Introduction
Ultraviolet (UV) radiation reaching the Earth’s surface has increased significantly over the last 20 years from increased ozone depletion. UV radiation is a component of sunlight that is divided into three parts: UVA (320-400nm), UV-B (280-320nm) and UVC (less than 280nm) [25]. Wavelength determines the transmission of UV radiation through the Earth’s atmosphere. UVC is completely absorbed by the atmospheric gases; UV-B radiation is absorbed by ozone layer and only a small amount reaches the Earth’s surface while UVA radiation is hardly absorbed. The decreased UV-B-filtering capacity of the ozone layer due to pollutants like chlorofluorocarbons (CFC), methylbromide and halons has increased the amount of solar UV-B radiation that plant life is exposed to [2]. A thorough understanding of the UV-B radiation levels is especially important in agriculture as its effects on crop species is essential to design crops that can produce food and other raw materials for the increasing world population. Increased UV-B exposure has the potential to damage DNA, generate reactive oxygen species (ROS) and disrupt cellular process in many plant species [10]. Specifically, the primary deleterious effects of increased UV-B occur on the efficiency of the photosynthetic apparatus and the reduction of photosynthetic genes. Damage to the thylakoid membrane and destruction of chlorophyll (Fig. 6) along with the decrease in the amount of photosynthesis are also attributed to over exposure of UV-B [9]Moreover, in the chloroplast thylakoid membrane the D1 and D2 proteins of photosystem II (water-plastoquinone oxidoreductase complex) are rapidly degraded in course of UV-B irradiation [9]. Under conditions where UV-B impairs photosynthetic electron transport, excess ROS would likely be generated by a reduced ability to dissipate excitation energy causing extreme damage to the cell or even cell death. DNA lesions such pyrimidine dimers (CPDs) and pyrimidine-pyrimidone photoproduct can also form because of UV-B exposure thus blocking transcription and replication of the altered DNA causing various mutations to plant [19]. Furthermore, UV-B has shown to increase the frequency of somatic homologous DNA rearrangements in Arabidopsis and tobacco plants [22].
UV-B can also have a broader ecological effect by influencing the balance of competition between plant species and could result from UV-susceptible plants to be less resistant to pathogens and insects as compared with non-susceptible or adapted plants. Increased UV-B level in aquatic ecosystems have been linked to adverse effects on the growth, pigment content and on reproduction of phytoplankton, thus directly affecting the balance of aquatic food webs [8,27].
In general the most damaging effects observed in plants can be attributed to above-ambient levels of UV-B while low exposure levels can initiate photomorphogenic and regulatory responses. It is not possible to understand fully how light controls plant development without knowledge of the regulatory effects of UV-B. Despite the negative effects of above-ambient levels UV-B on plants there are sufficient defence mechanisms that plants have generated to protect themselves against UV-B. The focus of this paper will be on specific UV-B defence mechanism in plants such as accumulation of UV-absorbing compounds, DNA repair machinery, free radical scavenging, anti-oxidants and UV signal transduction pathways. Morphological Changes
Differences in the level of adaptation or acclimation to UV-B determine the response to UV-B exposure and in turn can cause various morphological changes to plants. Genotypes within a species differ in their tolerance and responsiveness to UV-B, for a given genotype the extent of prior acclimation to UV-B affects the nature and magnitude of the response. Plants grown in light lacking UV-B are more likely to suffer stress on first exposure whereas plants grown in UV-B are more likely to tolerate an increase in exposure because of elevated UV-B express genes that help the plant to counteract any stress effect, repair damage, and establish increased protection [10, 14]. Ultimately, over exposure of high levels of UV-B will cause morphological changes to almost plants such as decreases in stem length, leaf expansion, decrease in hypocotyl length in seedlings and even necrosis. Wang et. al (2008) treated Cerastium glomeratum Thuill, sticky weed, with UV-B radiation from seedling emergence to leaf fall. Enhanced UV-B radiation was provided by three filtered 40-W fluorescence sun lamps while the desired irradiation was obtained by changing the distance between the lamps and the top of plants. The graph in Fig. 4 portrays the decrease in plant height with enhanced UV-B exposure in C. glomeratum. The importance of this is that with increasing UV-B exposure to plant life across the biosphere when succession occurs in the ecosystem. Early growth stages might keep it at a disadvantage at the very start in natural communities when it is competing with other species in which the plant height was not affected by enhanced UV-B radiation [10].
Recently, Navarro et. al (2010) studied the effects of different intensities of UV-B radiation on growth and morphology of early development stages of Iridaea cordata in germlings, young gametophytes originated in the laboratory and young fronds collected in the Magellan Strait, Chile were tested [20]. Three irradiances of UV-B exposure were provided for only 3 h a day in the middle of the light period: 0.17, 0.5, and 0.83 W m−2 (UV-B1, UV-B2, and UV-B3, respectively) and the experiments were carried out during a four week process where the temperature and photoperiod were controlled. A profound result of this study was the lack of development of initial upright fronds from germlings exposed to UV-B treatments (Fig. 7). In Fig. 8, a gradual bleaching was observed in apical section of those young gametophytes exposed to UV-B2 and UV-B3 treatments after about 2 weeks of exposure time [20]. Yet, from this knowledge of the effects of UV-B what are the cellular and molecular mechanism of this photoregulatory pathway. Fascinatingly, research has been done on the UV signal transduction pathway.

UV signal transduction pathway
The importance of studying how the UV signal transduction pathway and the photoregulatory pathway work is that it will provide us more knowledge on how plants adapt to UV-B stress. Photomorphogenesis is the process by which plant development is controlled by light. As mentioned previously, adequate levels of UV-B actually induce positive regulatory responses and many of these responses occur through a signal transduction pathway. Some of the key regulatory factors involved in the UV-B-induced photomorphogenic pathway are E3 ubiquitin ligase called constitutively photomorphogenic 1 (COP1) that is negative regulator of seedling photomorphogenesis [6, 10]. COP1 represses photomorphogenic gene expression and development in darkness and targets HY5 and other positive regulators of photomorphogenic gene expression for destruction by the proteasome [6, 10]. Another important protein is UV response locus 8 (UVR8) that acts specifically to mediate responses to UV-B, including the gene expression responses that establish UV protection. Additionally, an essential regulator would be the transcription factor elongated hypocotyl 5 (HY5) which is a key effector of the COP1 pathway and UVR8 [6].
Favory et al. (2009) demonstrated that COP1 and UVR8 proteins are required for the UV-B photoregulatory pathway and that UV-B induces direct interaction of UVR8 with COP1. In Fig. 1A, a bimolecular fluorescent complementation (BiFC) assay was used to show the direct interaction of wild type UVR8 and COP1. Fig. 1B indicated the visualization of UVR8 dimerization independent of UV-B while Fig. 1C and D showed no interaction of mutant UVR8 proteins with wild-type COP1 under UV-B and no interaction of mutant COP1 proteins with wild-type UVR8 under UV-B, respectively.
It was also seen that in plant defence to UV-B stress UV-B-induced photomorphogenesis is critical in establishing UV-B acclimation and tolerance. Specifically this study showed that UVR8 levels are rate limiting in this process as seen Fig. 2A demonstrating quantitative RT–PCR data showing overexpression of UVR8 but no effect on COP1 expression in lines Ox nos. 2 and 3 (both Ox 2 and 3 were transgenic lines that over expressed UVR8) compared with wild type [6]. The interaction of COP1–UVR8 occurs very early on in the UV-B regulatory network responsible for allowing UV-B protection. This light response of COP1 occurs in the range of minutes, much faster than any of the presently known reactions of COP1 [6]. The rapid effects of UV-B stems from the fact that light acts quickly on gene expression and stabilization of COP1 target proteins [4, 6]. UVR8 provides UV-B-specific signalling function to the multifunctional COP1 protein, which is necessary to relay the UV-B signal. Transcription factor HY5 have a prominent role in UV-B signalling downstream of COP1 and UVR8 (Fig. 3). It was shown that HY5-dependent genes are also dependent on UVR8 and COP1 under broadband UV-B [4]. UVR8 protein levels in cop1 mutants are similar to wild-type levels suggesting that COP1 is not targeting UVR8 for proteasomal degradation [4, 6]. This was a very important research study that helped in elucidating the signal transduction pathway of photomorphogenesis and the protein-protein interactions that regulate this pathway.

Is UVR8 a Photoreceptor?
Although it is known that COP1 and UVR8 directly interact with one another and that UVR8 is the rate limiting step in photomorphogenic pathway, does this mean that UVR8 could function as photoreceptor? This is an ongoing controversy that has had little research done in this area. Firstly, one of the ideas to suggest UVR8 could be photoreceptor would be its accumulation in the nucleus in response to sunlight, which may indicate that it is a phytochrome, photoreceptor that use pigments to detect light. One of the first studies to show the dual role of UV-B in regulating UVR8 nuclear accumulation and function was conducted by Kaiserli and Jenkins (2007) [13]. One of their main results indicated that when plants grown in white light lacking UV-B are examined by confocal microscopy, the green fluorescent protein (GFP)-UVR8 fusion is detected in both the cytosol and nucleus (Fig. 5A). However, UV-B exposure causes a marked increase in the number of nuclei displaying bright GFP-UVR8 fluorescence. Contrastingly, when GFP was alone, driven by the 35S promoter, it was not present in the nucleus and did not change its localization following UV-B exposure indicating that only UVR8 localizes the GFP to the nucleus (Fig. 5B) [13]. Additionally, as little as five minutes of UV-B exposure promotes a substantial increase both in the number of nuclei that contain GFP-UVR8 and the brightness of nuclear fluorescence [13]. Further experiments indicated that a 23- amino-acid region at the N terminus of UVR8 is required for efficient nuclear accumulation [13]. This region does not contain a nuclear localization signal (NLS) and could be required for interaction with other components that mediate the response [10]. One possibility is that UVR8 is translocated into the nucleus through a protein containing a NLS, similar to the nuclear import of phytochrome A mediated by far-red elongated hypotcotyl1 (FHY1) this may suggest that UVR8 is potentially a photoreceptor [13]. What is known for certain through transcriptomic analysis is that approximately 70 genes are stimulated upstream of the signal transduction pathway by UVR8, which connects UV stress with enhanced expression of UV adaptive genes [3]. In these genes are several known to have key roles in the creation of enzymes of flavonoid biosynthesis, the DNA photolyases, and enzymes involved in removal of oxidative stress and photooxidative damage. By gaining a grasp of the cellular mechanisms behind UV-B signalling more insight toward specific adaptations that plants have developed will be better understood as seen in later sections.
UV-B Defences in Plants
Sunscreens
One of the greatest assets that plants possess to protect themselves against UV-B is the deposition of UV-absorbing compounds in epidermal tissues such as flavonoids, phenylpropanoid derivatives (sinapate esters) and anthocyanins. Phenylpropanoids are a diverse family of organic compounds that are synthesized by plants from the amino acid phenylalanine while flavonoids are polyphenolic compounds that are easily recognised as pigments (absorb the light in the region of 280~320 nm) in many flowering plants [21]. These compounds act as a sunscreen, reducing penetration of UV-B into the leaf while those plants that are without such protection suffer the detrimental effects of UV-B exposure. For instance, Landry et al. (1995) investigated UV-B-induced injury in wild type Arabidopsis thaliana and two mutants that were defective in the ability to synthesize UV-B-absorbing compounds. One mutant transparent testa 5 (tt5) was deficient in flavonoids while ferulic acid hydroxylase 1 (fah1) was deficient in sinapate esters. Fig. 9 indicates that growth inhibition, leaf cupping, and foliar injury were most prominent in fah1 mutants compared to the tt5 and the wild type [15]. Consistent with the whole-plant response, the highest levels of lipid and protein oxidation products were seen in fah1 [15]. Another experiment conducted on Arabidopsis thalania and Glycine max used chlorophyll fluorescence imaging (Fig. 10) which is an interesting and relatively fast method to estimate the degree of UV penetration into photosynthetic tissue [16]. The intensity of chlorophyll fluorescence in the red region of the spectrum induced by UV radiation (RFUV) was measured for intact leaves and leaf discs. After this to quantify the fluorescent signal a Fluor-S MultiImager was used [16]. The major use of this technique was to separate the UV-hypersensitive tt5 and tt6 mutants from the wild type (WT) and tt3, tt4, and tt7 mutants. The soybeans grown at different levels of leaf phenolics and under different UV-B condition showed significant alterations in UV-B penetration. The effects on DNA revealed that the number of cyclobutane pyrimidine dimers caused by a short exposure to solar UV-B was much larger in leaves with high UV transmittance than in leaves pre-treated with solar UV-B to increase the content phenylpropanoids [16]. Moreover, their main results indicated that phenolic sunscreens in soybean are highly responsive to the wavelengths that are most affected by variations in ozone levels. This is an intriguing finding as this would have great implications on the effects of UV-B protection in actual crop fields. Although evidence is there about mutants that lacks the ability to generate phenolic compounds, a study conducted by Bieza and Lois (2001) looked into mutants that were hypersensitive to UV-B radiation. This was a powerful tool to learn about the mechanisms that protect plants against UV-induced damage. A single gene dominant mutation (uvt1) was isolated and had remarkable tolerance to UV-B radiation. Fig. 13 exhibits a constitutive increase in accumulation of UV-absorbing compounds in uvt1 that increases the capacity of the leaves to block UV-B radiation and therefore is likely to be responsible for the elevated resistance of this mutant to UV-B radiation [1]. Possible changes in gene expression due to increases in absorption were found in this study because of expression of chalcone synthase (CHS) mRNA. This was accomplished by a northern blot from total RNA samples isolated from aerial tissues of 13 day old wild-type, uvt1, and uvs plants not exposed and exposed to 0.15 W m-2 of UV- B radiation for 21 hours [1]. The northern blot was hybridized with a CHS gene probe. The uvt1 mutant could be established a valuable tool to uncover the exact role and mechanism of UV-absorbing pigments in UV protection [1]. Anthocyanins are the largest group of water-soluble pigments in the plant kingdom are responsible for most of the red, blue, and purple colors of fruits, vegetables, flowers, and other plant tissues or products [17]. They are synthesized via the phenylpropanoid pathway and belong specifically to the flavonoids group of molecules. Thus, they are part of the UV-absorbing compounds that help protect plants again UV-B exposure. Many of the studies looking at anthocyanins focus on black soybean (Glycine max (L.) Merr). It was found that treatment with anthocyanins reduced UV-B-induced reactive oxygen species levels and inhibited UV-B-induced apoptotic cell death through the prevention of caspase-3 pathway activation and reduction of proapoptotic Bax protein levels [24]. Therefore, the protective effect of anthocyanins on UV-B-induced apoptosis may be due to inhibition of caspases pathway by blocking ROS production.
It can be seen that UV-B absorbing compounds are extremely important and those plants without these adaptive measures will succumb to the stresses of UV-B exposure.

Free radical scavenging / Anti-oxidant Defences
As previously mentioned, UV-B induces oxidative stress through the formation of ROS which causes lipid and protein oxidation. ROS includes not only free radicals (superoxide radical, O2·–, and hydroxyl radical, OH-), but also molecules such as hydrogen peroxide (H2O2), singlet oxygen and ozone (O3) [2]. The source of ROS in the many plants is from the electron transport chains (ETC) of chloroplasts and mitochondria. Plant mitochondrial ETC, with its redox‐active electron carriers, is considered as the most probable candidate for intracellular ROS formation [2]. Moreover, mitochondria have shown to produce ROS because of electron leakage at the ubiquinone: cytochrome b region and at the matrix side of complex I (NADH dehydrogenase) [2, 18]. Additionally, another source of ROS and radical formation could be the lipoxgenase (LOX) reaction. The actual reaction itself catalyzes the hydroperoxidation of polyunsaturated fatty acids. The hydroperoxyderivatives of the polyunsaturated fatty acids can undergo autocatalytic degradation and thus produce radicals to initiate lipid peroxidation [2].
To combat ROS species and prevent damage to the cell it has to produce enzymes and non-enzymatic pathways to deal with problem. The antioxidant defence system consists of several enzymes such as superoxide dismutase (SOD), catalase (CAT), peroxidase (POD) and ascorbate peroxidase (APX) as well as non-enzymatic antioxidants such as ascorbate, glutathione, tocopherol and carotenoids [25]. SOD catalyzes O2 – radicals into H2O2 and O2 and CAT converts H2O2 into water and O2. POD dismutates H2O2 by oxidation of co-substrates such as phenolic compounds and/or antioxidants (ascorbate and glutathione) [2, 18]. APX is a plant-specific H2O2-scavenging enzyme, which is active in chloroplasts in the ascorbate-glutathione cycle [18].
The non-enzymatic antioxidants are small molecules that play a significant role in alleviating oxidative stress. Ascorbate and glutathione are localized in the intracellular fluid while tocopherol and carotenoids are active in cell membranes [2]. Ascorbate deficient mutants vtc1 (vitamin c-1) of Arabidopsis are hypersensitive to a number of oxidative stresses including UV-B. Furthermore, fig. 14 shows that levels of ascorbate and glutathione in Arabidopsis plants in vtc1 mutants are very low when transferred to the supplemental UV-B treatment [7]. The level of reduced ascorbate and total ascorbate in the wild type plants were found to be 5.2 times and 3.1 times higher than that of vtc1 mutants after eight hours of UV-B treatment [7]. Fig. 14A and B indicated that ascorbate in the vtc1 mutants was more oxidized after only eight hours of UV-B treatment compared to the wild type. Fig. 14C had some interesting results in that total glutathione levels in the wild type plants increased during the course of UV-B exposure (ranges from 3.10 to 9.30, expressed as μmol g−1 DW), whereas the ratio of reduced to total (GSH/GSHt) was not significantly affected (Fig. 14D) [7].
Various other enzymes such as phenylalanine ammonia-lyase (PAL) and CHS that are involved in the phenylpropanoid pathway can be induced by UV-B light to express their genes [2]. Plants synthesize secondary metabolites such as flavonoids, hydroxycinnamic acids and sinapate esters in the vacuoles of epidermal cell layers that can absorb UV-B and also act as free radical scavengers [7].

Proteomics of UV-B defence
The presence of UV-B radiation on plants has shown to increase the production of many proteins involved in UV-B defence. A very recent study conducted by Du et. al (2011) took a more proteomic approach a looked a variety of proteins that were upregulated, downregulated and were induced as a result of UV-B exposure. This was an excellent research study that compared the expression patterns of mRNA and protein abundance of UV-responsive proteins while also suggesting the involvement of some new proteins in UV-B protection in plants. Using physiological, proteomic and quantitative real-time PCR (qPCR) methods, systematically studied the response of 16-day-old rice seedlings to UV exposure for 6, 12 and 24 hours [5]. A two-dimensional gel electrophoresis (2DGE) map found that twenty proteins were up-regulated and three proteins were induced during UV exposure (Fig. 11). After this tryptophan synthase alpha chain (spot 3), glyoxalase I (spot 5) and Bet v I allergen family protein (spot 23) were selected for further investigation as seen by the comparison of mRNA levels to protein levels (Fig. 12). It was also deduced that tryptophan synthase α chain was essential for the removal of radical oxygen species; glyoxalase I was critical in detoxification/ anti-oxidation; and a Bet v I family protein was used in defence [5].
The other proteins induced wide variety of responses including phytohormone-regulative responses, injurious responses (photosynthesis suppression, lipid peroxidation and visible injury); and protective responses (accumulation of UV-absorbing compounds and differential expression of proteins involved in detoxification/anti-oxidation, defence, protein processing, RNA processing, carbohydrate metabolism and secondary metabolism) [5, 10]. This indicates that there are cumulative responses of various molecular mechanisms that help a plant cope and adapt to UV-B stress.
DNA repair mechanisms
It is known DNA is one of major targets of the UV damage. UV photoproducts such as DNA lesions and CPDs hamper the ability of DNA to replicate properly and can cause unwanted mutations. Plants possess two major mechanisms known as photorepair and dark repair. Photorepair uses photolyases, DNA repair enzymes that repair damage caused by exposure to UV light, to remove removes photoproducts [2]. Two types of cofactors are present in these photolyases that help to ameliorate DNA damage. The two cofactors FAD which is excited by blue/UVA light energy and monomerizes the photoproducts and methenyltetrahydrofolate that acts as a photoantenna get rid of DNA damage [2, 11]. Arabidopsis mutants were CPD photolyase and were hypersensitive to UV radiation [12]. Jiang et al (1997) isolated and characterized two mutants of Arabidopsis, uvr2 and uvr3, which are defective in the photorepair mechanisms of CPDs and pyrimidinone dimer [12]. The results indicated that the CPD photolyase mutation plants were less resistant to UV-B exposure and that photorepair mechanism allow for the alleviation of UV-B stress on Arabidopsis. In dark repair, photoproducts are removed from DNA by the evolutionarily conserved nucleotide excision repair (NER) mechanism in all organisms. When DNA lesions are in the regions of transcribed genes another NER pathway called global genomic repair (GGR) is used to repair damage [2,11,12]. Lesion recognition appears to be initiated by a complex of XPC/Rad23 (xeroderma pigmentosum, complementation group C/Rad23) or DDB1- DDB2 (UV-damaged DNA binding protein) in the GGR pathway [11]. NER is a complex multi-step process which requires the delicate cooperation of many enzymes and gene products. Firstly, damaged DNA is unwound by helicases and excision of damaged DNA is done by two nucleases [2]. A nuclease XPF /ERCC1 (xeroderma pigmentosum, complementation group F/excision repair complementing defective repair in Chinese hamster 1) makes a cut at the 5’ end of the DNA lesion [25]. At the 3’ end of the DNA lesion, XPG (xeroderma pigmentosum, complementation group G) nuclease makes the incision [12,25]. DNA polymerase then fills in the missing gaps in the DNA and DNA ligase binds these nucleotides together. DNA repair mechanisms help plants to further cope with UV-B stress, and allow them some tolerance when over exposed to UVB.

Future Directions
UV-B clearly activates a number of distinct signalling pathways in plants. Progress has been made in identifying components of the pathways but much remains to be done. It will not be possible to establish how many distinct pathways mediate UV-B responses until we know more about their components. Furthermore, little is known about the relative importance of the different UV-B signalling pathways in plants growing in the natural environment thus studies can be conducted to find this out. Moreover, how these pathways to UV-B response are integrated is also an area of further study. Also, it would be interesting to see what mechanisms are involved in the regulation of morphogenesis by UV-B. In this review UV-hyper-resistant plants were discussed, but testing how these mutant plants would operate under natural conditions has not been tested. Not only would its growth and survival need to be examined, but if it were a prevalent crop that is used for food its ability to produce fruit would have to be monitored. With the increase depletion of ozone in our atmosphere increased UV-B levels with have a drastic effect on agriculture, thus an observational study would have to first be undertaken with proper transgenic plants. Another area of research that would be fascinating would be to look at aquatic ecosystems. In one aquatic study, Spirodela polyrhiza, duckweed, was investigated and the influence of UV-B on various enzymes was conducted. Nitrate reductase (NR), nitrite reductase (NiR), glutamine synthetase (GS), NADH-dependent glutamate synthase (NADH-GOGAT) and ferredoxin-dependent glutamate synthase (Fd-GOGAT) were investigated in fronds and turions of duckweed [23]. The activities of all enzymes investigated, except for the cytoplasmic isoform of GS, were inhibited and also there was decrease in growth in fronds and turions [23]. This was a good study as there was a correlation between the enzyme activities and their protein amounts was found by doing a western blot analysis. Yet, further research on the whether there is a relationship between mRNA and protein amount can be done. Similar to the study mentioned above my experiment would focus of algae in aquatic systems. Would aquatic algae be more susceptible to UV-B exposure and is there an optimum intensity for photosynthesis to occur? By testing the chlorophyll content in these algae at various exposure times and intensities and the using chlorophyll fluorescence this could help to quantify the amount photosynthesis that may be occurring. Additionally, quantitative RT-PCR could test the gene expression of genes responsive to UV-B. Using other proteomic tools such as 2D-gel-electrophoresis to test what proteins were up regulated, down regulated, or induced and using mass spectroscopy would be the next step in the process.

There are also relatively few comparative studies that were found between plants that were more tolerant to UV-B stress and those that were less tolerant. What proteins would be over-expressed or less-expressed in each plant? Two plants of the same species where one is native to conditions with increased UV-B exposure (example from southern Argentina or Russia) and the other is found under decreased UV-B exposure conditions. By looking at the epidermal cells of the leaves of Arabidopsis thalania that inhabited each of these places we could detect effects. By again doing a 2D- Gel Electrophoresis at various times to determine what proteins are being over expressed or being induced in each plant respectively. It would also be interesting to see from Du et al. 2011 study which proteins of tryptophan synthase alpha chain, glyoxalase I and Bet v I allergen family protein were being phosphorylated. By looking at post-translational modifications in each of these proteins further explanations of how plants adapt to UV-B stress can be elucidated.

Conclusion
Sunlight is important to plants, both as the ultimate energy source and as an environmental signal regulating growth and development. Thus, the balance of UV-B exposure is critical for a plant to survive. The effect of UV-B on plants can be extensive and very damaging without proper precautions. Various morphological defects, disabling of photosynthetic machinery and even necrosis can occur under high UV-B intensity. When exposed to adequate and tolerable levels plants grow problem free and also initiate defence systems for the possibility of UV-B increase through signal transduction pathways. Some of the key regulatory factors involved in the UV-B-signal transduction pathway are the COP1, HY5 and another protein called UVR8 that all work together to mediate responses to UV-B. Although we have some regulatory components discovered, there still research to be done on different UV-B signalling pathways in plants growing in the natural environment, and how are these pathways functionally integrated.
One of the most important adaptations is the accumulation of UV-absorbing compounds like flavonoids and phenylpropanoids that act as a sunscreen for plants. Consequently, anti-oxidants and free radical scavenging enzymes help to alleviate ROS and prevent serious cellular damage. On top of this, plants have DNA repair machinery to fix DNA lesions and CPDs from causing mutations which helps plants to heal from exposure to high intensity UV-B. Even development of mutants that are hyper-sensitive to UV-B can assist in creating transgenic plants that can be used as crops to feed the ever growing population without the predicament of increased UV-B.
With increasing amount of pollution that enters our atmosphere and the depletion of ozone that gives humans and all organism protection from cosmic radiation there is a definite impact of UV-B research in plants. We know that plants have certain genes that protect them from UV-B damage, but are these genes conserved in humans and other animals? Answering these types of questions can help humans tackle the dilemma of increasing UV-B exposure and can help us create feasible applications that not only help humans, but the entire ecosystem.

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