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. 2020 Jun 19;16(6):e1008885. doi: 10.1371/journal.pgen.1008885

Fig 9. Tctp interacts with other Cora complex proteins.

Fig 9

(A) GST-pulldown of Tctp with Yrt and ATPα. GST-Yrt and GST-ATPα bind to MBP-Tctp. (B) Tctp binds to Yrt N-terminal FERM and FERM Adjacent (FA) domain but not to C-terminal VR domain. (C) Co-immunoprecipitation of Tctp with Yrt and ATPα. Myc-Tctp is coimmunoprecipitated with Flag-Yrt and Flag-ATPα in S2 cell extracts. (D-G’) Genetic interaction of Tctp and Cora partners at 25°C. ey>+ control (D). Tctp RNAi shows reduced eye (D’). yrt RNAi shows normal eye (E) but enhances Tctp RNAi eye phenotype (E’). ATPα RNAi causes about 11% (n = 37) lethality. Most flies show small eye phenotype (F). Double RNAi for Tctp and ATPα leads to 100% (n = 41) lethality (F’). Nrx-IV RNAi by ey-Gal4 causes semi-lethality. Escapers show reduced eyes (G). Double knockdown of Tctp and Nrx-IV results in 100% (n = 40) lethality (G’). (H) Quantification of lethality shown in (D, F, G) (n ≥ 37). Scale bar, 100 μm. (I) A model for Tctp interaction with Cora complex proteins. Cora is required for the maintenance of Tctp. Tctp may stabilize the Cora complex by interacting with Yrt, ATPa and NrxIV. Cora and Tctp may act redundantly to regulate junctional integrity. Hence, the reduction of both Cora and Tctp results in tissue-specific defects such as embryo lethality, loss of eye disc, and overgrowth of the wing disc.