**6. Genetic response**

Several studies have focused on changes in gene expression in plants exposed to long- and short-wave UV-B radiation to identify the cellular components that regulate response to UV [85]. The results showed that UV-B radiation triggers cell growth and morphogenesis pathways [86]. UV-B response signals are also transmitted from cell to cell and are usually organ-specific [87].

Genetic approaches for phenotypic responses to UV-B are based on models of increased tolerance or aberrant responses (e.g., changes in hypocotyl growth) to UV-B irradiation [86]. Transcriptomic analysis from *Arabidopsis* seedlings exposed to different UV-B radiation intensities showed that more than 20% of the genes that modified their expression are transcription factors [85]. These approaches allowed the identification of mutants that lacked or overexpressed photoprotective compounds or inhibited hypocotyl growth in response to UV-B [14, 88].

UV-B radiation induces changes in the expression of genes that affect growth and development, as seen in *UV-B light insensitive* (*uli*) mutant plants, which present reduced hypocotyl growth relative to wild-type after UV-B exposure. Also, UV-B affects *chalcon synthase (CHS)* expression [14]; low levels of irradiation activate this gene, which is key in the biosynthesis of phenylpropanoids [89]. *CHS,* along with transcription factors, allows plants to protect themselves against UV-B.

*LONG HYPOCOTYL5 (HY5)* is a bZIP transcription factor that regulates morphogenesis in response to UV-B. *HY5* gene expression is a component of the UV-B-induced signaling network. Transcriptomic analysis in *Arabidopsis thaliana* showed the importance of HY5-dependent regulation in response to low-level UV-B irradiation [85]. If HY5 is lost, transcriptional induction of the UV-B response genes is impaired [86] and cells undergo programmed death [90].

HY5 is a light-induced transcription factor required for many light-responsive genes; in the dark, it is degraded by the proteasome [91]. This transcription factor is key for phytochrome and cryptochrome regulation networks [85, 92, 93]. So, it seems that HY5 does not respond to UV-B radiation exclusively, which opens the door for research on other components that specifically drive plants' response to UV-B.

Several genes are induced by UV-B independently from traditional photoreceptors, such as phytochromes and cryptochromes, through the activity of the LONG HYPOCOTYL5 (HY5) transcription factor [85]. This independence suggests that there must be a specific UV-B photoreceptor that activates HY5; however, the identity of this putative element is still unclear [94].

CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1) is an E3 ubiquitin ligase that participates in the UV-B response [95]. COP1 has three functional domains, a RING finger (ligase activity), a coiled-coil for dimerization, and a WD40 repeat domain with binding activity [93]. COP1 targets bZIP transcription factors and is required to activate *HY5* gene expression. Both proteins are localized in the nucleus and regulate photomorphogenesis under UV-B conditions in a specialized pathway [95]. COP1 was identified as a photomorphogenesis repressor in darkness and light [93, 96]. Visible light inactivated COP1 and separated it from HY5 [93], allowing HY5 stabilization and, therefore, activation of light-responsive genes [91, 97] through the

interaction of phytochromes and cryptochromes [98, 99]. Phytochromes and cryptochromes interact with the SUPPRESOR OF PHYTOCHROME A (SPA) proteins, causing light-dependent COP1 inactivation. COP1 response to UV-B radiation is independent of the SPA proteins [95, 100]; rather, COP1 responds to UV-B through the interaction with the UV RESPONSE LOCUS 8 (UVR8) protein [96].

UVR8 is a seven-bladed b-propeller protein that forms a homodimer in its inactive state [101, 102] and is capable of UVR-B perception [103, 104]. In contrast to other photoreceptors (phytochrome and cryptochrome), UVR8 does not employ a bound chromophore; instead, it uses a tryptophan residue localized in the b-propeller blade [101, 102, 105]. Upon UV-B absorption, the UVR8 dimer destabilizes and the monomeric form interacts with COP1 [104]. The UVR8-COP1 heterodimer activates the transcription factor HY5, consequently activating downstream genes that are implied in metabolic and morphological alterations [104, 106]; this mechanism activates UV-B acclimation and tolerance [96]. UVR8 is usually located in the cytoplasm, while COP1 is in the nuclear bodies of hypocotyl cells. When plants are irradiated with UV-B, UVR8 translocates to the nucleus [107] and colocalizes to the COP1-rich nuclear bodies [96]. After UV-B exposition, the UVR8 dimer COP1 prevents HY5 degradation, so that HY5 can exert its transcriptional activation function [108].

In Arabidopsis plants, *uvr8* mutants do not respond when grown under UV-B radiation; they lack a photomorphogenic signal and therefore do not display the damage usually found in wild-type plants [96]. UV-B-induced gene expression is important for UV acclimation and survival. When *urv8* and *cop1* mutants are initially grown in weak UV-B exposure and later moved to high UV-B irradiance, the mutants do not show an acclimation effect. When exposed to a natural spectral balance, the *uvr8* mutant shows leaf damage. Also, *HY5* or *CHS* gene expression is undetectable

**Figure 2.** *ELONGATED HYPOCOTYL5 (HY5) transcription factor activation.*

*Ultraviolet Radiation and Its Effects on Plants DOI: http://dx.doi.org/10.5772/intechopen.109474*

in both mutants. Consequently, the interaction between COP1 and UVR8 proteins is required for the regulation of UV-B response and confers UV-B protection. On the other hand, overexpression of *UVR8* leads to UV-B photomorphogenic hypersensitivity, presenting inhibition of hypocotyl growth, activation of *HY5* and *CHS* gene, and accumulation of anthocyanin [96].

COP1 is related to the repression of photomorphogenesis but it seems that UVR8 provides UV-B-specific signaling and that the interaction COP1-UVR8 occurs within minutes [96]. UVR8 is reverted to homodimer (inactive form) through the REPRESSOR OF UV-B PHOTOMORPHOGENESIS proteins (RUP1 and 2). RUP1 and RUP2 are two highly related WD40-repeat proteins that interact directly with UVR8 promoting its homodimerization, thus acting act as negative regulators [104, 108, 109]. *RUP 1* and *RUP 2* are induced by UV-B but act downstream of UVR8-COP1 forming a negative feedback loop that balances UV-B defense [109] (**Figure 2**).

Inhibition of the transcription factor HY5 by binding with COP1 in the absence of UV-B light, the expression of the response genes remains inactive (left). In the presence of UV-B light, the monomeric form of UVR8 enters the nucleus, binds to COP1, and activates HY5 (right).
