Fig. 6: Defects in the NCT complex leads to transcriptional de-repression of cdr1B and over-production of CDR1B protein.

a Expression levels of cdr1B transcripts in the nctA null and the nctB null mutant in RNA-seq analysis: *, FDR < 0.05. b In vivo binding of NctA on the 5′-upstream region of cdr1B. Tracks for the NctA ChIP-seq (ChIP) and their input DNA control (Input) are visualised in the UCSC genome browser together with annotated gene models and their transcript, which are expressed in the no-drug conditions. The direction of the target gene and the 5′-proximal gene are shown in red arrows and blue arrows, respectively. c Representative western blot (WB) showing the increase in CDR1B protein levels in the ∆nctA mutant. Cell-free extracts were resolved via SDS-PAGE, and probed for CDR1B using a CDR1B-specific antibody. Ponceau S staining was performed as an overall loading control. d Relative protein levels of CDR1B. The relative intensity of the CDR1B signal was quantified by densitometric scanning. The data represent the mean results of two biological replicates, and the error bars signify the standard deviations. Source data are provided as a Source Data file.