Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair

In the paper

“Recently, it has been reported that the mechanisms of BER and NER (but not photoreactivation) in higher plants are active in proliferating cells [172].”

What the sources say

• Disputed

  The paper supports excision repair in proliferating cells, but explicitly contradicts the exclusion of photoreactivation. The Abstract (p. 1) says both photoreactivation and excision repair are active in proliferating cells; the Discussion (p. 5) likewise says the meristem may need both. (LLM, conf=0.91)

  Checked by a reasoning model — may be wrong.

  cites [172] sourceExperimental — accuracy not yet measured

In the paper

“which is one of the most effective and carcinogenic exogenous agents that can interact with DNA and alter the genome integrity and may affect the normal life processes of all organisms ranging from prokaryotes to mammals [2–10].”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [2]
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [3]
• ?Not checked — no full text of the sourcecites [4] source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [5]
• ?Not checked — no full text of the sourcecites [6] source
• ?Not checked — no full text of the sourcecites [7] source
• Partly supported

  The Human health section (page unavailable) links solar UV exposure to skin cancer, while the Aquatic ecosystems section reports UV-associated DNA damage and effects on bacterioplankton. The paper does not establish that UVR is among the most effective carcinogenic agents or that it affects the normal life processes of all organisms from prokaryotes to mammals. (LLM, conf=0.86)

  cites [8] sourceExperimental — accuracy not yet measured
• Partly supported

  The Introduction reports that UV-B impairs photosynthesis and growth and has harmful effects on plants; the Discussion reports cellular damage in cyanobacteria. Our copy does not establish that UVR is carcinogenic, interacts with DNA or alters genome integrity, or that these effects extend to mammals. (LLM, conf=0.85)

  cites [9] sourceExperimental — accuracy not yet measured
• Partly supported

  The Introduction (page not supplied) says UVR damages DNA and can inhibit phytoplankton production; the Discussion reports UVR-induced mortality in Mediterranean picocyanobacteria. The paper does not establish that UVR is carcinogenic or extend these effects to all organisms from prokaryotes to mammals. (LLM, conf=0.88)

  cites [10] sourceExperimental — accuracy not yet measured

In the paper

“One of the transcription factors, TATA-box binding protein (TBP), promotes the selective formation of 6-4PPs in the TATA-box, where the DNA is bent, but CPDs are formed preferentially at the edge of the TATA box and outside where the DNA is not bent [53].”

What the sources say

• Supported

  The Discussion (page not provided) reports that 6-4PP formation was restricted to an internal cluster within the presumed TBP contacts, while other clusters formed CPDs. It also describes the sharp bend induced by TBP; the in vitro results (page not provided) identify CPDs in the flanking regions. (LLM, conf=0.92)

  cites [53] source

In the paper

“Solar UV radiation is responsible for a wide range of biological effects including alteration in the structure of protein, DNA, and many other biologically important molecules, chronic depression of key physiological processes, and acute physiological stress leading to either reduction in growth and cell division, pigment bleaching, N2 fixation, energy production, or photoinhibition of photosynthe”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [3]
• Partly supported

  Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [9] sourceExperimental — accuracy not yet measured
• Partly supported

  The Introduction (page not provided) describes UV-induced DNA damage, inhibition of primary production, pigment degradation, and changes in nitrogen metabolism; the Discussion reports UV-induced cell mortality. The copy does not support the more specific claims about altered protein structure, chronic versus acute effects, N2 fixation, or reduced energy production. (LLM, conf=0.88)

  cites [10] sourceExperimental — accuracy not yet measured

In the paper

“In all the groups of UVR (i.e., UV-A: 315–400 nm; UV-B: 280–315 nm; UV-C: <280 nm) UV-B radiation produces adverse effects on diverse habitats, even though most of the extraterrestrial UV-B is absorbed by the stratospheric ozone [12].”

What the sources say

• Partly supported

  The section on factors affecting surface UV says shorter UV-B wavelengths are particularly sensitive to ozone depletion and that reduced ozone increases damaging radiation for environmental processes (page not provided). This supports the general link between ozone and harmful UV-B, but the copy does not establish that most incoming UV-B is absorbed by stratospheric ozone or document adverse effects across diverse habitats. (LLM, conf=0.78)

  cites [12] sourceExperimental — accuracy not yet measured

In the paper

“Certain UV-absorbing pigments are produced by a number of organisms as a first line of defense; however, they are unable to avoid UV-radiation completely from reaching DNA in superficial tissue [28–32].”

What the sources say

• ?Not checked — no full text of the sourcecites [28]
• ?Not checked — no full text of the sourcecites [29] source
• ?Not checked — no full text of the sourcecites [30] source
• Partly supported

  The Marine photoprotective compounds section (page not available) says organisms synthesize or accumulate UV-protective compounds, supporting the claim that such compounds serve as a defense. It does not say they are a 'first line' of defense or that UV radiation can still reach DNA in superficial tissue. (LLM, conf=0.84)

  cites [31] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [32] source

In the paper

“A number of endogenous factors such as free radicals [34] generated during metabolic processes as well as exogenous factors such as UV or ionizing radiations [35] are known to interfere with genome integrity.”

What the sources say

• Supported

  The citation to this paper, [34], is attached to the claim about endogenous free radicals, not the separate claim about UV and ionizing radiation cited to [35]. In the section accompanying Figure 1 (page not provided), the paper says the mitochondrial electron transport chain generates reactive oxygen species and that mitochondrial DNA is damaged by them. (LLM, conf=0.91)

  cites [34] source
• ?Not checked — no full text of the sourcecites [35] source

In the paper

“However, Su et al. [61] have reported a new photoproduct of 5-Methylcytosine and Adenine characterized by high-performance liquid chromatography and mass spectrometry.”

What the sources say

• Supported

  The paper’s title identifies it as a report of a new 5-methylcytosine–adenine photoproduct characterized by HPLC and mass spectrometry. The Experimental Procedures sections on RP-HPLC analysis and MS analysis document both methods. (LLM, conf=0.95)

  cites [61] source

In the paper

“Recently, Rumora et al. [82] have examined the thymine dimer-induced structural changes to the DNA duplex with several small, base-selective reactive chemical probes.”

What the sources say

• Supported

  The paper’s Discussion, under “Examining the Structure of Lesion-Containing DNA with Small Reactive Probes,” says the authors probed lesion-containing DNA with small reactive molecules and identifies KMnO4, DEPC, and DMS as the probes selected to examine base pairing and stacking. The Results section identifies the lesion studied as a central thymine dimer in a DNA duplex. (LLM, conf=0.95)

  cites [82] source

In the paper

“UV-induced DNA lesions such as CPDs and 6-4PPs show differential effects on DNA conformation, impairing their regulatory functions and other dynamic processes [24, 26, 75, 76].”

What the sources say

• ?Not checked — no full text of the sourcecites [24] source
• Partly supported

  The Figure 1 discussion reports different effects of the (6–4) adduct and the Dewar product on DNA distortion and polymerase bypass; the Abstract says UV photoproducts can block replication. The comparison in this source is not between CPDs and 6-4PPs, and the passages do not support the claim about impaired regulatory functions. (LLM, conf=0.84)

  cites [26] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [75] source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [76]

In the paper

“the existence of repair mechanisms was observed by Kelner [154] and Dulbecco [155] independently.”

What the sources say

• Partly supported

  The Discussion reports Kelner’s observation that visible light restored viability to UV-irradiated cells and proposes restoration of an altered cellular constituent as a working hypothesis. It does not identify that constituent as DNA or establish a DNA repair mechanism; it also does not address whether Dulbecco’s observation was independent. (LLM, conf=0.84)

  cites [154] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [155] source

In the paper

“To avoid the deleterious effects of UVR, plants have acquired two main protective strategies; shielding by flavonoids and phenolic compounds [168, 169] and DNA repair by photoreactivation.”

What the sources say

• Partly supported

  The paper’s Results (page not supplied) show that flavonoid-containing maize tissue had less UV-induced DNA damage, supporting flavonoid shielding. Our copy does not establish shielding by phenolic compounds beyond flavonoids. The citation is attached to the shielding clause, not the subsequent photoreactivation clause. (LLM, conf=0.84)

  cites [168] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [169] source

In the paper

“Deprotonated reduced flavin adenine dinucleotide (FADH−) is found in all known photolyases as a catalytic cofactor, which transfers energy in the form of an electron to the CPD, splitting the cyclobutane ring with the generation of two monomeric bases [157, 167]”

What the sources say

• ?Not checked — no full text of the sourcecites [157] source
• Supported

  The paper describes fully reduced FADH− as photolyase’s catalytic cofactor and says the excited cofactor transfers an electron to the pyrimidine dimer, whose ring then splits (Abstract). The Results and Discussion report direct electron transfer and electron return from repaired thymine monomers. Its general description of photolyase supports the citing sentence’s broad cofactor statement, although the experiments used E. coli photolyase. (LLM, conf=0.89)

  cites [167] source

In the paper

“The CSA protein (44 kDa) which belongs to “WD repeat” family of proteins exhibits structural and regulatory roles and CSB proteins (168 kDa) which belong to SWI/SNF family of proteins exhibit DNA-stimulated ATPase activity [217–219].”

What the sources say

• ?Not checked — no full text of the sourcecites [217] source
• ?Not checked — no full text of the sourcecites [218] source
• Supported

  The introductory passage gives CSA as a 44 kDa WD-repeat protein and CSB as a predicted 168 kDa SWI/SNF protein. The Discussion describes structural and regulatory roles for the WD-repeat family, and the paper reports DNA-stimulated ATPase activity for CSB. No page numbers are available in our copy. (LLM, conf=0.90)

  cites [219] source

In the paper

“hHR23B-XPC complex or only XPC exhibits a similar high affinity for both UV-induced single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) [230, 259], preferentially binds to DNA with various lesions [259] and even to small bubble structures with or without a lesion [260].”

What the sources say

• Partly supported

  The Results report that the XP-C–HHR23B complex bound strongly to a single-stranded DNA-cellulose column. The Discussion says this indicates high affinity for ssDNA but explicitly leaves open which component is responsible. The paper does not establish similarly high affinity for UV-damaged double-stranded DNA or for XPC alone; the citing sentence assigns the lesion and bubble claims to other references. (LLM, conf=0.88)

  cites [230] sourceExperimental — accuracy not yet measured
• Partly supported

  The DNA Binding Properties section (page not supplied) reports comparable high-affinity binding of the XPC–HHR23B complex to single- and double-stranded DNA, with slightly higher affinity for UV-irradiated duplex DNA; XPC alone also binds DNA strongly. It does not establish comparable binding to UV-damaged DNA in both strand forms or a preference for DNA with various kinds of lesions. The bubble-structure claim is attached to a different citation, [260], so it is not assessed against this paper. (LLM, conf=0.89)

  cites [259] sourceExperimental — accuracy not yet measured
• Supported

  The citation to this paper is attached to the small-bubble claim. In the section “XPC-HR23B binds a small bubble structure regardless of the presence or absence of lesions,” the authors report efficient binding to 3- and 5-base bubbles without AAF damage and binding to a 3-base bubble regardless of whether the lesion is present. (LLM, conf=0.94)

  cites [260] source

In the paper

“hHR23B-XPC is absolutely required for dual incision as well as for open complex formation during GG-NER [243, 261].”

What the sources say

• Partly supported

  In “XPC and XPA participate in open complex formation,” XPC-defective extracts failed to form the full open complex around a platinum lesion, and adding XPC-hHR23B restored both opening and dual incision. The same section says that repair of certain other lesions does not require XPC in vitro, so the paper does not support “absolutely required” as an unqualified statement about GG-NER. (LLM, conf=0.85)

  cites [243] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [261] source

In the paper

“Both XPA and RPA can recruit with the DNA lesions in absence of XPG, and similarly XPG can also join the damage sites in the absence of XPA [238, 239].”

What the sources say

• ?Not checked — no full text of the sourcecites [238] source
• Partly supported

  The introduction (page unavailable) says XPA binds preferentially to damaged DNA, and the paper reports an XPA–RPA interaction. It does not establish that XPA or RPA is recruited to lesions without XPG, or that XPG reaches damage sites without XPA. (LLM, conf=0.82)

  cites [239] sourceExperimental — accuracy not yet measured

In the paper

“Both hHR23A and -B harbor a ubiquitin-like moiety at their amino terminus [230].”

What the sources say

• Supported

  Figure 7B compares the N-terminal conserved regions of HHR23A and p58/HHR23B with ubiquitin-like domains. The text also identifies a ubiquitin-like N-terminus in the RAD23 homologues. Page numbers are not provided in our copy. (LLM, conf=0.94)

  cites [230] source

In the paper

“Overall, it has been distinguished that RNA pol II with the recruitment of two proteins (i.e., CSA and CSB) proceeds the TCR while hHR23B-XPC complex is the first factor in NER that initiates GGR by sensing and binding lesions, locally distorting the DNA double helix and recruiting the other factors of the system [227].”

What the sources say

• Supported

  The paper states that elongating RNA polymerase II detects lesions in transcription-coupled NER and that CSA and CSB are needed for efficient repair of transcribed strands. In the XPC-hHR23B section, it explicitly says the complex initiates global-genome NER by binding lesions, distorting the helix locally, and recruiting other repair factors. (LLM, conf=0.95)

  cites [227] source

In the paper

“Genetic and genomic analysis indicates that plant NER pathway is homologous to that of mammals and fungi and unrelated to the bacterial system [204, 271–273].”

What the sources say

• ?Not checked — no full text of the sourcecites [204] source
• Partly supported

  The Results (page not specified) identify plant homologs of eukaryotic NER genes, and the Discussion (page not specified) concludes that the repair pathway is highly conserved among plants, mammals, and fungi. But the Results describe the bacterial mechanism as similar, with little homology between bacterial and eukaryotic proteins; that does not support calling the systems wholly unrelated. (LLM, conf=0.84)

  cites [271] sourceExperimental — accuracy not yet measured
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [272]
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [273]

In the paper

“For instance, 6-4PPs are removed much faster from the genome than CPDs, possibly because of disparity in affinity of the damage sensor hHR23B-XPC.”

What the sources say

• Partly supported

  The Introduction and results on repair in specific sequences (page not supplied) report that 6-4PPs are repaired much faster than CPDs in normal human fibroblasts. The Discussion reports similar repair kinetics for the two lesions in XP-C fibroblasts. Our copy does not support the proposed explanation involving differential affinity of hHR23B-XPC. (LLM, conf=0.88)

  cites [211] sourceExperimental — accuracy not yet measured

In the paper

“XPC is the sole XP factor not essential for TCR and is restricted to GGR [211].”

What the sources say

• Partly supported

  The Introduction says XP-C fibroblasts retain transcription-coupled repair (TCR), and the Discussion contrasts their TCR-only repair with normal cells’ TCR and global repair. This supports that XPC is not essential for TCR and is associated with global repair, but the paper does not establish that XPC is the sole XP factor with that distinction. (LLM, conf=0.84)

  cites [211] sourceExperimental — accuracy not yet measured

In the paper

“Rad51 (a functional homolog of the E. coli RecA) [298] is the central protein in HR, binds the exposed single-stranded tails forming a nucleoprotein filament and this early step is promoted by a Rad55/Rad57 protein heterodimer [299] by overcoming the inhibitory effects of the heterotrimeric single-stranded DNA binding protein RPA [300].”

What the sources say

• ?Could not verify

  Citation [300] is attached to the claim that Rad55/Rad57 overcomes RPA’s inhibition of Rad51 filament formation. The paper’s passage labeled Abstract (page unavailable) says RPA binding is essential for Rad51 loading, but does not address that proposed inhibitory effect or how Rad55/Rad57 might overcome it. Searches for Rad55/Rad57 and RPA inhibition found no decisive passage. (LLM, conf=0.73)

  cites [298] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [299] source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [300]

In the paper

“It has been shown that Ku complex (a heterodimer of Ku70/Ku80 [≈86]) is a major end binding factor in mammalian cells, possess end bridging activity [308, 309].”

What the sources say

• ?Not checked — no full text of the sourcecites [308] source
• Supported

  The Introduction identifies Ku as a heterodimer of 70 and 86 kDa subunits that binds duplex-DNA ends and is implicated in mammalian end joining. The ‘Ku promotes association of two DNA molecules’ section reports a pulldown assay showing that Ku bridges DNA molecules, while the Discussion describes its role in end joining as a critical component of its function in vivo. The copy does not quantify ‘major,’ but it supports the broad characterization. (LLM, conf=0.89)

  cites [309] source

In the paper

“The eukaryotic RAD51s play a significant role in HR, maintaining genome integrity in both mitotic as well as meiotic cell cycle [288, 289].”

What the sources say

• ?Not checked — no full text of the sourcecites [288] source
• Partly supported

  The Abstract (page not available) says Rad51 plays a central role in homologous recombination, and the discussion of RAD51-paralog mutants reports chromosomal aberrations alongside impaired Rad51-mediated recombination. The paper identifies DMC1 as meiosis-specific, but the passages do not establish that RAD51 proteins maintain genome integrity in both mitotic and meiotic cell cycles; that part of the claim is more specific than the evidence. (LLM, conf=0.82)

  cites [289] sourceExperimental — accuracy not yet measured

In the paper

“Genetic and biochemical evidence suggest that Mre11-Rad50-Xrs2 (MRX) act as end bridging factor in yeast NHEJ, since DNA-PKcs is absent in them [319, 320].”

What the sources say

• Partly supported

  The Discussion’s “A DNA End-Bridging Model” proposes that Mre11, or the MRX complex, holds two DNA ends together; the Discussion also cites yeast genetic and biochemical observations linking MRX to NHEJ. Our copy does not say that DNA-PKcs is absent in yeast or give its absence as the reason MRX may bridge ends. Page numbers were not available in the indexed passages. (LLM, conf=0.88)

  cites [319] sourceExperimental — accuracy not yet measured
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [320]

In the paper

“Moreover, a plant homologue of human NER gene of the endonuclease, ERCC1, has been cloned from Lilium longiflorum which showed a similar role in DNA repair in plants [279].”

What the sources say

• Partly supported

  The Isolation of cDNA clone and sequence analysis section identifies a Lilium longiflorum clone homologous to human ERCC1. The DNA repair activity section shows that lily ERCC1 corrected sensitivity to mitomycin C in ERCC1-deficient hamster cells, but did not correct UV sensitivity. The paper infers a conserved DNA-repair role in plants; it does not demonstrate that role in plant cells, as the claim's 'showed' implies. (LLM, conf=0.88)

  cites [279] sourceExperimental — accuracy not yet measured

In the paper

“SOS repair system is initiated by interaction of two crucial proteins the RecA and the LexA repressor which curbs the expression of SOS genes by binding to their promoters [327] (Figure 14).”

What the sources say

• Supported

  The Results and discussion section (‘4 – Other repair related proteins,’ subsection ‘A – SOS system’) says LexA represses SOS genes by binding their promoters and that RecA inactivates LexA to induce the system. This supports the cited description of how SOS repair is initiated. (LLM, conf=0.94)

  cites [327] source

In the paper

“The recA gene encodes a DNA-dependent ATPase that binds to ssDNA and promotes strand invasion and exchange between homologous DNA molecules [285].”

What the sources say

• Supported

  The introductory passage identifies recA protein as the product of the recA gene and says it promotes assimilation of single-stranded DNA into homologous duplex DNA, forming a D-loop. The Results describe recA binding to single-stranded DNA, and the abstract reports ATP hydrolysis catalyzed by recA in its presence. Page numbers are not available in our copy. (LLM, conf=0.91)

  cites [285] source

In the paper

“When the repair mechanisms are unsuccessful, it may cause cellular senescence (permanent cell cycle arrest), oncogenesis or apoptosis [354].”

What the sources say

• Partly supported

  The Introduction (page not specified) says cells with damage beyond repair may undergo apoptosis. It does not identify senescence or oncogenesis as outcomes of failed repair; the section on malfunctioning apoptosis links cancer to faulty apoptosis instead. (LLM, conf=0.86)

  cites [354] sourceExperimental — accuracy not yet measured

In the paper

“Recently, the genes imuA and imuB have been described that induce SOS mutagenesis in Caulobacter crescentus, but absent in E. coli [332].”

What the sources say

• Partly supported

  The Discussion (page unavailable) states that the SOS-regulated imuAB–dnaE2 operon is responsible for most damage-inducible mutagenesis in Caulobacter crescentus. It contrasts this machinery with that of E. coli, but the passages do not establish that both imuA and imuB are absent from E. coli. (LLM, conf=0.84)

  cites [332] sourceExperimental — accuracy not yet measured

In the paper

“The occurrence of DNA damage response in G2-phase, leads to checkpoint mediator (claspin) dependent activation of Chk1/2, followed by SCFβTrcP mediated degradation of CDK-activating phosphatase Cdc25A [341, 342], that results in arrest of multiple cell-cycle transition including the G2 checkpoint [343, 344].”

What the sources say

• Partly supported

  The Abstract and Discussion (page not provided) support SCFβ-TRCP-mediated Cdc25A turnover in response to DNA damage and Chk1-dependent Cdc25A ubiquitination. They do not establish claspin-dependent Chk1/2 activation specifically in G2 phase. The sentence attaches separate citations to its later claim about arresting multiple cell-cycle transitions. (LLM, conf=0.86)

  cites [341] sourceExperimental — accuracy not yet measured
• Partly supported

  The introductory passage (page unavailable) says that DNA damage activates Chk1 and Chk2, promoting SCF-dependent Cdc25A degradation, and describes β-TrCP-dependent ubiquitination. It does not establish that this response occurs specifically in G2 or that Chk1/2 activation depends on claspin. The cell-cycle-arrest clause has separate citations [343, 344] and is not assessed against this source. (LLM, conf=0.85)

  cites [342] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [343] source
• Partly supported

  The Results report that DNA damage induced G2 arrest with proteasome-dependent Cdc25A destruction, and that restoring Cdc25A partially abrogated the G2 checkpoint. The Introduction also describes Chk1- or Chk2-mediated Cdc25A phosphorylation in earlier checkpoint responses. Our copy does not establish claspin-dependent Chk1/2 activation or identify SCFβTrcP as the mediator of Cdc25A degradation. (LLM, conf=0.88)

  cites [344] sourceExperimental — accuracy not yet measured

In the paper

“It has been reported that translesion synthesis past a CPD, facilitated by pol. η, with the insertion of adenines opposite both bases of a T∧T CPD [352], where as 6-4TT may lead to a G insertion.”

What the sources say

• Supported

  The citation is attached to the CPD clause, not the subsequent 6-4TT clause. In the translesion-synthesis section (p. 3102), the paper reports that polymerase η efficiently bypassed a TT CPD; its discussion reports preferential dAMP incorporation opposite the thymines of a CPD and preferential extension from primers with A opposite a dimer thymine. The paper presents the dAMP-incorporation result as a finding from steady-state kinetic experiments, rather than as a determination made in its own incorporation assay. (LLM, conf=0.90)

  cites [352] source

In the paper

“Interestingly, it has been found that DNA polymerase IV (dinB) is also involved in translesion synthesis in E. coli [331].”

What the sources say

• Partly supported

  The Results identify dinB as E. coli DNA polymerase IV, and the Discussion links it to spontaneous mutation when replication is stalled. Neither passage establishes that it performs translesion synthesis; the paper discusses mutation on ostensibly undamaged templates instead. (LLM, conf=0.82)

  cites [331] sourceExperimental — accuracy not yet measured

In the paper

“Additionally, double-strand break repair (by homologous recombination and nonhomologous end joining), SOS response, cell-cycle checkpoints, and programmed cell death (apoptosis) are also operative in various organisms with the expense of specific gene products.”

In the paper

“The hydrolytic deamination (loss of an amino group) can directly convert one base to another; for example, deamination of cytosine results in uracil and at much lower frequency adenine to hypoxanthine.”

In the paper

“The formation of “spore photoproduct” has been detected in UV-irradiated bacterial spores by the addition of methyl group of one thymine residue to the C5 position of an adjacent thymine. In most cellular environments, there is no much significance of this photoproduct, since it requires anhydrous conditions for its formation [49].”

What the sources say

• ?Not checked — no full text of the sourcecites [49] source

In the paper

“The 6-4PPs are eagerly converted into their Dewar valence isomers upon exposure to UV-B or UV-A radiation that may further undergo reversion to the 6-4PPs upon exposure to short-wavelength UV radiation [45].”

What the sources say

• ?Not checked — no full text of the sourcecites [45] source

In the paper

“Although UV-B radiation has less than 1% of total solar energy, it is a highly active component of the solar radiation that brings about chemical modification in DNA and changes its molecular structure by the formation of dimers.”

In the paper

“Certain enzymes, such as superoxide dismutase (SOD), catalase (CAT), peroxidase (POD), and scavengers such as vitamin C, B, and E, cysteine, and glutathione play an additional role in defense against UV radiation [33].”

What the sources say

• ?Not checked — no full text of the sourcecites [33] source

In the paper

“The amounts of CPDs and 6-4PPs are about 75 and 25%, respectively, of the total UV-mediated DNA damage products [22]; however, the ratio between the yield of CPDs and 6-4PPs mainly depends upon the two adjacent bases involved in the formation of dimers [54].”

What the sources say

• ?Not checked — no full text of the sourcecites [22] source
• ?Not checked — no full text of the sourcecites [54] source

In the paper

“Moreover, ozone depletion followed by increased UV exposure has been predicted to continue throughout most of this century [11].”

What the sources say

• ?Not checked — no full text of the sourcecites [11] source

In the paper

“It has been demonstrated that the main photoproducts are cis-syn-configured CPD lesions, while trans-syn-configured CPD lesions are formed in much less quantity [47].”

What the sources say

• ?Not checked — no full text of the sourcecites [47] source

In the paper

“In depurination/depyrimidination, there are complete removals of purine/pyrimidine bases, leaving the deoxyribose sugar depurinated/depyrimidinated, that may cause breakage in the DNA backbone.”

In the paper

“Thus the heterogeneous distribution of the UV-induced photolesions in the DNA depends on the sequences that facilitate DNA bending as well as the chromatin modulation through the binding of specific protein [55].”

What the sources say

• ?Not checked — no full text of the sourcecites [55] source

In the paper

“CPDs correspond to the formation of a four-member ring structure involving C5 and C6 of both neighboring bases whereas 6-4PPs are formed by a noncyclic bond between C6 (of the 5′-end) and C4 (of the 3′-end) of the involved pyrimidines via spontaneous rearrangement of the oxetane (when the 3′-end is thymine) (Figure 3(a)) or azetidine (when the 3′-end is cytosine) (Figure 3(b)) intermediates [5, 44”

What the sources say

• ?Not checked — no full text of the sourcecites [5] source
• ?Not checked — no full text of the sourcecites [44] source

In the paper

“DNA damage results in (i) misincorporation of bases during replication process, (ii) hydrolytic damage, which results in deamination of bases, depurination, and depyrimidination [36], (iii) oxidative damage, caused by direct interaction of ionizing radiations (IR) with the DNA molecules, as well as mediated by UV radiation-induced free radicals or reactive oxygen species [37, 38], and (iv) alkyl”

What the sources say

• ?Not checked — no full text of the sourcecites [36] source
• ?Not checked — no full text of the sourcecites [37] source
• ?Not checked — no full text of the sourcecites [38] source

In the paper

“One of the most prominent targets of solar UV-radiation is cellular DNA, which absorbs UV-B radiation and causes adverse effects on living systems such as bacteria [15, 16], cyanobacteria [17], phytoplankton [18], macroalgae [19], plants [20], animals, and humans [21–23].”

What the sources say

• ?Not checked — no full text of the sourcecites [15] source
• ?Not checked — no full text of the sourcecites [16] source
• ?Not checked — no full text of the sourcecites [17]
• ?Not checked — no full text of the sourcecites [18] source

In the paper

“At high concentrations oxygen-free radicals or, more frequently, reactive oxygen species (ROS) can induce damage to cell structure, lipids, proteins as well as DNA and results in oxidative stress which has been implicated in a number of human diseases [40].”

What the sources say

• ?Not checked — no full text of the sourcecites [40] source

In the paper

“CPDs are formed at higher quantity by cycloaddition reaction between two pyrimidine bases [47] in single-stranded DNA (ssDNA) and at the flexible ends of poly (dA)-(dT) tracts, but not at their rigid centre [50, 51].”

What the sources say

• ?Not checked — no full text of the sourcecites [47] source
• ?Not checked — no full text of the sourcecites [50] source
• ?Not checked — no full text of the sourcecites [51] source

In the paper

“UV-C radiation is quantitatively absorbed by oxygen and ozone in the Earth's atmosphere, hence does not show much harmful effects on biota.”

In the paper

“It has been documented that UV-B severely affects survival, fecundity, and sex-ratio in several intertidal copepods [14].”

What the sources say

• ?Not checked — no full text of the sourcecites [14] source

In the paper

“In double stranded B-DNA, where the dimer entails two adjoining pyrimidine bases on the same DNA strand, only the syn isomers can be generated, whereas the cis isomer is preferred over the trans isomer to a great extent [42].”

What the sources say

• ?Not checked — no full text of the sourcecites [42] source

In the paper

“Photodimerization of adenine (A) involves the cycloaddition of N7-C8 double bond of the 5′-A across the C6 and C5 positions of the 3′-A [65, 69] and generates a very unstable azetidine intermediate.”

What the sources say

• ?Not checked — no full text of the sourcecites [65] source
• ?Not checked — no full text of the sourcecites [69] source

In the paper

“There is little information concerning the formation of cytosine hydrates in UV-irradiated DNA due to instability of the resulting photoproduct [63].”

What the sources say

• ?Not checked — no full text of the sourcecites [63] source

In the paper

“Overall, it has been concluded that UV-induced DNA lesions such as CPDs, 6-4PPs, abasic site, strand breaks, and oxidative product are the predominant and most persistent lesions and if not repaired may cause severe structural distortions in the DNA molecule, thereby affecting the important cellular processes such as DNA replication and transcription, compromising cellular viability and functional”

What the sources say

• ?Not checked — no full text of the sourcecites [30] source
• ?Not checked — no full text of the sourcecites [36] source

In the paper

“Although dipyrimidine photoproducts are the preferential outcome of UV-B radiation, the biological importance of UV radiation-induced modifications of DNA purine bases has also been recognized [64].”

What the sources say

• ?Not checked — no full text of the sourcecites [64] source

In the paper

“UV-B-induced ROS [89] as well as DNA lesions (CPDs and 6-4PPs) may cause primary as well as secondary breaks, respectively.”

What the sources say

• ?Not checked — no full text of the sourcecites [89] source

In the paper

“The extent of adenine-containing photoproduct (A-T) is very low (1 × 10−5 in native DNA) but these lesions may contribute to the biological effects of UV radiation in view of the fact that the A-T adduct has been shown to be mutagenic [67, 68].”

What the sources say

• ?Not checked — no full text of the sourcecites [67] source
• ?Not checked — no full text of the sourcecites [68] source

In the paper

“DNA photolyases (45–66 kDa) having 420–616 amino acid residues [158] are monomeric flavin-dependent repair enzymes, consisting of two known cofactors, a catalytic cofactor and a light-harvesting cofactor.”

What the sources say

• ?Not checked — no full text of the sourcecites [158] source

In the paper

“The process of photoreactivation is executed by means of a photoreactivating enzyme known as “photolyase”, which is well conserved and found throughout the three domains of life (Table 2).”

In the paper

“6-4 photolyases have been identified in certain organisms like Drosophila, silkworm, Xenopus laevis, and rattle snakes [22].”

What the sources say

• ?Not checked — no full text of the sourcecites [22] source

In the paper

“CPD photolyases have been reported in diverse groups such as archaea, bacteria, fungi, virus, plants, invertebrates, and many vertebrates including aplacental mammals (Table 2).”

In the paper

“It has been observed that about 240 KJ/mol of energy is captured upon absorption, out of which about 125 KJ/mol energy is consumed during the initial electron transfer from the excited FADH to CPD lesions [177].”

What the sources say

• ?Not checked — no full text of the sourcecites [177] source

In the paper

“UV-induced replication arrest in the xeroderma pigmentosum variant (XPV) followed by the accumulation of Mre11/Rad50/Nbs1 complex and phosphorylated histone H2AX (γ-H2AX) in large nuclear foci at sites of stalled replication forks also suggests that UV damage leads to the formation of DSBs during the course of replication arrest [90, 95].”

What the sources say

• ?Not checked — no full text of the sourcecites [90] source
• ?Not checked — no full text of the sourcecites [95] source

In the paper

“The enzyme binds specifically to the CPDs (CPD photolyase) or 6-4PPs (6-4 photolyase) and directly monomerizes the cyclobutane ring of the pyr <> pyr, using the energy of visible/blue-light and protects the genome from deleterious effects of UVR [157, 158].”

What the sources say

• ?Not checked — no full text of the sourcecites [157] source
• ?Not checked — no full text of the sourcecites [158] source

In the paper

“Studies on Arabidopsis seedling, rice, and alfalfa indicate that photoreactivation greatly enhances the rate of removal of dimers, although, in the absence of photoreactivating (blue) light, dimers are slowly eliminated from bulk DNA and 6-4PPs are generally observed to be repaired more quickly than CPDs [173, 174].”

What the sources say

• ?Not checked — no full text of the sourcecites [173] source
• ?Not checked — no full text of the sourcecites [174] source

In the paper

“A number of workers have identified a human photolyase which shows homology with Cry gene (plant blue-light receptor) and about 40% sequence identity to the Drosophila 6-4 photolyase”

What the sources say

• ?Not checked — no full text of the sourcecites [164] source

In the paper

“Overall, it seems that UV radiation does not directly produce DNA DSBs but rather produces pyrimidine dimers and other photoproducts leading to replication arrest and DSBs.”

In the paper

“MacFarlane and Stanley [178] have suggested that photolyase enzyme is indeed left in the semiquinonid state after accomplishment of repair of the CPD lesion.”

What the sources say

• ?Not checked — no full text of the sourcecites [178] source

In the paper

“Recently, Almeida and Sobol [184] have proposed a unified model of SP-BER and LP-BER.”

What the sources say

• ?Not checked — no full text of the sourcecites [184] source

In the paper

“Eukaryotic NER is known to be similar to prokaryotes regarding the biochemical strategy used but differs widely in the nature and number of proteins used [210].”

What the sources say

• ?Not checked — no full text of the sourcecites [210] source

In the paper

“The AP-site is removed by the action of AP endonuclease-1 (APE-1) along with phosphodiesterase that breaks the DNA strand along 5′ or 3′ to the AP site, respectively, and subsequently the gap is filled by a repair DNA polymerase and the strand is joined by a DNA ligase (Figure 10) [182, 191].”

What the sources say

• ?Not checked — no full text of the sourcecites [182] source
• ?Not checked — no full text of the sourcecites [191] source

In the paper

“Discovery of NER was first described in E. coli [212, 213] where about six proteins such as UvrA, B, and C (known as ABC-complex, which shows excinuclease activity), UvrD (helicase II), DNA polymerase I (pol. I), and DNA ligase are recruited to complete the repair [214, 215].”

What the sources say

• ?Not checked — no full text of the sourcecites [212] source
• ?Not checked — no full text of the sourcecites [213] source
• ?Not checked — no full text of the sourcecites [214] source
• ?Not checked — no full text of the sourcecites [215] source

In the paper

“DNA having one nucleotide lesion is removed by short-patch BER (SP-BER) whereas two/more nucleotide lesion is repaired by long-patch BER (LP-BER) pathway [195] (Figure 10).”

What the sources say

• ?Not checked — no full text of the sourcecites [195] source

In the paper

“The flap endonuclease (Fen1) protein then displaces the ensuing DNA flap leaving a nick which is ligated by DNA ligase I (Lig. I) [200, 201].”

What the sources say

• ?Not checked — no full text of the sourcecites [200] source
• ?Not checked — no full text of the sourcecites [201] source

In the paper

“The formation of AP sites has been observed in seeds of Zea mays during early germination. This phenomenon was attributed to the action of DNA glycosylases on lesions accumulated during seed storage [207], implying the presence of BER in this species.”

What the sources say

• ?Not checked — no full text of the sourcecites [207] source

In the paper

“Unlike SP-BER, LP-BER involves proliferating cell nuclear antigen (PCNA) coupled with DNA pol. −δ/ε or β which extends and fills the gap by inserting 2–13 nucleotide [184].”

What the sources say

• ?Not checked — no full text of the sourcecites [184] source

In the paper

“It has been suggested that the RNA pol II backs up some nucleotides upon encountering the lesion to facilitate the accessibility of the repair machinery to the lesion site [220, 221].”

What the sources say

• ?Not checked — no full text of the sourcecites [220] source
• ?Not checked — no full text of the sourcecites [221] source

In the paper

“It is expected that the CSB protein ubiquitinates the stalled elongating RNA pol II complex at the lesion and enhances the assembly of repair factors [222].”

What the sources say

• ?Not checked — no full text of the sourcecites [222] source

In the paper

“Recently, Fousteri et al. [224] has revealed that CSB is a prerequisite factor in vivo to assemble NER proteins while it is not essential to recruit TFIIH or NER complex in vitro.”

What the sources say

• ?Not checked — no full text of the sourcecites [224] source

In the paper

“TFIIH is usually involved in initiation of RNA Pol II transcription, but upon DNA damage can be employed in cell cycle regulation and NER (both in global genome and TC-NER) [228, 235].”

What the sources say

• ?Not checked — no full text of the sourcecites [228] source
• ?Not checked — no full text of the sourcecites [235] source

In the paper

“In mammalian cells, the quantity of hHR23B is higher than the XPC [255]”

What the sources say

• ?Not checked — no full text of the sourcecites [255] source

In the paper

“Sugasawa et al. [226] showed that hHR23B-XPC attaches directly to DNA damage and alters the DNA conformation around the lesion.”

What the sources say

• ?Not checked — no full text of the sourcecites [226] source

In the paper

“TFIIH is a ten-subunit protein complex (Table 4) composed of a core complex (XPB, XPD, p62, p44, p34, p52, p8) and of a cdk activating kinase (CAK) subunit (Mat1, Cdk7, CyclinH) [236].”

What the sources say

• ?Not checked — no full text of the sourcecites [236] source

In the paper

“XPA and heterotrimeric replication protein A (RPA; RPA70, 32 and 14) are recruited to confirm the presence of DNA damage and form a more stable preincision complex [185].”

What the sources say

• ?Not checked — no full text of the sourcecites [185] source

In the paper

“It has been found that the XPD helicase activity is dispensable for in vitro transcription [262] but seems to play an additional architectural role within the complex by connecting the core TFIIH with the CAK subunit [228, 236].”

What the sources say

• ?Not checked — no full text of the sourcecites [262] source
• ?Not checked — no full text of the sourcecites [228] source
• ?Not checked — no full text of the sourcecites [236] source

In the paper

“very recently it has been reported that mostly ligase III, in cooperation with its partner XRCC1 seals the DNA nicks and ligase I plays a minor role in actively replicating cells, but not in quiescent cells [268].”

What the sources say

• ?Not checked — no full text of the sourcecites [268] source

In the paper

“Several observations provide evidence that “dark” repair of UV-induced NER is a significant DNA repair mechanisms in plants that is capable of excising dimers, particularly 6-4PPs [30, 270].”

What the sources say

• ?Not checked — no full text of the sourcecites [30] source
• ?Not checked — no full text of the sourcecites [270] source

In the paper

“It was shown that DDB complex is recruited first to the lesion (CPD) before the XPC complex, on little distorted DNA helix; however, in case of large distortion of the DNA helix caused by 6-4PPs, direct recognition by XPC is also possible for this”

What the sources say

• ?Not checked — no full text of the sourcecites [216] source
• ?Not checked — no full text of the sourcecites [253] source

In the paper

“It was reported that XPC and UV-DDB materialize to assist for the efficient recognition of UV-induced photolesions and that both factors are ubiquitylated [250, 253].”

What the sources say

• ?Not checked — no full text of the sourcecites [250] source
• ?Not checked — no full text of the sourcecites [253] source

In the paper

“Lesions that cause little distortion can be recognized by the DDB complex which is also part of an E3 ubiquitin (Ub) ligase that poly-ubiquitinates XPC and XPE [216].”

What the sources say

• ?Not checked — no full text of the sourcecites [216] source

In the paper

“A UV-specific endonuclease resembling UvrABC nuclease in activity was partially characterized from spinach [206].”

What the sources say

• ?Not checked — no full text of the sourcecites [206] source

In the paper

“XPG, which belongs to flap endonuclease-1 (FEN-1) family of structure-specific endonucleases [264], is not only involved in performing the 3′ incision in NER but also required for stabilizing the fully open DNA bubble structure and to permit the 5′ incision by ERCC1- XPF [265].”

What the sources say

• ?Not checked — no full text of the sourcecites [264] source
• ?Not checked — no full text of the sourcecites [265] source

In the paper

“Recombinational repair is a significant UV-tolerance mechanism in plants where UV-induced chromosomal rearrangements including homologous intrachromosomal recombination events have been found [296].”

What the sources say

• ?Not checked — no full text of the sourcecites [296] source

In the paper

“In E. coli, this HJ is resolved by the positioning of RuvABC resolvasome, however in eukaryotic cell, how this HJ is resolved to give crossover products is not known.”

In the paper

“The accumulation of massive amount of DNA lesions within the cells under different specific physiological responses [324] may lead to the occurrence of SOS repair system which was well described in E. coli, where the involvement of more than 40 genes have been found [325].”

What the sources say

• ?Not checked — no full text of the sourcecites [324] source
• ?Not checked — no full text of the sourcecites [325] source

In the paper

“When HR is inactivated, an alternate pathway, that is, NHEJ becomes operative for the repair of DSBs [303], that also involves a multi-protein complex and has been found in organisms ranging from a few prokaryotes to mammals.”

What the sources say

• ?Not checked — no full text of the sourcecites [303] source

In the paper

“Homologues of most of the genes are highly conserved among all eukaryotes including human [282, 283] highlighting these genes for cell survival.”

What the sources say

• ?Not checked — no full text of the sourcecites [282] source
• ?Not checked — no full text of the sourcecites [283] source

In the paper

“The proteolytic activity of RecA protein inactivates the LexA repressor and induces all the genes to which LexA is associated.”

In the paper

“For instance, mutation of at least one of these repair proteins, called BRCA1 may lead to hereditary breast cancer [280].”

What the sources say

• ?Not checked — no full text of the sourcecites [280] source

In the paper

“Among all, E. coli recA gene and its eukaryotic homologs RAD51s are the best recombination genes [284].”

What the sources say

• ?Not checked — no full text of the sourcecites [284] source

In the paper

“The Rad51 nucleoprotein filament in association with other repair protein searches the genome for an intact copy of the broken DNA on the sister chromatid to form a heteroduplex joint molecules or D-loop that is matured in to a Holliday junctions (HJs). HJ is then resolved to give crossover products (Figure 13).”

In the paper

“Virtually, the joint molecule formation is followed by extension of the incoming strand by DNA polymerases and branch migration, leading to restoration of the genetic information [283, 302].”

What the sources say

• ?Not checked — no full text of the sourcecites [283] source
• ?Not checked — no full text of the sourcecites [302] source

In the paper

“Among eukaryotes, the yeast S. cerevisiae and Schizosaccharomyces pombe have four RAD51-like genes (RAD51, DMC1, RAD55/rhp55, and RAD57/rhp57) [286, 287] whereas vertebrate animals and plants have seven types of RAD51-like genes (RAD51, -51B, -51C, -51D, DMC1, XRCC2, and XRCC3) [288].”

What the sources say

• ?Not checked — no full text of the sourcecites [286] source
• ?Not checked — no full text of the sourcecites [287] source
• ?Not checked — no full text of the sourcecites [288] source

In the paper

“There are 59% identity between S. cerevisiae, human and mouse in the case of Rad51 protein (Rad51p) and 30% identity to RecA protein of bacteria [290], whereas yeast and human proteins are 60% identical in case of Rad52 proteins (Rad52p) [291].”

What the sources say

• ?Not checked — no full text of the sourcecites [290] source
• ?Not checked — no full text of the sourcecites [291] source

In the paper

“It has been suggested that as in mammals, breaks are repaired by nonhomologous recombination far more frequently than via HR [202, 323].”

What the sources say

• ?Not checked — no full text of the sourcecites [202] source
• ?Not checked — no full text of the sourcecites [323] source

In the paper

“DSB repair through HR process is an error free pathway, since, it requires an extensive region of sequence homology between the damaged and template strands, whereas NHEJ is an error prone, alternate pathway for the repair of DSBs, essentially joins broken chromosomal ends independent of sequence homology.”

In the paper

“Recently, a third protein, designated as XLF or Cernunnos [313] that has homology to Xrcc4, has been identified and shown to co-associate with the DNA ligaseIV/Xrcc4 complex [314, 315].”

What the sources say

• ?Not checked — no full text of the sourcecites [313] source
• ?Not checked — no full text of the sourcecites [314] source
• ?Not checked — no full text of the sourcecites [315] source

In the paper

“The intermediate component of this pathway is β-TrcP (an adaptor protein) that links both WEE1 [346] and claspin [347–349] with the SCF ubiquitin ligase complex and this SCFβTrcP acts as trigger of checkpoint initiation where recognition of phosphodegron β-TrcP is exposed after Chk1 mediated Phosphorylation of Cdc25A [350], as well as checkpoint recovery which is linked with Plk1 mediated Phospho”

What the sources say

• ?Not checked — no full text of the sourcecites [346] source
• ?Not checked — no full text of the sourcecites [347] source
• ?Not checked — no full text of the sourcecites [348] source
• ?Not checked — no full text of the sourcecites [349] source
• ?Not checked — no full text of the sourcecites [350] source

In the paper

“Under normal conditions, this latter complex being active promotes G2/M transition and upon inactivation due to DNA damage, blocks the G2 cell-cycle and unlike the G1/S checkpoint this arrest seems to be partly p53/p21 independent [183].”

What the sources say

• ?Not checked — no full text of the sourcecites [183] source

In the paper

“Activation of both ATM and ATR results in phosphorylation of Chk2 and Chk1 respectively which transfer the DNA damage signal to the cell-division cycle proteins Cdc25(A-C).”

In the paper

“It has been shown that ATM and DNA-PK are activated by the presence of DSBs where as activation of ATR takes place by single strand regions of DNA [337, 338].”

What the sources say

• ?Not checked — no full text of the sourcecites [337] source
• ?Not checked — no full text of the sourcecites [338] source

In the paper

“The SOS response is induced with damage signal but it is highly mutagenic due to engagement of error-prone DNA polymeraseV (UmuC/UmuD2 complex) [329] and DNA polymerase IV [330] in E. coli.”

What the sources say

• ?Not checked — no full text of the sourcecites [329] source
• ?Not checked — no full text of the sourcecites [330] source

In the paper

“Majchrzak et al. [324] examined the effects of SOS response on genome stability of trinucleotide repeat sequences (TRS) in E. coli and observed that SOS response genes destabilized the TRS tracts and also altered the superhelical density of the plasmids.”

What the sources say

• ?Not checked — no full text of the sourcecites [324] source