Managed to break a main stem, tried my best to get her back on in rapid fashion, but it was a 95% clean break, so I can't expect 🙃 much. Oh well, that's what I get for cracking bad jokes.
Genetics is the study of heredity, the passing of traits from parents to offspring, while photomorphogenesis is the developmental process in plants where light influences growth and development. Genetics focuses on the fundamental principles of heredity and gene expression, while photomorphogenesis specifically investigates how light signals affect plant morphology, including growth, elongation, and overall development.
Photomorphogenesis, the light-mediated developmental process in plants, involves complex gene expression regulation. This regulation occurs at multiple levels, from the initial perception of light signals by photoreceptors to the activation of specific gene networks and post-transcriptional modifications.
Recommend this literature.
https://onlinelibrary.wiley.com/doi/full/10.1111/pce.12934
Photomorphogenic responses to ultraviolet-B light
Gareth I. Jenkins
First published: 09 February 2017
https://doi.org/10.1111/pce.12934
Citations: 173
A further response involving UVR8 and auxin signaling is leaf epinasty, which is the downward curling of leaf edges away from incident light.
A recurrent theme in recent research is that UVR8 often functions through interaction with other signaling pathways. In particular, several studies highlight an interaction between UVR8 and the hormonal pathways that regulate extension growth. One example is the role of UVR8 in suppressing the shade avoidance response. Many plant species respond to the presence of neighbouring vegetation by stimulating extension growth as a result of increased auxin biosynthesis. Leaves absorb red light but reflect far-red light, and therefore shading by vegetation leads to a relative decrease in the ratio of ambient red:far-red light, which is detected by phytochrome, causing a decrease in Pfr relative to Pr (Casal 2013; Fraser et al. 2016). In turn, the decrease in Pfr/Pr leads to an increase in stability and activity of several PHYTOCHROME INTERACTING FACTOR (PIF) transcription factors, notably PIFs 4, 5 and 7, which stimulate expression of auxin biosynthesis genes, leading to extension growth (Hornitschek et al. 2012; Li et al. 2012). Hayes et al. (2014) showed that UV-B antagonizes shade avoidance responses in Arabidopsis elicited by low red:far-red light, and the UV-B effect was strongly impaired in uvr8 mutant plants. UV-B, detected by UVR8, inhibited the increase in expression of auxin biosynthesis and signaling genes promoted by reduced red:far-red light. Furthermore, UVR8 signaling stimulated GA2OXIDASE1 expression, which causes reduced levels of gibberellic acid and consequent stabilization of DELLA proteins, which antagonize PIF activity (De Lucas et al. 2008; Feng et al. 2008). Whereas the effect of UV-B on GA2OXIDASE1 expression required HY5/HYH, that on the auxin related genes did not. The experiments further showed that UV-B elicited destruction of PIFs 4 and 5 and the stabilization of DELLA proteins, although it remains to be established directly whether the effects on these proteins are mediated by UVR8. Thus, UV-B, detected by UVR8, signals to plants that they are in sunlight and negates shade-induced extension growth by antagonizing PIF action and auxin biosynthesis.
UV-B also inhibits the morphogenic responses caused by exposure to elevated temperature, which include hypocotyl extension in seedlings and petiole extension and leaf elevation in mature plants; again, the effect of UV-B is substantially mediated by UVR8 (Hayes et al. 2016). However, in contrast to the action of UV-B in suppressing shade avoidance, UV-B inhibition of thermomorphogenesis does not involve either PIF destruction or an effect on DELLA proteins. PIF4 is a key regulator of thermomorphogenesis, promoting expression of genes concerned with auxin biosynthesis and signaling. UV-B inhibits PIF4 transcript accumulation, consequently preventing an increase in PIF4 protein, and also stabilizes the LONG HYPOCOTYL IN FAR-RED 1 transcription factor, which binds to PIF4, impairing its ability to bind to DNA. Together, these mechanisms block the accumulation and activity of PIF4 at elevated temperature (Hayes et al. 2016). The inhibition of thermomorphogenesis by UV-B is likely to be advantageous for plants, as it will prevent detrimental extension growth under natural conditions where elevated temperature is often accompanied by exposure to relatively high levels of UV-B.
Another auxin-regulated growth response is phototropism. It is well established that phototropism in response to unilateral UV-A/blue light is mediated by phototropins, which direct accumulation of auxin on the non-illuminated side of the stem, causing localized extension and hence bending towards the light source (Christie & Murphy 2013). Vandenbussche et al. (2014) reported that UV-B can also induce phototropic bending and that the UV-B response in phot1phot2 mutant plants requires UVR8. However, UV-B-induced bending is slower in phot1phot2 than in wild type, indicating that phototropin action is involved in the wild-type UV-B response, and that the phototropin-mediated response is faster than that mediated by UVR8 (Vandenbussche & Van Der Straeten 2014; Vandenbussche et al. 2014). Moreover, the response mediated by phototropin is initiated at lower fluence rates than that mediated by UVR8 (Vanhaelewyn et al. 2016b). The UV-B-induced phototropic response involves the establishment of an auxin gradient across the hypocotyl, as in the UV-A/blue light response, but formation of the gradient in UV-B does not require phototropins and involves some different auxin signaling components to phototropism mediated by UV-A/blue light (Vandenbussche et al. 2014). UVR8 mediates repression of genes involved in auxin biosynthesis and signaling, which likely contributes to the generation of the auxin gradient across the hypocotyl. Vandenbussche & Van Der Straeten (2014) showed that the accumulation of HY5 on the UV-B exposed side of the hypocotyl (demonstrated using a HY5-YFP fusion) correlated with UVR8 response kinetics and is likely to mediate the repression of auxin biosynthesis genes on the illuminated side.
A further response involving UVR8 and auxin signaling is leaf epinasty, which is the downward curling of leaf edges away from incident light. Epinasty is stimulated by UV-B exposure (Wilson & Greenberg 1993; Jansen 2002) and also by the action of phyB, whereas phototropins promote leaf flattening (Kozuka et al. 2013). Fierro et al. (2015) showed that the epinastic response to UV-B in Arabidopsis is mediated by UVR8, most likely through the regulation of auxin transport. Moreover, they found considerable overlap in the sets of genes regulated by UVR8 and phyB, notably in the repression of genes involved in auxin action. The phyB action in epinasty involves the regulation of specific PIFs (Johansson & Hughes 2014), and there is evidence that PIFs are required for the UV-B-induced response (Fierro et al. 2015). A possible scenario is that UV-B de-stabilizes PIFs, as in the inhibition of shade avoidance, causing the repression of auxin response genes and consequently initiating the changes in auxin transport associated with the epinastic response.
Fasano et al. (2014) highlighted the potential interactions between UVR8 and abiotic stress signaling pathways and proposed that the cross-talk may involve auxin signaling. They reported that high salt and osmotic stress stimulate UVR8 expression and that a uvr8 mutant has increased salt tolerance under UV-B conditions. In addition, the reduced extension growth of plants over-expressing UVR8, previously observed by Favory et al. (2009), was enhanced under osmotic stress. Fasano et al. (2014) found that the UVR8 over-expression phenotype is due to reduced cell expansion and suggested that the phenotype could be explained by altered auxin signaling. Abiotic stresses such as drought, salinity and high temperature will often be accompanied by relatively high fluence rates of UV-B in nature, and the interplay between UVR8 signaling and auxin signaling could be modulated under such conditions to regulate growth and promote survival.
The stimulation of stomatal closure by UV-B involves interaction of UVR8 with different signaling pathways to those that regulate growth responses. In species such as Vicia faba (Jansen & Noort 2000) and Arabidopsis (Eisinger et al. 2003; He et al. 2013; Tossi et al. 2014), low fluence rates of UV-B stimulate stomatal opening whereas higher fluence rates promote closure. He et al. (2013) showed that the closure response in Arabidopsis is mediated by an increase in H2O2, generated through NADPH oxidase activity. UV-B-induced cytosolic alkalinization is involved in mediating the increase in H2O2 production (Zhu et al. 2014). In turn H2O2 stimulates NO production (He et al. 2013). Inhibition of endogenous NO accumulation prevents closure even under conditions where H2O2 remains high (Tossi et al. 2014). Tossi et al. (2014) found that UV-B-induced stomatal closure is impaired in uvr8, with a concomitant reduction in H2O2 and NO accumulation in the guard cells. Nevertheless, the mutant stomata were viable, and they closed when either a NO donor or abscisic acid was added. It is likely that UVR8 acts to promote H2O2 and hence NO accumulation, but it is not clear how it does so. The UVR8 action likely involves gene expression, because a mutant lacking the HY5/HYH transcription factors is impaired in the closure response (Tossi et al. 2014), but the relevant target genes are not known.
The ability of UVR8 to influence auxin and gibberellic acid signaling, as well as redox signaling, is likely to affect a larger number of physiological processes than reported to date. Furthermore, it is likely that interactions between UVR8 and additional signaling pathways will be discovered. UVR8 photoreception leads to sequestration of COP1 and stimulation of HY5 accumulation, and both these proteins participate in a range of cellular processes (Lau & Deng 2012; Huang et al. 2014a; Gangappa & Botto 2016). For instance, COP1 is involved in controlling abundance of the flowering time regulator CONSTANS (Jang et al. 2008; Liu et al. 2008; Sarid-Krebs et al. 2015), and hence UVR8 activation might influence flowering time, as suggested in some studies (Morales et al. 2013; Fasano et al. 2014). HY5 binds to over 9000 genomic loci in Arabidopsis (Zhang et al. 2011) and regulates genes in numerous processes (Gangappa & Botto 2016). Thus, regulation of HY5 provides a potential mechanism for UVR8 to influence several aspects of plant physiology. Figure 3 illustrates some of the known and potential interactions involving UVR8.