Figure 7.
Sdk controls the timing of Pyd localization to vertices. (Refers to Fig. S4 and Video 6.) (A–H) Pyd::GFP dynamics relative to F-actin (A–D) and mC::Abi (E–H) at 28 h APF. (A and E) Snapshots of a dynamic cell contact. (A′ and C′) Kymographs of the LC–LC contacts shown above. Pyd::GFP at vertices increases during expansion and decreases during contraction. (B–D) Pearson correlation charts for contact length, F-actin, and Pyd in WT. Contact length correlates positively with F-actin at a shift of −1 min (B) and with Pyd at a shift of +2 min (C). (D) Actin correlates positively with Pyd at a shift of +1 min. (F–H) Pearson correlation charts for contact length, Abi, and Pyd in WT eyes. (F and G) Contact length correlates positively with Abi at a shift of −3 min and with Pyd at a shift of +3 min. (H) Abi correlates positively with Pyd at a shift of +2 min. (I) 26 h APF; a sdk mutant MARCM clone stained for Pyd and E-cad. Pyd levels decrease at vertices in the sdk clone. Representative vertices are marked with arrowheads. (J) Pyd accumulation at vertices is reduced in sdk clones at 26 h APF (unpaired t test, n = 77 sdk and 73 WT contacts in 2 eyes, P = 0.0001; left) but not at 28 h APF (unpaired t test, n = 30 sdk and 30 WT contacts in 2 eyes, P = 0.8824; right). (K) Snapshots of Pyd::GFP localization in a sdk mutant eyes. (K′) Kymograph of the above contact. Pyd accumulation during expansion is delayed compared with WT. (L) Pearson correlation for contact length versus Pyd in sdk eyes shows peak correlation at a shift of +5 min. (M) The time shift of the peak r values for individual contacts is significantly higher in sdk mutants compared with WT (Mann–Whitney U test, P < 0.0001, n = 24 WT and 15 sdk contacts across 3 retinas each). Scale bars, 5 μm.

Sdk controls the timing of Pyd localization to vertices. (Refers to Fig. S4 and Video 6.) (A–H) Pyd::GFP dynamics relative to F-actin (A–D) and mC::Abi (E–H) at 28 h APF. (A and E) Snapshots of a dynamic cell contact. (A′ and C′) Kymographs of the LC–LC contacts shown above. Pyd::GFP at vertices increases during expansion and decreases during contraction. (B–D) Pearson correlation charts for contact length, F-actin, and Pyd in WT. Contact length correlates positively with F-actin at a shift of −1 min (B) and with Pyd at a shift of +2 min (C). (D) Actin correlates positively with Pyd at a shift of +1 min. (F–H) Pearson correlation charts for contact length, Abi, and Pyd in WT eyes. (F and G) Contact length correlates positively with Abi at a shift of −3 min and with Pyd at a shift of +3 min. (H) Abi correlates positively with Pyd at a shift of +2 min. (I) 26 h APF; a sdk mutant MARCM clone stained for Pyd and E-cad. Pyd levels decrease at vertices in the sdk clone. Representative vertices are marked with arrowheads. (J) Pyd accumulation at vertices is reduced in sdk clones at 26 h APF (unpaired t test, n = 77 sdk and 73 WT contacts in 2 eyes, P = 0.0001; left) but not at 28 h APF (unpaired t test, n = 30 sdk and 30 WT contacts in 2 eyes, P = 0.8824; right). (K) Snapshots of Pyd::GFP localization in a sdk mutant eyes. (K′) Kymograph of the above contact. Pyd accumulation during expansion is delayed compared with WT. (L) Pearson correlation for contact length versus Pyd in sdk eyes shows peak correlation at a shift of +5 min. (M) The time shift of the peak r values for individual contacts is significantly higher in sdk mutants compared with WT (Mann–Whitney U test, P < 0.0001, n = 24 WT and 15 sdk contacts across 3 retinas each). Scale bars, 5 μm.

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