Skip to main content
. Author manuscript; available in PMC: 2021 Jan 6.
Published in final edited form as: Curr Biol. 2019 Dec 12;30(1):17–30.e3. doi: 10.1016/j.cub.2019.11.005

Figure 7. Regulation of I-a identity by seven Grs.

Figure 7.

(A) Summary of previous data showing that misexpression of Gr59c in I-b induced a change in response profile to one resembling I-a, and that loss of Gr59c from I-a induced a change in profile to one resembling I-b [19]. (B) Confirmation that misexpression of Gr59c in I-b suppresses response to bitter compounds. The values for the control genotype “+” were from Figure 2. One-way ANOVA followed by Dunnett’s multiple comparison test, n=6-10. (C) New mutations confirm that loss of Gr59c or Gr89a from I-a leads to novel responses to TPH, CAF, THE, and COU; these responses depend on Gr66a, Gr93a, Gr33a, and Gr39a as shown. One-way ANOVA followed by Dunnett’s multiple comparison test, n=10-23. (D) Model for regulation of bitter response in I sensilla. Expression of four receptors, Gr33a, Gr39a.a, Gr66a, and Gr93a, together confer response to CAF, COU, THE, TPH, and UMB. In I-a, Gr32a, Gr59c, and Gr89a are all required to block the four receptors from conferring responses to these tastants. See also Figure S6.