Fig. 3: MiR-155 primarily controls KDM2A expression in high affinity cMyc⁺ LZ GC-B cells.

a Heat map showing the transcript levels of the enzymes involved in the demethylation of histone H3K36me2. The bulk RNA-seq dataset from WT and KO cMyc⁺ LZ GC-B cells was used. FDR values are shown. b Sequence alignment of a part of the 3’UTR of Kdm2a. The 8-mer miR-155 binding site is highlighted in a box. c Immunofluorescence staining of splenic section from a WT mouse seven days after SRBC immunization, showing IgD (white), MYC (red) and KDM2A (blue). Scale bar, 50 µm. Representative section images from two experiments (WT n = 4; KO n = 4). d Scatter plots show the MI of MYC and KDM2A within segmented GC cells in spleen sections from immunized WT and KO mice. The Pearson correlation coefficient (r) is presented with a 95% confidence interval in red. A.U., arbitrary unit. e Relative MFI of KDM2A in cells from four GC-B cell subpopulations. GC-B cells were derived from WT or KO donor B cells seven days after HEL^3 × -SRBC immunization. Pooled from two independent experiments (WT n = 11; KO n = 9). Unpaired student’s t-test, two-tailed. f Relative MFI of KDM2A in cells from four GC-B cell subpopulations. GC-B cells were derived from WT or KO donor B cells seven days after HEL^3 × -SRBC immunization. Low and high affinity were determined based on HEL^3 × binding within Igκ⁺ GC-B cells. Pooled from two independent experiments (WT n = 11; KO n = 9). RCN, relative cell number. Paired student’s t-test, two-tailed. Unless otherwise stated, mean ± SEM is indicated. n.s., not significant.