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. Author manuscript; available in PMC: 2016 May 27.
Published in final edited form as: Annu Rev Neurosci. 2015 Apr 22;38:331–349. doi: 10.1146/annurev-neuro-071714-034145

Figure 4.

Figure 4

An unfolded protein response (UPR)–based model for tas1R feedback. (a) Some cells choose tas1R2 for expression, leading to production of TAS1R2 protein. This protein fails to exit the endoplasmic reticulum (ER), activating the UPR. The UPR in turn promotes transcription of tas1R3, which couples with TAS1R2 to allow exit from the ER, similar to the role of RTP1 with olfactory receptors (ORs). Feedback could also act to prevent transcription of tas1R1. (b) Likewise, tas1R1 choice promotes UPR activation, driving transcription of tas1R3, ER exit of the coreceptor, and cell surface expression. (c) In contrast, choice of a deleted tas1R2 copy would fail to activate the UPR, allowing for choice of a second tas1R gene and explaining how, in tas1R1 mutants, tas1R2 expression expands.