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PubMed2003

Improved preservation of coagulation factors after pre-storage leukocyte depletion of whole blood.

Plasma and red blood cell quality are affected both by citrate concentration and the levels of extracellular leukocyte and platelet derived substances, accumulated during storage of blood. The effect of leukocyte filtration on the storage stability of whole blood was therefore studied in blood collected in standard CPD and 0.5CPD (CPD with half strength citrate concentration). A total of 52 units, 12 of them with reduced citrate concentration, were leukocyte-filtered with Pall( whole blood filter (WBF1 or 3). No differences in leukocyte or platelet reduction were observed with the two citrate concentrations. However, with 0.5CPD a significantly longer filtration time and increased complement activation was observed. The effect of pre-storage leukocyte filtration on the plasma quality of whole blood was therefore only studied with standard CPDA1 anticoagulant solution (normal strength citrate concentration). Leukocyte filtration did not affect the von Willebrand factor concentration, while a small reduction (7%, p=0.04) in factor VIII (FVIII) concentration was observed. During storage, however, FVIII decreased more slowly in the filtered than in the unfiltered product, and, from day two, the FVIII content was significantly higher in the filtered product (46% versus 30% at 28 days, p<0.001). Factor V (FV) demonstrated a 16% reduction (p<0.001) upon filtration, followed by an additional 8% in the next 24 h and only a 4% reduction the next 27 days, while unfiltered products demonstrated a continuous reduction to 26% at 28 days. While the beta-thromboglobulin (beta-TG) concentration significantly increased (from 836 to 2483 IU/ml, p<0.001) during leukocyte filtration, no further increase was observed during storage. In contrast, unfiltered products demonstrated an increase to 5762 IU/ml (p<0.001) at 14 days, followed by a slight, not significant, reduction. This indicates platelet activation during filtration and explains a parallel reduction in FV. Filtration induced no increase in prothrombin fragment 1+2, while a slight increase was observed in some unfiltered products after 28 days of storage.Pre-storage leukocyte depletion thus improves the coagulation factor content of plasma in stored whole blood.

Blood Coagulation Factors↗
PubMed2002

Ultraviolet-sensitive syndrome cells are defective in transcription-coupled repair of cyclobutane pyrimidine dimers.

Patients with ultraviolet-sensitive syndrome (UV(S)S) are sensitive to sunlight, but present neither developmental nor neurological deficiencies. Complementation studies with hereditary DNA repair syndromes show that UV(S)S is distinct from all known xeroderma pigmentosum (XP) and Cockayne syndrome (CS) groups. UV(S)S cells exhibit some characteristics typical of CS, including normal global genomic (GGR) repair of UV-photoproducts, poor clonal survival and defective recovery of RNA synthesis after UV exposure. Those observations have led us to suggest that UV(S)S cells, like those from CS, are defective in transcription-coupled repair (TCR) of cyclobutane pyrimidine dimers (CPD). We have now examined the repair of CPD in the transcribed and non-transcribed strands of the active dihydrofolate reductase (DHFR) and p53 genes, and of the silent alpha-fetoprotein (AFP) and mid-size neurofilament (NF-M) genes in normal human cells and in cells belonging to UV(S)S and CS complementation group B. Our results provide compelling evidence that the UV(S)S gene is essential for TCR of CPD and probably other bulky DNA lesions. As a possible distinction between UV(S)S and CS patients, we postulate that the UV(S)S gene may not be required for TCR of oxidative lesions. We have also found that repair of CPD in either DNA strand of the genomic fragments examined, occurs at a slower rate in TCR-deficient cells than in the non-transcribed strands in normal cells; we suggest that in the absence of TCR, global repair complexes have hindered access to lesions in genomic regions that extend beyond individual transcription units.

Cells, Cultured↗
PubMed2003

Tumor suppressor p53 dependent recruitment of nucleotide excision repair factors XPC and TFIIH to DNA damage.

Functional tumor suppressor p53 is mainly required for efficient global genomic repair (GGR), a subpathway of nucleotide excisions repair (NER). In this study, the regulatory effect of p53, on the spaciotemporal recruitment of XPC and TFIIH to DNA damage sites, was investigated in repair-proficient and -deficient human cells in situ. Photoproducts were induced through micropore UV irradiation of discrete subnuclear areas of intact cells and the specific lesions, as well as recruited repair factors, were detected by immunofluorescent intensity and density of the damaged DNA subnuclear spots (SNS). Both cyclobutane pyrimidine dimers (CPD) and 6-4 photoproducts (6-4PP) were visualized in situ at SNS within irradiated nuclear foci. The in situ repair kinetics revealed that p53-WT normal fibroblasts are proficient for the repair of both CPD and 6-4PP, whereas, p53-Null Li-Fraumeni syndrome (LFS) fibroblasts fail to efficiently repair CPD but not 6-4PP. Colocalization experiments of the NER factors showed that in normal human cells, XPC and TFIIH are rapidly and efficiently recruited to DNA damage within SNS. By contrast, recruitment of both XPC and TFIIH to DNA damage in SNS occurred much less efficiently in p53-Null or p53-compromised cells. The total cellular levels of XPC and XPB were similar in both p53-WT and -Null cells and remained unchanged up to 24h following UV irradiation. The results also showed that dispersal of recruited XPC and TFIIH from DNA damage SNS occurs within a short period after DNA damage. Such dispersal requires functional XPA, XPF and XPG proteins. Taken together, the results demonstrated that p53 plays a pronounced role in the damage recognition and subsequent assembly of repair machinery during GGR and the recruitment of XPC and TFIIH to CPD is p53-dependent. Most likely mechanism of this p53 action is through its downstream effector protein, DDB2.

Blotting, Western↗
PubMed1991

Characterization of an inhibitory metal binding site in carboxypeptidase A.

The specificity of metal ion inhibition of bovine carboxypeptidase A ([(CPD)Zn]) catalysis is examined under stopped-flow conditions with use of the fluorescent peptide substrate Dns-Gly-Ala-Phe. The enzyme is inhibited competitively by Zn(II), Pb(II), and Cd(II) with apparent KI values of 2.4 x 10(-5), 4.8 x 10(-5), and 1.1 x 10(-2) M in 0.5 M NaCl at pH 7.5 and 25 degrees C. The kcat/Km value, 7.3 x 10(6) M-1 s-1, is affected less than 10% at 1 x 10(-4) M Mn(II) or Cu(II) and at 1 x 10(-2) M Co(II), Ni(II), Hg(II), or Pt(IV). Zn(II) and Pb(II) are mutually exclusive inhibitors. Previous studies of the pH dependence of Zn(II) inhibition [Larsen, K. S., & Auld, D. S. (1989) Biochemistry 28, 9620] indicated that [(CPD)Zn] is selectively inhibited by a zinc monohydroxide complex, ZnOH+, and that ionization of a ligand, LH, in the enzyme's inhibitory site (pKLH 5.8) is obligatory for its binding. The present study allows further definition of this inhibitory zinc site. The ionizable ligand (LH) is assigned to Glu-270, since specific chemical modification of this residue decreases the binding affinity of [(CPD)Zn] for Zn(II) and Pb(II) by more than 60- and 200-fold, respectively. A bridging interaction between the Glu-270-coordinated metal hydroxide and the catalytic metal ion is implicated from the ability of Zn(II) and Pb(II) to induce a perturbation in the electronic absorption spectrum of cobalt carboxypeptidase A ([(CPD)Co]).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Ultraviolet damage and nucleosome folding of the 5S ribosomal RNA gene.

The Xenopus borealis somatic 5S ribosomal RNA gene was used as a model system to determine the mutual effects of nucleosome folding and formation of ultraviolet (UV) photoproducts (primarily cis-syn cyclobutane pyrimidine dimers, or CPDs) in chromatin. We analyzed the preferred rotational and translational settings of 5S rDNA on the histone octamer surface after induction of up to 0.8 CPD/nucleosome core (2.5 kJ/m(2) UV dose). DNase I and hydroxyl radical footprints indicate that UV damage at these levels does not affect the average rotational setting of the 5S rDNA molecules. Moreover, a combination of nuclease trimming and restriction enzyme digestion indicates the preferred translational positions of the histone octamer are not affected by this level of UV damage. We also did not observe differences in the UV damage patterns of irradiated 5S rDNA before or after nucleosome formation, indicating there is little difference in the inhibition of nucleosome folding by specific CPD sites in the 5S rRNA gene. Conversely, nucleosome folding significantly restricts CPD formation at all sites in the three helical turns of the nontranscribed strand located in the dyad axis region of the nucleosome, where DNA is bound exclusively by the histone H3-H4 tetramer. Finally, modulation of the CPD distribution in a 14 nt long pyrimidine tract correlates with its rotational setting on the histone surface, when the strong sequence bias for CPD formation in this tract is minimized by normalization. These results help establish the mutual roles of histone binding and UV photoproducts on their formation in chromatin.

Animals↗
PubMed2006

In silico design of a mutant of cytochrome P450 containing selenocysteine.

A mutant of P450(cam), in which the cysteine ligand was replaced by selenocysteine, was designed theoretically using hybrid QM/MM (quantum mechanical/molecular mechanical) calculations. The calculations of the active species, Se-CpdI (selenocysteine-Compound I), of the mutant enzyme indicate that Se-Cpd I will be formed faster than the wild-type species and be consumed more slowly in C-H hydroxylation. As such, our calculations suggest that Se-Cpd I can be observed unlike the elusive species of the wild-type enzyme (Denisov, I. G.; Makris, T. M.; Sligar, S. G.; Schlichting, I. Chem. Rev. 2005, 105, 2253-2277). Spectral features of Se-Cpd I were calculated and may assist such eventual characterization. The observation of Se-Cpd I will resolve the major puzzle in the catalytic cycle of a key enzyme in nature.

Amino Acid Substitution↗
PubMed2006

Rapid freeze-quench ENDOR study of chloroperoxidase compound I: the site of the radical.

The classical heme-monooxygenase active intermediate, compound I (Cpd-I), incorporates a heme which is oxidized by two equivalents above the resting ferric state, one equivalent associated with a ferryl center, [Fe=O]2+ (FeS = 1), and the other with an active-site radical (RS = 1/2). Theoretical calculations on models of a Cpd-I with a thiolato axial ligand have presented divergent views about its electronic structure. In one picture, the radical is on the porphyrin; in the other, it is on the sulfur. In this report, ENDOR spectroscopy answers the question, does Cpd-I of the enzyme chloroperoxidase contain a porphyrin pi-cation radical or an iron-bound cysteinyl radical: the radical is predominantly on the porphyrin, with spin density on sulfur having an upper bound, rhoS </= rhoSmax approximately 0.23. We further suggest that the same answer applies to Cpd-I of cytochromes P450.

Chloride Peroxidase↗
PubMed2006

The Poulos-Kraut mechanism of Compound I formation in horseradish peroxidase: a QM/MM study.

QM/MM calculations are used to elucidate the Poulos-Kraut (Poulos, T. L.; Kraut, J. J. Biol. Chem. 1980, 255, 8199-8205) mechanism of O-O bond activation and Compound I (Cpd I) formation in HRP, in conditions corresponding to neutral to basic pH. Attempts to generate Compound I directly from the Fe(H2O2) complex by migrating the proton from the proximal oxygen to the distal one (1,2- proton shift) result in high barriers. The lowest energy mechanism was found to involve initial deprotonation of ferric hydrogen peroxide complex (involving spin crossover from the quartet to the doublet state) by His42 to form ferric-hydroperoxide (Cpd 0). Subsequently, the distal OH group of Cpd 0 is pulled by Arg38 and reprotonated by His42(H+) to form Cpd I and a water molecule that bridges the two residues. The structures of the intermediate and the transition state reveal the manner by which the Arg-His residues promote cooperatively the electronic reorganization that is required to attend the heterolytic O-O cleavage.

Ferric Compounds↗
PubMedDate not supplied

Parallel pathways, noise masking and glaucoma detection: behavioral and electrophysiological measures.

PURPOSE: We tested the hypothesis that because of their reduced neural efficiency, glaucoma patients should have increasingly impaired thresholds as external noise is added to a stimulus. METHOD: We compared the performance of 20 normals (mean age = 39 years) with that of 15 patients with early glaucoma or at very high risk for glaucoma (mean age 45 years). All patients had normal visual acuity. Contrast thresholds were measured on two sets of tasks: (1) behavioral and (2) sweep visually evoked potentials (VEPs). Two stimuli were used (a) 7.5 Hz reversing gratings of 0.69 cpd, and (b) 5.5 cpd gratings. Noise was binary and contrast varied from 0 to 80%. Psychophysical thresholds were determined using a staircase which employed a spatial four alternative forced choice procedure (4AFC) and converged on 50% correct. Sweep VEP thresholds were determined by extrapolation to zero volts as a function of log contrast. RESULTS: Differences between normal subjects and patients with early glaucoma were not significant without noise. Both the absolute size of the difference and its significance increased as noise level increased. For the behavioral thresholds these trends were clearer with the 5.5 cpd grating, while for the sweep VEPs they were more clear for the 0.69 cpd grating. CONCLUSION: The performance deficit of glaucoma patients which may be minimal under normal testing conditions is magnified when external noise is added to the stimulus. VEPs and psychophysical thresholds show interesting differences in their sensitivity to this effect. Implications for the early detection of glaucoma are discussed.

Adult↗
PubMed1998

Induction of interleukin-6 production by ultraviolet radiation in normal human epidermal keratinocytes and in a human keratinocyte cell line is mediated by DNA damage.

The sunburn reaction is the most common consequence of human exposure to ultraviolet radiation (UVR), and is mediated at least in part by interleukin-6 (IL-6). The aim of this study was to determine if DNA is a major chromophore involved in the induction of IL-6 following UV irradiation of a human epidermoid carcinoma cell line (KB), and of normal human epidermal keratinocytes. We first confirmed that IL-6 release was associated with enhanced levels of IL-6 mRNA transcripts. The wavelength dependence for IL-6 release was then investigated by irradiating the cells at defined wavelengths (254, 302, 313, 334, and 365 nm) with a monochromator. The maximum effect on IL-6 release was observed at 254 nm with only low levels of induction observed at wavelengths above 313 nm. The wavelength dependence for UV-induced IL-6 release was similar to that for DNA absorption or for the induction of cyclobutane pyrimidine dimers (CPD). To determine whether UV-induced DNA damage mediated IL-6 secretion, the role of CPD was investigated by treating keratinocytes with photosomes (photolyase encapsulated in liposomes) followed by photoreactivating light. This photoreversal procedure led to a reduction in the levels of the UVC-induced secretion of IL-6, which in normal human keratinocytes was unambiguously associated with repair of CPD. We conclude that the release of IL-6 from human keratinocytes following short-wave UVC and UVB irradiation is mediated by DNA damage and that CPD play an important role in this process.

Carcinoma, Squamous Cell↗
PubMed2001

The changing training needs of clinical nurse managers: exploring issues for continuing professional development.

AIMS OF THE STUDY: To identify areas where clinical nurse managers perceived that they would benefit from further training and to make recommendations for planning future programmes to meet their needs. BACKGROUND: The effectiveness of the clinical nurse manager has traditionally been associated with maintaining standards of care. Continuing professional development (CPD) is essential to ensure this important group feel adequately prepared to perform their role and has been recognized as an important factor in maintaining job satisfaction and reducing wasteful staff turnover. A review of the literature indicated that since the 1980s the CPD needs of clinical nurse managers have tended to be overlooked despite increasing complexity of the tasks expected of them. Thus it appeared that a fresh study to address these needs would be justified and should take into account sources of work-related stress and variables relating to job satisfaction. METHODS: The study involved clinical nurse managers employed in all four acute hospital National Health Service (NHS) trusts where training needs were served by a major inner city educational consortium. Data collection proceeded in two stages. Initially interviews were undertaken with a random sample of 15 clinical nurse managers to provide in-depth, qualitative data. This information was used to develop a survey questionnaire distributed to the remaining 182 clinical nurse managers in each of the trusts. RESULTS: Data from the interviews indicated that clinical nurse managers appeared to feel clinically competent but generally experienced lack of confidence when dealing with a range of issues, in particular; human resources, managing budgets, deputizing for senior colleagues across the trust ('acting up') and using information technology in everyday practice. Response rate to the survey was good (65%). The results corroborated the interview findings, indicating a need for updating in the same wide range of topics. There were few differences in training needs across all four trusts. Clinical nurse managers who perceived that they had been well-prepared for their role demonstrated higher levels of job satisfaction. Perceived preparation for clinical leadership was the same irrespective of the employing trust, length of time in post and other sociodemographic variables. CONCLUSIONS: The study findings confirm that CPD remains a major issue for clinical nurse managers in the United Kingdom (UK) and that providing opportunities for such development may be an important factor in enhancing job satisfaction. The study findings should help those providing CPD to plan more effectively for this group and have implications for staff recruitment and retention.

Attitude of Health Personnel↗
PubMed1997

Drying cells for SEM, AFM and TEM by hexamethyldisilazane: a study on hepatic endothelial cells.

Critical point drying (CPD) is a common method of drying biological specimens for scanning electron microscopy (SEM). Drying by evaporation of hexamethyldisilazane (HMDS) has been described as a good alternative. This method, however, is infrequently used. Therefore, we reassessed HMDS drying. Cultured rat hepatic sinusoidal endothelial cells (LEC), possessing fragile fenestrae and sieve plates, were subjected to CPD and HMDS drying and evaluated in the scanning electron microscope, atomic force microscope (AFM) and transmission electron microscope (TEM). We observed no differences between the two methods regarding cellular ultrastructure. In contrast with CPD, HMDS drying takes only a few minutes, less effort, low costs for chemicals and requires no equipment. We conclude that HMDS-dried specimens have equal quality to CPD ones. Furthermore, the method also proved useful for drying whole-mount cells for TEM and AFM.

Animals↗
PubMed1999

Class II DNA photolyase from Arabidopsis thaliana contains FAD as a cofactor.

The major UV-B photoproduct in DNA is the cyclobutane pyrimidine dimer (CPD). CPD-photolyases repair this DNA damage by a light-driven electron transfer. The chromophores of the class II CPD-photolyase from Arabidopsis thaliana, which was cloned recently [Taylor, R., Tobin, A. & Bray, C. (1996) Plant Physiol. 112, 862; Ahmad, M., Jarillo, J.A., Klimczak, L.J., Landry, L.G., Peng, T., Last, R.L. & Cashmore, A.R. (1997) Plant Cell 9, 199-207], have not been characterized so far. Here we report on the overexpression of the Arabidopsis CPD photolyase in Escherichia coli as a 6 x His-tag fusion protein, its purification and the analysis of the chromophore composition and enzymatic activity. Like class I photolyase, the Arabidopsis enzyme contains FAD but a second chromophore was not detectable. Despite the lack of a second chromophore the purified enzyme has photoreactivating activity.

Arabidopsis↗
PubMedDate not supplied

Continuous peritoneal dialysis-associated peritonitis: a review and current concepts.

The percentage of end-stage renal disease (ESRD) patients in the United States maintained on continuous peritoneal dialysis (CPD) therapy is decreasing. Complications from CPD therapy, including peritonitis, may be the reason for the decline. Improvements in CPD technology and a better understanding of the risk factors that predispose patients to the development of peritonitis have been responsible for a decline in the rate of peritonitis. Yet peritonitis remains a significant cause of patient morbidity and mortality and the overall outcome of peritonitis is not acceptable. Factors that have limited our ability to lessen the impact of peritonitis include a lack of data on dosing antibiotics in patients on continuous cycling peritoneal dialysis (CCPD) therapy, a lack of knowledge concerning the biology of bacterial biofilm, and the development of resistance to the current prophylactic antibiotic protocols. Further studies are needed concerning the optimal management of the peritoneal catheter and whether it is feasible to resume CPD therapy after catheter removal.

Anti-Bacterial Agents↗
PubMed2003

Protein and energy nutrition among adult patients treated with chronic peritoneal dialysis.

Protein-energy malnutrition (PEM) in adult patients treated with chronic peritoneal dialysis (CPD), which is highly prevalent and frequently severe in its manifestation, poses a significant therapeutic dilemma. The causes of PEM include inflammation, low nutrient intake, nutrient losses during dialysis, metabolic acidemia, coexisting illnesses, and possibly the endocrine disorders of uremia. Treatment strategies for PEM in CPD patients include the following: attempt to treat the potentially reversible causes of anorexia, increase nutrient intake (by nutritional counseling, oral food supplements, consideration of appetite stimulants and intraperitonial amino acid solutions), and the correction of metabolic acidosis. Coexisting illnesses engendering PEM should be treated. Experimental evidence suggests that such agents as anabolic steroids, human growth hormone, insulin-like growth factor-I, and L-carnitine may engender positive protein balance in these individuals. Finally, the use of anti-inflammatory agents to improve the nutritional status of malnourished CPD patients remains to be defined. There is a need to carry out clinical trials that examine whether an improvement in the nutritional status of CPD patients is associated with an improvement in their mortality, morbidity and/or quality of life.

Acidosis↗
PubMed2002

Differential diagnosis of hyperthyroidism: Doppler sonographic quantification of thyroid blood flow distinguishes between Graves' disease and diffuse toxic goiter.

The aim of our study was to evaluate the usefulness of color duplex sonography to distinguish Graves' disease from diffuse toxic goiter. 24 patients with Graves' disease and 13 patients with diffuse toxic goiter underwent B-mode- and color duplex sonography of the thyroid gland. All patients had hyperthyroidism and elevated (99m)Tc-uptake. Spectral Doppler recordings were obtained at all thyroid arteries. Representative color flow maps of the thyroid gland were analyzed, calculating the percentage area of the thyroid gland, occupied by color pixels (color pixel density). The B-mode ultrasound pattern was subjectively assessed on a 4-point rating scale. In patients with Graves' disease the mean peak systolic velocity (PSV) (SD) was 110 (+/- 49) cm/s, the mean volume flow rate (VFR) was 123 ( +/- 67) ml/min and the mean color pixel density (CPD) was 33 (+/- 12) %. For patients with diffuse toxic goiter mean PSV (SD) was 43 ( +/- 9) cm/s (p < 0.001), mean VFR was 23 (+/- 10) ml/min (p < 0.001) and mean CPD was 9 (+/- 6) % (p = 0.007). CPD and spectral duplex recordings were positively correlated (CPD/PSV: rs = 0.77, CPD/VFR: rs = 0.75; p < 0.0001). No significant differences were observed concerning RI values. Sensitivity was 87% and specificity 92% for CPD and VFR and 87% and 100% for PSV. We conclude, that color duplex sonography can reliably distinguish diffuse toxic goiter from Graves' disease and therefore contributes significantly to the differential diagnosis of hyperthyroidism in diffuse thyroid disease.

Adult↗
PubMed2002

Dobzhansky-Muller incompatibilities in protein evolution.

We study fitness landscape in the space of protein sequences by relating sets of human pathogenic missense mutations in 32 proteins to amino acid substitutions that occurred in the course of evolution of these proteins. On average, approximately 10% of deviations of a nonhuman protein from its human ortholog are compensated pathogenic deviations (CPDs), i.e., are caused by an amino acid substitution that, at this site, would be pathogenic to humans. Normal functioning of a CPD-containing protein must be caused by other, compensatory deviations of the nonhuman species from humans. Together, a CPD and the corresponding compensatory deviation form a Dobzhansky-Muller incompatibility that can be visualized as the corner on a fitness ridge. Thus, proteins evolve along fitness ridges which contain only approximately 10 steps between successive corners. The fraction of CPDs among all deviations of a protein from its human ortholog does not increase with the evolutionary distance between the proteins, indicating that substitutions that carry evolving proteins around these corners occur in rapid succession, driven by positive selection. Data on fitness of interspecies hybrids suggest that the compensatory change that makes a CPD fit usually occurs within the same protein. Data on protein structures and on cooccurrence of amino acids at different sites of multiple orthologous proteins often make it possible to provisionally identify the substitution that compensates a particular CPD.

Amino Acid Sequence↗
PubMed1997

Photorepair mutants of Arabidopsis.

UV radiation induces two major DNA damage products, the cyclobutane pyrimidine dimer (CPD) and, at a lower frequency, the pyrimidine (6-4) pyrimidinone dimer (6-4 product). Although Escherichia coli and Saccharomyes cerevisiae produce a CPD-specific photolyase that eliminates only this class of dimer, Arabidopsis thaliana, Drosphila melanogaster, Crotalus atrox, and Xenopus laevis have recently been shown to photoreactivate both CPDs and 6-4 products. We describe the isolation and characterization of two new classes of mutants of Arabidopsis, termed uvr2 and uvr3, that are defective in the photoreactivation of CPDs and 6-4 products, respectively. We demonstrate that the CPD photolyase mutation is genetically linked to a DNA sequence encoding a type II (metazoan) CPD photolyase. In addition, we are able to generate plants in which only CPDs or 6-4 products are photoreactivated in the nuclear genome by exposing these mutants to UV light and then allowing them to repair one or the other class of dimers. This provides us with a unique opportunity to study the biological consequences of each of these two major UV-induced photoproducts in an intact living system.

Arabidopsis↗