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Research shows that sea urchins living around Anvers Island, Antarctic Peninsula, contain the mycosporine-like amino acids (MAAs) palythine, porphyra-334, mycosporine-glycine and shinorine. The MAAs, which absorb ultra-violet light, are found in varying concentrations in adult Sterechinus neumayeri urchins. Low levels of MAAs are found in the organisms' body wall. Up to 1389 micrograms per gram dry weight of MAAs are found in the ovaries.

Annual springtime losses of stratospheric ozone over the Antarctic during the past two decades have resulted in increased levels of biologically-harmful UVB radiation reaching the ocean. This phenomenon occurs at a time when embryos and larvae of the sea urchin Sterechinus neumayeri and the sea star Psilaster charcoti are developing in surface waters. Eggs and embryos of these species were exposed to ambient sunlight in outdoor tanks and in the water column (from surface to 7 m) under normal and depleted ozone conditions (i.e., low and high UV fluences) during spring of 1996 and 1997. Increased exposure to UVB caused increases in cellular damage, abnormal cleavage, mortality and total development time. Under non-depleted ozone conditions, UVB effects on embryos were detected to a maximum depth of 3 m. Under a depleted ozone column, detectable damage occurred to depths of 5-7 m. Overall, the success of development to a normal blastula stage was inversely related to the total ambient UVB exposure, which in mm, was inversely correlated to ozone levels. The reproductive success of S. neumayeri and P. charcoti may be affected by the recurring springtime losses of ozone over Antarctica. Detailed information is needed on the timing of spawning and the residence times of eggs and embryos in surface waters before the magnitude of this stress can be fully determined.

The article presents a study which estimates the carbon biomass distributions of the global marine plankton know as coccolithophores. The study used remote sensing approaches, a quality control procedure, and statistical analyses. Results show that biomass distributions in North Atlantic were the highest biomass values, and all planktons were seen across the latitudes of the Northern Hemisphere.

Mycosporine-like amino acids (MAAs) that absorb UV radiation (310-360 nm) were investigated in 34 species of benthic marine invertebrates(fourteen sponges, two cnidarians, one nemertean, four molluscs, onebryozoan, two arthropods, eight echinoderms and two tunicates), two species of benthic fish and two species of red algae collected duringthe spring of 1992 from McMurdo Sound. In addition, MAAs were measured in the ripe ovaries, testes and brooded juveniles of four species of echinoderms. While 90% of the species had MAAs in their tissues, both quantitative and qualitative measurements reflected a general lack of UV protectants among these fauna. Eight MAAs were detected amongthe species examined, but only four of these (mycosporine-glycine, shinorine, porphyra-334 and palythine) occurred in any appreciable number of the species. Palythinol only occurred in the sponge Isodictya erinacea and asterina-330 and palythene only occurred in the red algaIridaea cordata. MAAs were detected in the ripe ovaries and testes of the sea urchin Sterechinus neumayeri and the ripe ovaries and brooded young of the sea cucumber Cucumaria ferrari. Low levels and abundances of MAAs may reflect a reduced need for UV protectants in marine organisms inhabiting subtidal (>20 m depth) benthic environments thatexperience seasonal sea-ice cover. Low concentrations of MAAs may also be a function of diet, since the majority of benthic species present in McMurdo Sound are not herbivorous. [ABSTRACT FROM AUTHOR]

SignificanceTranscription-coupled repair (TCR) involves four core proteins: CSA, CSB, USP7, and UVSSA. CSA and CSB are mutated in the severe human neurocutaneous disease Cockayne syndrome. In contrast UVSSA is a mild photosensitive disease in which a mutated protein sequence prevents recruitment of USP7 protease to deubiquitinate and stabilize CSB. We deleted the UVSSA protein using CRISPR-Cas9 in an aneuploid cell line, HEK293, and determined the functional consequences. The knockout cell line was sensitive to transcription-blocking lesions but not sensitive to oxidative agents or PARP inhibitors, unlike CSB. Knockout of UVSSA also activated ATM, like CSB, in transcription-arrested cells. The phenotype of UVSSA, especially its rarity, suggests that many TCR-deficient patients and tumors fail to be recognized clinically.

The ability to repair DNA is a ubiquitous characteristic of life on Earth and all organisms possess similar mechanisms for dealing with DNA damage, an indication of a very early evolutionary origin for repair processes. James E. Cleaver's career (initiated in the early 1960s) has been devoted to the study of mammalian ultraviolet radiation (UVR) photobiology, specifically the molecular genetics of xeroderma pigmentosum and other human diseases caused by defects in DNA damage recognition and repair. This work by Jim and others has influenced the study of DNA damage and repair in a variety of taxa. Today, the field of DNA repair is enhancing our understanding of not only how to treat and prevent human disease, but is providing insights on the evolutionary history of life on Earth and how natural populations are coping with UVR-induced DNA damage from anthropogenic changes in the environment such as ozone depletion., (© 2014 The American Society of Photobiology.)

Ultraviolet B (UVB, 280-315nm) radiation is detrimental to both of larvae of the digenetic trematode Schistosoma mansoni and its snail intermediate host, Biomphalaria glabrata. We explored effects of UVB on three aspects of the interaction between host and parasite: survival of infected snails, innate susceptibility and resistance of snails to infection, and acquired resistance induced by irradiated miracidia. Snails infected for 1 week showed significantly lower survival than uninfected snails following irradiation with a range of UVB intensities. In contrast to known immunomodulatory effects in vertebrates, an effect of UVB on susceptibility or resistance of snails to infection could not be conclusively demonstrated. Finally, exposure of susceptible snails to UVB-irradiated miracidia failed to induce resistance to a subsequent challenge with nonirradiated miracidia, a result similar to that reported previously with ionizing radiation.

Schistosoma mansoni occurs in tropical regions where levels of ultraviolet B (UVB; 290-320 nm) light are elevated. However, the effects of UVB on parasite transmission are unknown. This study examines effects of UVB on the miracidia and sporocysts of S. mansoni, focusing specifically on intramolluscan development, infectivity, and the ability to photoreactivate (repair DNA damage using visible light). Histology revealed that miracidia irradiated with 861 J x m(-2) underwent abnormal development after penetrating Biomphalaria glabrata snails. Total number of sporocysts in snail tissues decreased as a function of time postinfection (PI), among both nonirradiated and irradiated parasites; however, this decrease was greater in the latter. Moreover, whereas the proportion alive of nonirradiated sporocysts increased PI, that of irradiated sporocysts, i.e., derived from irradiated miracidia, decreased. Irradiation of miracidia with UVB resulted in decreased prevalence of patent infection (defined by presence of daughter sporocysts) in a dose-dependent manner, and no infections occurred at a dose of 861 J x m(-2). Like many aquatic organisms, including the snail host, parasites were able to photoreactivate if exposed to visible light following UVB irradiation, even subsequent to penetrating snails. These photoreactivation results suggest cyclobutane-pyrimidine dimers in DNA as the primary mechanism of UVB damage, and implicate photoreactivation, rather than nucleotide excision, as the main repair process in S. mansoni.

Although Schistosoma mansoni occurs mainly in the tropics, where intense levels of solar radiation are present, the impact of ultraviolet (UV) light on schistosome transmission is not known. The purpose of this study was to investigate potential effects of UVB (290-320nm) on juvenile Biomphalaria glabrata, the snail intermediate host of S. mansoni. Albino and wild-type snails were exposed to doses of UVB from UV-fluorescent lamps, and the following were measured: survival, photoreactivation (light-mediated DNA repair), effects on feeding behavior, and morphological tissue abnormalities. Irradiation with UVB is lethal to B. glabrata in a dose-dependent manner. Exposure to white light subsequent to UVB irradiation enhances survival, probably by photoreactivation. The shell offers some, but not complete, protection. Experiments in which UVB transmittance through the shell was blocked with black nail polish suggest that injury to both exposed (headfoot) and shell-enclosed (mantle and visceral mass) tissues contributes to mortality in lethally irradiated snails. Wild-type (pigmented) snails are less susceptible to lethal effects of UVB than albino snails, and they may be more capable of photoreactivation. UVB exposure inhibits snail feeding behavior, and causes tentacle forks and growths on the headfoot. Thus, UVB may influence the life cycle of S. mansoni by both lethal and sub-lethal damage to the snail intermediate host. However, the ability of snails to photoreactivate may mitigate these effects.

We investigated the interaction of diet and accumulation of UV-absorbing mycosporine-like amino acids (MAAs) in body tissues and spawn of the sea hare Aplysia dactylomela to determine if MAA accumulation reflects type and level of dietary intake. Food sources were the red algae Acanthophora spicifera, Centroceras clavulatum, and Laurencia sp., and the green alga, Ulva lactuca. Adults were maintained on these foods for 40 days, after which feces were collected and tissues separated by dissection. Field animals were similarly sampled at this time. All spawn from experimental and field animals was collected over the study period. Samples, including seaweed foods, were analysed for six MAAs. Overnight consumption experiments using a variety of common seaweeds and one seagrass from A. dactylomela's habitat showed that the four seaweeds selected as foods were among those best-eaten by Aplysia. After 40 days levels of specific MAAs in the tissues of experimental animals showed excellent correlation with those in their diets, suggesting that the MAAs were dietarily-derived. Relative MAA contents in spawn from all diet groups correlated well with those in spawn from field animals. Commonest MAAs in spawn were porphyra-334, shinorine, and palythine, in this order. Concentrations of these MAAs were maintained at constant levels over time in spawn from all diet groups eating red algae and from field animals. Spawn from the Ulva dietary group showed an initial significant decline in MAA concentrations, but levels stabilized after the first 2 weeks. Skin was rich in porphyra-334 and shinorine, and levels of these in experimental animals correlated well with comparable levels in the skin of field animals. Digestive glands contained high levels of asterina-330, particularly those of the Centroceras dietary group, where concentrations reached a maximum of 21 mg dry g(-1).

A series of ultraviolet (UV)-resistant cell lines have been generated from a UV-sensitive XP group A cell line homozygous for a stop codon (TGA) in the chromosome 9 XPA gene. Three lines generated by chemical mutagenesis acquired the ability to excise (6-4) photoproducts but not cyclobutane dimers from the whole genome; two lines generated by a fusion procedure with hamster cells acquired the ability to excise both (6-4) photoproducts and cyclobutane dimers from the whole genome. A central region of the hamster XPA gene was cloned and sequenced. With the use of species-specific primers in the polymerase chain reaction, we found that the hybrid cell lines do not contain a hamster XPA gene. Sequence analysis showed that all of the UV-resistant cell lines contain reversions of the human stop codon, resulting in missense mutations (glycine or leucine for arginine) or wild-type sequences. The concentration of XPA protein in revertant cell lines was about one-half that in normal cells, which would be expected from heterozygous cells; there was no evidence that the mutant proteins were less stable than the wild-type proteins. These results are consistent with the idea that the XPA protein initiates repair by binding to damaged sites with various affinities, depending on the photoproduct and the transcriptional state of the region. A concentration of XPA protein near 50% is needed before repair can proceed into nontranscribed regions of the genome. The revertant cell lines represent a class of missense mutations in the XPA gene that may have altered specificity and that can be used to understand some of the regulatory differences in repair of photoproducts in various regions of the genome.

The ultraviolet light-sensitive phenotype of xeroderma pigmentosum (XP) has been corrected by the incorporation into XP cells of small chromosome fragments from Chinese hamster ovary cells. Like normal human and hamster cells, these XP-hamster hybrids are able to excise both of the photoproducts produced by ultraviolet light: cyclobutane pyrimidine dimers and the minor photoproduct, (6-4) pyrimidine-pyrimidone dimers. This excision capacity contrasts with that of an XP revertant, of the same cell line used in this study, which is able to excise only the (6-4) photoproducts. The excision defect of XP has been fully corrected in the hybrids; therefore, the small hamster chromosome fragments they contain should carry the gene for complementation group A of XP.

DNA repair in xeroderma pigmentosum complementation groups C and D occurs at a low level. Measurements of pyrimidine dimers remaining in bulk DNA from the whole genome indicated very little excision in either complementation group. The repair sites in group C cells were, however, clustered together in small regions of the genome which appeared to be mended nearly as efficiently as the whole genome is mended in normal cells, while repair in group D cells was randomly distributed. Growth of normal cells in cycloheximide or 3-aminobenzamide neither inhibited repair nor altered the distribution of repair sites. Growth of normal cells in novobiocin or aphidicolin inhibited excision but repair remained randomly distributed. On the basis of these observations, and consideration of other cellular features of group C and D, we suggest that group C may represent a mutation which results in a low level of repair enzymes with normal function. Group D, on the other hand, may represent a mutation resulting in functionally defective repair enzymes.