c, qPCR analysis of hbegfa, hif1ab, vegfaa and alcama mRNA expression levels in hbegfa, hif1ab, vegfaa and alcama wild-type and heterozygous zebrafish, using primers specific for the wild-type allele. d, qPCR analysis of Fermt1 and Rel mRNA expression levels in wild-type and Fermt2 and Rela knockout cells transfected with empty vectors (control) or plasmids encoding wild-type FERMT2 or RELA. e, Western blot analysis of FERMT2 and ACTB levels in Fermt2 knockout cells transfected with empty vectors (control) or plasmids encoding wild-type FERMT2. f, Western blot analysis of RELA and ACTB levels in Rela knockout cells transfected with empty vectors (control) or plasmids encoding wild-type RELA. g, qPCR analysis of Actg1 mRNA expression levels in wild-type and heterozygous Actb mESCs. n = 3 biologically independent samples. Wild-type or control expression levels were set at 1 for each assay. Data are mean ± s.d., and a two-tailed Student’s t-test was used to calculate P values (a–d, g). The experiments in e, f were performed only once. For the source data for western blots, see Supplementary Fig. 1.
