Ultraviolet-B radiation (UV-B, 280-320 nm) is an important environmental signal that regulates growth and development in plants. There are two dose-dependent UV-B response pathways in plants: a specific one, mediated by UVR8 (the specific UV-B receptor) and an unspecific one, which is activated by the oxidative damage produced by radiation. The receptor is constitutively expressed, and, in the presence of UV-B, induces the monomerization of the UVR8 dimer. The monomer then interacts with COP1, an ubiquitin ligase, hindering its ability to ubiquitine the transcriptional factor HY5, thus averting its degradation and activating the photomorphogenic response. HY5 induces the synthesis of proteins RUP1 and RUP2, which interact with UVR8, liberating COP1 and inducing dimerization of UVR8. This mechanism has been thoroughly characterized in Arabidopsis, and it has been demonstrated that the UVR8 receptor is key to the UV-B response. Although Arabidospis is the model plant, due to its characteristics and the wide variety of available mutants, many of the mechanisms described in Arabidopsis differ in other plants. In this paper, we review the latest information regarding UV-B response mediated by UVR8 in different species, focusing on the differences reported compared to Arabidopsis. For instance, UVR8 is not only induced by UV-B but also by other agents that are expressed differentially in diverse tissues. Also, in some of the species analyzed, proteins with low homology to RUP1 and RUP2 were detected. We also discuss how UVR8 is involved in other developmental and stress processes that are not UV-B dependent. We conclude that the receptor is highly versatile and that there is a differential response between Arabidopsis and other species.

The phytohormone ABA regulates seed germination and stress responses. The identification of clade A protein phosphatase type 2C (PP2C)-interacting proteins PYRABACTIN RESISTANCE 1 (PYR1)/RCAR (REGULATORY COMPONENT OF ABA RECEPTOR) and PYR1-LIKEs (PYLs) as ABA receptors has been a major advance in understanding this process. Here, our aim was to identify additional ABA response loci by suppressor screening of the jasmonate (JA)-insensitive coronatine insensitive 1-16 (coi1-16) mutant using its ABA-hypersensitive phenotype. The identification and genetic characterization of Coi1-16 Resistant to ABA (CRA) loci revealed several unknown and three previously known abi mutants (abi1, abi3 and abi4), thus providing proof-of-concept evidence for this study. The synergistic effect of ABA and JA on seed germination and cotyledon expansion was analyzed in depth and the roles of cra5 coi1-16, cra6 coi1-16, cra7 coi1-16 and cra8 coi1-16 in ABA signaling during seed germination and stress responses were functionally characterized. The cra5 coi1-16 mutant showed resistance to ABA, paclobutrazol, and abiotic stresses during germination and early developmental stages. Furthermore, the cra5 coi1-16 mutation was mapped to the short arm of chromosome V and mutants exhibited differential expression of ABA-responsive genes, suggesting that CRA5 may function as a positive regulator of ABA signaling. Interestingly, cra6 coi1-16, cra7 coi1-16 and cra8 coi1-16 mutants display similar ABA- and abiotic stress-insensitive phenotypes during seed germination and seedling establishment. Taken together, our results demonstrate a key role for CRA genes in regulating the onset of seed germination by ABA, and highlight how cra mutants can be used as powerful tools to analyze novel molecular components of ABA signaling in seeds.