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. 2015 Sep 21;34(20):2537–2556. doi: 10.15252/embj.201488044

Figure EV1.

Figure EV1

tmem-17 loss-of-function phenotypes, TZ markers in tmem-138 mutants, and TZ negative interaction hierarchy data
  1. Disruption of tmem-17 alone does not cause overt ciliary defects as measured by uptake of fluorescent dye through environmentally exposed cilia. tmem-17;nphp-4 double mutants are defective in dye uptake while tmem-17;mks-2,tmem-17;mksr-1 and tmem-17;mks-3 take up the dye similar to tmem-17 alone. Scale bar: 20 μm.
  2. tmem-17 mutants avoid high-osmolarity solutions, as do tmem-17;mks-2,tmem-17;mksr-1, and tmem-17;mks-3 double mutants. tmem-17;nphp-4 double mutants are partially defective in sensing osmolarity, though not as severely as osm-5 (IFT mutant) animals, which are completely oblivious of the hyperosmotic barrier (*P < 0.0001, chi-squared test).
  3. TZ markers expressed in wild-type and the tmem-138 mutants. MKS-5, TMEM-231 (MKS module), and NPHP-4 (NPHP module) do not require TMEM-138 for TZ localisation. Scale bars: 4 μm.
  4. Model showing all of the negative interaction amongst MKS/NPHP proteins, where a particular MKS/NPHP protein (at the arrowhead) is localised properly in a specific TZ mutant; a white circle on the arrowhead indicates new data obtained in this study.