Figure 6: DYNC2LI1 mutations delay retrograde IFT and lead to the ciliary accumulation of IFT components.
From: Mutations in DYNC2LI1 disrupt cilia function and cause short rib polydactyly syndrome
(a) Immunofluorescence micrographs of control and SRPS cells stained as labelled. Cilia (2 × ) are shown on the right. (b) Expression of untagged wild-type DYNC2LI1 through an IRES-GFP vector (artificially coloured blue) rescues ciliary accumulation of IFT components. (c) Quantification of IFT88 signal: graph shows the mean ratio of IFT88 signal between the cilium body and its proximal end±s.e.m (n=20 × 3 independent experiments). Statistical analyses were performed using Mann–Whitney test, *P<0.05. Scale bar, 5 μm.
