Figure 1. Signalling with G-proteins. (a) Monomeric GTPases, RAC/ROP. These operate by shuttling between the inactive GDP-bound and the activated GTP-bound forms that activate downstream effectors. (b) Heterotrimeric G protein-coupled receptors (GPCRs). GPCRs have seven transmembrane spanning domains (orange). Binding of the agonist to GPCR stimulates its intrinsic GEF activity on G that allows GTP binding and dissociation of G and G subunits. Both these subunits can interact with downstream effectors (E1 and E2) and activate cellular responses.

Figure 2. Hormone perceptions by cell surface receptors of the two-component system. (a) The prototype of the so-called two-component phosphorelay signalling mechanism in prokaryotes. (b) The ethylene signal transduction. (c) The cytokinin signal transduction.

Figure 3. Signalling with receptor-like kinases. Upper panel illustrates the innate immunity signalling in response to the bacterial elicitor, flagellin, the clavata meristem maintenance signalling, the brassinosteroid hormone perception and the nod factor signalling during symbiosis. The lower panel shows the signalling pathway for the regulation of stomata density, the regulation of cell density-dependent proliferation by the photosulfokine peptides (PSKs) and the systemic wound response signalled by the binding of the systemin peptide to the SR160 LRR–RLK receptor.

Figure 4. Hormone perception involves direct binding to intracellular signalling proteins. (a) Auxin signal transduction. Within the cell the TIR1 and a small family of related F-box proteins were identified as the auxin receptor. Dependent on auxin binding, TIR1 associates with the Aux/IAA transcriptional regulators and targets these for degradation. (b) Studies of giberellin signal transduction in rice revealed a conceptually similar mechanism to auxin. However, GA binds to an adaptor protein, GID1 and regulates the recruitment of the DELLA transcriptional repressor protein, called SLR1 in rice, to the F-box protein, GID2 and thus SLR1 is targeted for degradation. (c) Central to JA-signalling is also an F-box protein, COI1, which is part of an E3 Ubiquitin ligase complex. How JA signalling operates is less understood; we only know some of the components involved. (d) ABA is mostly known for its effects during dormancy. Recently, it was found to regulate flowering time by binding to the FCA protein and thereby disrupting its interaction with FY. The FCA–FY complex prevents the accumulation of the FLC mRNA. FLC is a potent repressor of flowering.

Figure 5. Light signalling mechanisms. (a) The rapid pathway. Red/far red light induces the conversion of phytochrome B (phyB) from its red (PrB) to farred (PfrB) form leading to its translocation from the cytoplasm to the nucleus to promote gene transcription. (b) Gene expression based on light-dependent protein degradation. The b-ZIP transcription factor HY5 is rapidly turned over by the COP1-dependent proteolysis system in the dark, but white light induces the translocation of COP1 from the nucleus to the cytoplasm while blue light alters COP1 function in a CRY-dependent fashion, leading to the inactivation of COP1 and thus the stabilization of HY5 that triggers the transcription of light-induced genes.