Desiccation protects two Antarctic mosses from ultraviolet-B induced DNA damage

2009 ◽  
Vol 36 (3) ◽  
pp. 214 ◽  
Author(s):  
Johanna D. Turnbull ◽  
Simon J. Leslie ◽  
Sharon A. Robinson
Keyword(s):  
Dna Damage ◽  
Ozone Depletion ◽  
Ultraviolet B ◽  
Cyclobutane Pyrimidine Dimers ◽  
Moss Species ◽  
Cosmopolitan Species ◽  
Ultraviolet B Radiation ◽  
Pyrimidine Dimers ◽  
Bryum Pseudotriquetrum ◽  
Antarctic Mosses

Antarctic mosses live in a frozen desert, and are characterised by the ability to survive desiccation. They can tolerate multiple desiccation-rehydration events over the summer growing season. As a result of recent ozone depletion, such mosses may also be exposed to ultraviolet-B radiation while desiccated. The ultraviolet-B susceptibility of Antarctic moss species was examined in a laboratory experiment that tested whether desiccated or hydrated mosses accumulated more DNA damage under enhanced ultraviolet-B radiation. Accumulation of cyclobutane pyrimidine dimers and pyrimidine (6–4) pyrimidone dimers was measured in moss samples collected from the field and then exposed to ultraviolet-B radiation in either a desiccated or hydrated state. Two cosmopolitan species, Ceratodon purpureus (Hedw.) Brid. and Bryum pseudotriquetrum (Hedw.) Gaertn., B.Mey. & Scherb, were protected from DNA damage when desiccated, with accumulation of cyclobutane pyrimidine dimers reduced by at least 60% relative to hydrated moss. The endemic Schistidium antarctici (Cardot) L.I. Savicz & Smirnova accumulated more DNA damage than the other species and desiccation was not protective in this species. The cosmopolitan species remarkable ability to tolerate high ultraviolet-B exposure, especially in the desiccated state, suggests they may be better able to tolerate continued elevated ultraviolet-B radiation than the endemic species.

Repeated exposures of human skin equivalent to low doses of ultraviolet-B radiation lead to changes in cellular functions and accumulation of cyclobutane pyrimidine dimers

2001 ◽  
Vol 79 (4) ◽  
pp. 507-515 ◽  
Author(s):  
Nadine Chouinard ◽  
Jean-Philippe Therrien ◽  
David L Mitchell ◽  
Marielle Robert ◽  
Régen Drouin ◽  
...  
Keyword(s):  
Dna Damage ◽  
Repeated Exposure ◽  
Ultraviolet B ◽  
Skin Equivalent ◽  
Basal Cells ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Cyclobutane Pyrimidine Dimers ◽  
Biochemical Alterations ◽  
Pyrimidine Dimers

Chronic exposure to sunlight may induce skin damage such as photoaging and photocarcinogenesis. These harmful effects are mostly caused by ultraviolet-B (UVB) rays. Yet, less is known about the contribution of low UVB doses to skin damage. The aim of this study was to determine the tissue changes induced by repeated exposure to a suberythemal dose of UVB radiation. Human keratinocytes in monolayer cultures and in skin equivalent were irradiated daily with 8 mJ/cm2 of UVB. Then structural, ultrastructural, and biochemical alterations were evaluated. The results show that exposure to UVB led to a generalized destabilization of the epidermis structure. In irradiated skin equivalents, keratinocytes displayed differentiated morphology and a reduced capacity to proliferate. Ultrastructural analysis revealed, not only unusual aggregation of intermediate filaments, but also disorganized desmosomes and larger mitochondria in basal cells. UVB irradiation also induced the secretion of metalloproteinase-9, which may be responsible for degradation of type IV collagen at the basement membrane. DNA damage analysis showed that both single and repeated exposure to UVB led to formation of (6–4) photoproducts and cyclobutane pyrimidine dimers. Although the (6–4) photoproducts were repaired within 24 h after irradiation, cyclobutane pyrimidine dimers accumulated over the course of the experiment. These studies demonstrate that, even at a suberythemal dose, repeated exposure to UVB causes significant functional and molecular damage to keratinocytes, which might eventually predispose to skin cancer.Key words: UVB, keratinocytes, skin structure, DNA damage, photoproducts.

scholarly journals A Role for Histone H2B During Repair of UV-Induced DNA Damage in Saccharomyces cerevisiae

Genetics ◽  
2002 ◽  
Vol 160 (4) ◽  
pp. 1375-1387
Author(s):  
Emmanuelle M D Martini ◽  
Scott Keeney ◽  
Mary Ann Osley
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Chromatin Structure ◽  
Specific Effect ◽  
Cell Killing ◽  
Cyclobutane Pyrimidine Dimers ◽  
Histone H2b ◽  
Uv Sensitivity ◽  
Pyrimidine Dimers

Abstract To investigate the role of the nucleosome during repair of DNA damage in yeast, we screened for histone H2B mutants that were sensitive to UV irradiation. We have isolated a new mutant, htb1-3, that shows preferential sensitivity to UV-C. There is no detectable difference in bulk chromatin structure or in the number of UV-induced cis-syn cyclobutane pyrimidine dimers (CPD) between HTB1 and htb1-3 strains. These results suggest a specific effect of this histone H2B mutation in UV-induced DNA repair processes rather than a global effect on chromatin structure. We analyzed the UV sensitivity of double mutants that contained the htb1-3 mutation and mutations in genes from each of the three epistasis groups of RAD genes. The htb1-3 mutation enhanced UV-induced cell killing in rad1Δ and rad52Δ mutants but not in rad6Δ or rad18Δ mutants, which are defective in postreplicational DNA repair (PRR). When combined with other mutations that affect PRR, the histone mutation increased the UV sensitivity of strains with defects in either the error-prone (rev1Δ) or error-free (rad30Δ) branches of PRR, but did not enhance the UV sensitivity of a strain with a rad5Δ mutation. When combined with a ubc13Δ mutation, which is also epistatic with rad5Δ, the htb1-3 mutation enhanced UV-induced cell killing. These results suggest that histone H2B acts in a novel RAD5-dependent branch of PRR.

scholarly journals γH2AX in the S Phase after UV Irradiation Corresponds to DNA Replication and Does Not Report on the Extent of DNA Damage

2020 ◽  
Vol 40 (20) ◽  
Author(s):  
Shivnarayan Dhuppar ◽  
Sitara Roy ◽  
Aprotim Mazumder
Keyword(s):  
Dna Damage ◽  
Uv Irradiation ◽  
S Phase ◽  
Dna Double Strand Breaks ◽  
Cyclobutane Pyrimidine Dimers ◽  
Environmental Mutagen ◽  
Strand Breaks ◽  
Pyrimidine Dimers ◽  
Replication Sites ◽  
A Cell

ABSTRACT Ultraviolet (UV) radiation is a major environmental mutagen. Exposure to UV leads to a sharp peak of γH2AX, the phosphorylated form of the histone variant H2AX, in the S phase within an asynchronous population of cells. γH2AX is often considered a definitive marker of DNA damage inside a cell. In this report, we show that γH2AX in the S-phase cells after UV irradiation reports neither on the extent of primary DNA damage in the form of cyclobutane pyrimidine dimers nor on the extent of its secondary manifestations in the form of DNA double-strand breaks or in the inhibition of global transcription. Instead, γH2AX in the S phase corresponds to the sites of active replication at the time of UV irradiation. This accumulation of γH2AX at replication sites slows down the replication. However, the cells do complete the replication of their genomes and arrest within the G2 phase. Our study suggests that it is not DNA damage, but the response elicited, which peaks in the S phase upon UV irradiation.

Suspended Sediment as an Attenuating Factor of Ultraviolet-B Radiation Effects on the Growth and DNA Damage of Chlorella Sp.

2012 ◽  
Vol 518-523 ◽  
pp. 5165-5171
Author(s):  
Yun Li ◽  
Yao Jia Huang ◽  
Xiao Rong Wang
Keyword(s):  
Dna Damage ◽  
Cell Growth ◽  
Suspended Sediment ◽  
Coastal Waters ◽  
Radiation Effects ◽  
Ultraviolet B ◽  
Light Penetration ◽  
Ultraviolet B Radiation ◽  
Laboratory Conditions ◽  
Chlorella Sp

Effects of enhanced ultraviolet-B (UV-B) radiation and suspended sediment (SS) separately as well as in combination on the growth and DNA damage of Chlorella sp. were studied under controlled laboratory conditions. The Chlorella sp. was exposed to UV-B of 17 µW cm-2for 0, 1 and 5 minutes in 0, 500 and 5000 mg L-1defined SS. The results showed that SS attenuated light penetration and suppressed the growth ofChlorellasp.. It also attenuated UV-B induced DNA damage and promoted the cell growth. The suppression and promotion of cell growth depended on the concentration of SS and dose of UV-B radiation. These results are important in understanding of the effects of elevated UV-B radiation on microalgae in sediments-dominate coastal waters.

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