Skip to main content
. 2021 May 6;106(6):1523–1540. doi: 10.1111/tpj.15250

Figure 6.

Figure 6

Proposed model of the role of the NIT1 family of nitrilases in hypocotyl elongation (thermomorphogenesis) in the absence and presence of the chemical compound Heatin.

(a) In absence of the chemical compound Heatin. Hypocotyl elongation in high temperature conditions (27°C; green letters) requires the NIT1‐subfamily of nitrilase enzymes (orange oval). Members of the NIT1‐subfamily convert the auxin precursor indole‐3‐acetonitrile (IAN) into bioactive auxin indole‐3‐acetic acid (IAA). Hence, in high temperature conditions IAN substrate levels are relatively low (grey letters) and IAA product levels are relatively high (black letters). A possible direct effect of IAN on hypocotyl elongation (bypassing IAA) cannot be excluded and is here indicated as a grey‐dotted arrow and black question mark. How high temperature interacts with NIT1‐subfamily enzymes is unknown, but IAN substrate conversion by NIT2 is promoted by higher temperatures. Furthermore, NIT2 displays an atypical temperature sensitivity profile (Vorwerk et al., 2001). Eventually, auxin perception and signalling are required for hypocotyl elongation.

(b) In presence of the chemical compound Heatin. In this study, we report on the identification of the chemical compound Heatin (red letters and chemical structure). We demonstrate that NIT1 and NIT2 are required for Heatin‐mediated hypocotyl elongation and propose that Heatin can directly interact with NIT1‐subfamily members to inhibit their activity (orange oval with dashed outline and grey letters). As a result, IAN substrate levels are high in the presence of Heatin (bold black letters). Unanticipated, also a significant rise in the NIT1‐subfamily enzyme product, bioactive IAA, was observed because of Heatin application, which occurs via an unknown mechanism (orange dashed line and question mark). Although unanticipated, a similar finding has been reported before (Piotrowski et al., 2001). This increase in IAA would likely contribute to observed Heatin‐induced hypocotyl elongation. However, as indicated above, we cannot exclude IAN to trigger hypocotyl elongation (bypassing IAA; dotted arrow). Nevertheless, it appears that the main effect of Heatin on hypocotyl elongation is probably not depending on the nitrilases, although nitrilases may indirectly affect the response to Heatin because of their role in the production of IAA. A possible alternative pathway for Heatin action may involve aldehyde oxidase 1 (AAO1) and AAO2 enzymes, as these redundantly contribute to Heatin‐mediated hypocotyl elongation. As AAO activity was proposed to be linked to IAA biosynthesis (Böttcher et al., 2014; Seo et al., 1998) it is possible that this AAO1/AAO2 route contributes to observed increased IAA levels in the presence of Heatin. AAO1/AAO2 might interfere with elongation growth via a yet unknown mechanism (blue dashed lines and question mark).