GNA13 loss results in abnormal GC architecture and altered chemokine-directed migration. (A) GNA13 mutations identified by exome sequencing in GC B-cell subtype (GCB) DLBCL and Burkitt lymphoma (BL) are depicted along the length of the gene, shown in gray. Colored lines indicate the type of mutation (blue corresponding to missense, red for nonsense, and green for deletion) and the colored boxes represent important functional domains. The switch domain, shown in yellow, is important for initiating conformational changes in GNA13 that affect its guanosine triphosphate binding affinity. The nucleotide binding (NB) domain, shown in orange, forms the guanosine triphosphate binding site. The pie chart (right) shows the percentage of GNA13 mutations that are missense, nonsense, or deletion. (B) Immunofluorescent staining of GC B cells (GL7⁺, white) in sections of spleen from 3-month-old AID-Cre⁺Gna13 cohort mice. Images are representative of 3 animals per genotype. (C) Dot plot showing the percentage of CXCR4⁺CD83⁻ GC cells (DZ) compared with CXCR4⁻CD83⁺ (LZ) cells in GC B cells from Peyer patches of AID-Cre⁺Gna13 mice. Dots represent individual animals, with DZ cells indicated in black and LZ cells indicated in white. (D) Box and whisker plot of the average DZ:LZ ratio across genotypes. Data are the summation of 3 experiments. (E) Transwell migration of splenic GC cells isolated from 2-month-old AID-Cre⁺Gna13 mice with and without CXCL12 stimulation. (F) Same as panel E, depicted as chemotactic index, the number of cells that migrated over 3 hours toward 100 ng/mL CXCL12 divided by the number of cells that migrated in the absence of chemokine. Data are the representative of 4 experiments.