Photoreceptors regulate cell growth through altered auxin synthesis, transport and signalling. ➀ Wavelength-specific activation of the photoreceptors UV Resistance Locus 8 (UVR8), cry, phyB and phyA triggers their nuclear accumulation [3]. PhyB activation by red light is reversed by far-red light and spontaneous conversion that is accelerated at high temperature [6,7,8]. ➁ Active photoreceptors trigger Phytochrome Interacting Factor (PIF) phosphorylation, which leads to degradation for PIF4 and PIF5 and inactivation for PIF7 [9]. ➂ Free PIFs bind to promotors of YUCCAs, HFR1 and many other target genes and stimulate their expression [10,11,12,13,14,15,16,17,18]. HFR1, which is stabilised in UV-B via UVR8, inhibits DNA binding of PIFs [19]. ➃ Auxin synthesis mainly occurs in a two-step pathway [20,21,22,23,24]. Trp is first converted to IPyA by TAA1 and TARs [21,23,24]. IPyA is next converted to active IAA auxin via YUCCA [20,22,24]. Negative feedback on IPyA levels occurs through reversal to Trp via VAS1 and IPyA glucosylation by UGT76F1 [25,26]. IAA is also inactivated by conjugation to amino acids via GH3 proteins [27]. ➄ In the nucleus, IAA interacts with the TIR1/AFB receptors of the SCFTIR1/AFB receptor complex. Upon IAA binding, SCFTIR1/AFB ubiquitinates Auxin/Indole Acetic Acids (AUX/IAA) proteins, which leads to AUX/IAA degradation [28]. In the absence of IAA, AUX/IAAs inhibit auxin signalling by interacting with Auxin Response Factors (ARFs), preventing their DNA binding and transcriptional activity. ARF activity is further reduced by photoreceptor stabilisation of AUX/IAAs, and the formation of a transcriptionally inactive photoreceptor-AUX/IAA-ARF complex [29,30,31]. PhyB inactivation in persistent shade enhances auxin signalling through reduced expression of the TIR1-targeting miR393 [32]. ➅ The transcriptional activity of ARFs is reinforced by the formation of a trans-activating transcription factor module together with BZR and PIF [33,34,35]. BZR1, ARF and PIF are all inhibited by interaction with growth-repressive DELLA proteins, forming the BAP/D module [36]. DELLA repression is alleviated by GA-mediated DELLA degradation in persistent shade conditions. Besides DELLAs, various active photoreceptors have also been shown to inhibit the activity of BZR1, ARF and PIF [37,38,39]. Active BZR1, ARF and PIF target many shared and unique target genes, including genes involved in auxin inactivation and transport, as well as gibberellin synthesis and cell growth [36,40]. ➆ Phot1 associates with NPH3 at the plasma membrane [41]. Phot1 activation by unilateral blue light leads to phot1 autophosphorylation. This triggers NPH3 dephosphorylation and a loss of PIN3 from the outer endodermal plasma membrane on the illuminated side of the hypocotyl (for details see Figure 2) [42,43,44]. ➇ Polar redistribution of PIN3 occurs in response to photoreceptor cues [43,44,45]. Moreover, PIN3 can be phosphorylated by PID, D6PK and AGC1-12 kinases that are required for various photoreceptor-mediated growth responses [43,46,47]. Polar localisation of PIN3 allows for directed auxin flow towards target tissues (for details see Figure 2). ➈ Auxin stimulates apoplast acidification through SAUR19-mediated activation of H+-ATPases [48,49,50]. This enhances the activity of cell wall modifying enzymes and results in acid growth [51,52,53,54,55]. This figure was created using BioRender.com.