Fig 1: Fat3 localizes WRC components that are essential for AC migration(A and B) Anti-Abi1/2 immunostaining of E16.5 WT(A) and Fat3?™/?™ (B) retinas shows a change in Abi1/2 localization in the absence of Fat3.(C–E) In P0 Fat3?™/+ retinas (C'), Abi1/2 is enriched in the nascent IPL. By contrast, significantly more Abi1/2+ processes point away from the IPL in Fat3?™/?™ retinas (D') (7.50 ± 0.86 processes per field, N = 3, n = 8) than in Fat3?™/+ controls (2.33 ± 0.66 processes per field, N = 3, n = 9, p = 0.0002, t test), quantified in (E).(F–G') Anti-Bhlhb5 and DAPI staining of retinal sections from P11 control (F) and Abi1 cKO homozygotes (G) reveals AC migration defects.(H) Quantification of nuclei in the IPL for Six3CRE/+; Abi1fl/+ (N = 3,n = 12) and Six3CRE/+;Abi1fl/fl (N= 3, n = 12). Mann–Whitney test was used.(I) Quantification of Bhlhb5+ cells in the IPL and GCL. t test was used.(J and K) Deletion of Abi1 from the retina does not induce ectopic synapses, as seen by anti-VGAT staining of P6 control (Six3CRE/+;Abi1fl/+) and mutant (Six3CRE/+;Abi1fl/fl) retinal sections.(L) Quantification of mean VGAT fluorescence intensity in IPL normalized to upper INL for Six3CRE/+; Abi1fl/+ (N = 3,n = 14) and Six3CRE/+;Abi1fl/fl (N= 4, n = 18) retinas. Mann–Whitney test was used. Scale bars: 20 µm. Each field is 291.2 µm long.(M) Diagrams summarizing the key findings of this study. Data are represented as mean ± SEM.See also Figure S7.