Skip to main content
. 2020 Mar 15;459(2):126–137. doi: 10.1016/j.ydbio.2019.12.009

Fig. 5.

Fig. 5

Apical FERM domain proteins and the Exocyst promote apical localisation of Crb.

A) Mutant clones for moesin, marked by absence of GFP, show normal Crb localization (n ​> ​12 stage 6–9 egg chambers; scale bar approximately 10 ​μm).

B) Double mutant clones for merlin and expanded, marked by absence of GFP, show normal Crb localization (n ​> ​6 stage 6–9 egg chambers; scale bar approximately 10 ​μm).

C) Double mutant clones for merlin and moesin, marked by absence of GFP, show normal Crb localization (n ​> ​14 stage 6–9 egg chambers; scale bar approximately 10 ​μm).

D) Triple mutant clones for merlin, expanded and moesin, marked by absence of GFP, show loss of apical Crb localization (n ​> ​4 stage 6–9 egg chambers; scale bar approximately 10 ​μm).

E) Mutant clones for crbΔFBM, marked by absence of GFP, showing weakly reduced apical Crb localization (n ​> ​3 stage 6–9 egg chambers; scale bar approximately 10 ​μm).

F) Mutant clones for crbΔFBM, marked by absence of GFP, showing strongly reduced apical Crb localization (n ​> ​6 stage 6–9 egg chambers; scale bar approximately 10 ​μm).

G) Mutant clones for sec15, marked by absence of GFP, show loss of apical Crb localization (n ​> ​5 stage 6–9 egg chambers; scale bar approximately 10 ​μm).

H) Mutant clones for sec15, marked positively by expression of GFP, show loss of apical Crb localization in extruded cells (n ​> ​7 stage 6–9 egg chambers; scale bar approximately 10 ​μm).

I) Quantification of average apical Crb fluorescence pixel intensity, measured with Image J in n ​> ​20 ​cells per genotype.

J) Zoom image of (G) showing mislocalisation of Crb in sec151 mutant cells.