Figure 5

Mll1 deficiency alters the retinal cell type composition at P24 but not at P0. (A) Immunostaining of retinal cross-sections from P24 CreNeg and Mll1KO mice with antibodies to specific markers for inner retinal cell types (green): Brn3a for Ganglion Cells (GC); Calbindin for Horizontal Cells (HC); Calretinin for starburst Amacrine Cells (AC); Protein Kinase C-alpha (PKC- A) for On-Bipolar Cells (BC); Glutamine Synthetase (GS) for Muller Glia (MG). Antibody information is given in Supplementary Table S2. (B) Cell count changes of each inner retinal cell type in Mll1KO retinas, presented as mean cell number relative to CreNeg, with error bars representing standard error of mean (SEM, n = 4). *p < 0.01, n.s. = not significant by two-way ANOVA. (C) Schematic diagram showing when progenitors of each retinal cell type exit the cell cycle. Early-born cell types include GC, HC, and Cone (light gray arrows); late-born cell types include Rod, BC, and MG (black bars). Different subtypes of amacrine cells (ACs) are born at both early and late times (indicated by dark gray bar). (D) Immunostaining of P0 retinal cross-sections for markers of early-born cell types: Brn3a for GC, Onecut1 (OC1) for HC, AP-2 alpha (AP-2a) for early-born AC and RXRγ for Cone. (E) The number of cells reactive for each marker per retina cross-section was counted. Results are presented as mean cell number relative to CreNeg with error bars representing SEM. n.s. = not significant by two-way ANOVA with Tukey’s multiple comparisons (n = 3).