Biomedical subjects

T Peng

Publications and source records attributed to T Peng.

At least 55 records · Page 3Linked to original sources

PubMed1999

Resistance to Coccidioides immitis in mice after immunization with recombinant protein or a DNA vaccine of a proline-rich antigen.

Two inbred strains of mice (BALB/c and C57BL/6) were vaccinated with either recombinant expression protein of a Coccidioides immitis spherule-derived proline-rich antigen (rPRA) in monophosphoryl lipid A-oil emulsion adjuvant or a DNA vaccine based on the same antigen. Four weeks after vaccination, mice were infected intraperitoneally with arthroconidia. By 2 weeks, groups of mice receiving saline or plasmids with no PRA insert exhibited significant weight loss, and quantitative CFUs in the lungs ranged from 5.9 to 6.4 log10. In contrast, groups of mice immunized with either rPRA or DNA vaccine had significantly smaller pulmonary fungal burdens, ranging from 3.0 to 4.5 log10 fewer CFUs. In vitro immunologic markers of lymphocyte proliferation and gamma interferon (IFN-gamma) release after splenocytes were stimulated with rPRA correlated with protection. Also, plasma concentrations of rPRA-specific total immunoglobulin G (IgG), IgG1, and IgG2a showed increases in vaccinated mice. These studies expand earlier work by demonstrating protection in mice which differ in H-2 background, by using an adjuvant that is potentially applicable to human use, and by achieving comparable protections with a DNA-based vaccine. Our in vitro results substantiate a Th1 response as evidenced by IFN-gamma release and increased IgG2a. However, IgG1 was also stimulated, suggesting some Th2 response as well. PRA is a promising vaccine candidate for prevention of coccidioidomycosis and warrants further investigation.

Animals↗

PubMed1999

Mammary gland expression of mouse mammary tumor virus is regulated by a novel element in the long terminal repeat.

Mouse mammary tumor virus (MMTV) infects both lymphoid tissue and lactating mammary gland during its infectious cycle, but some endogenous MMTVs are transcribed only in lymphoid cells. We found a lymphoid cell-specific endogenous MMTV that was converted to a milk-borne, infectious virus through recombination with an exogenously transmitted MMTV. The changed expression pattern correlated with the alteration of a single base pair in the long terminal repeat of the lymphoid cell-specific virus. Transgenic mice with the element from either the milk-borne or lymphoid cell-specific virus upstream of the chloramphenicol acetyltransferase reporter gene showed the same pattern of expression as the virus from which the regulatory sequences were derived. Electrophoretic mobility shift assays with mammary cell extracts showed that the site from the milk-borne virus was preferentially bound by a prolactin-inducible factor that poorly bound the altered site from the lymphoid cell-specific virus. The complex that formed on the milk-borne virus-specific oligonucleotide supershifted with anti-Stat5b antibody. Mice lacking either Stat5a or Stat5b had dramatically reduced levels of MMTV transcripts in mammary gland but not in lymphoid tissue. Thus, a member of the STAT family of transcription factors is involved in the tissue-specific expression of mouse mammary tumor virus in vivo. This is the first example of the involvement of a member of the STAT family of transcription factors in the control of tissue-specific expression.

Animals↗

PubMed1999

Angiotensin II activation of insulin-like growth factor 1 receptor transcription is mediated by a tyrosine kinase-dependent redox-sensitive mechanism.

We have recently shown that angiotensin II activation of insulin-like growth factor 1 receptor (IGF-1R) transcription is a critical requirement for angiotensin-stimulated vascular smooth muscle cell growth; therefore, we examined the signaling pathway involved. In rat aortic smooth muscle cells, the antioxidants N-acetyl-L-cysteine (5 mmol/L) and pyrrolidine dithiocarbamate (100 micromol/L) completely inhibited angiotensin II-stimulated increases in IGF-1R mRNA and protein levels, suggesting the involvement of reactive oxygen species. Indeed, catalase abolished the Ang II-stimulated increase of IGF-1R protein expression, and accordingly, H(2)O(2) (0.2 mmol/L) or the oxidized products of linoleic acid, hydroperoxyoctadecadienoic acids (10 micromol/L), increased IGF-1R mRNA levels at 3 hours by 74+/-20% and 107+/-22% and increased receptor number at 24 hours by 51+/-6.7% and 55+/-7.4%, respectively. The protein tyrosine kinase inhibitors genistein and tyrphostin A25 also blocked angiotensin II increases in IGF-1R mRNA and protein levels and blocked the ability of hydroperoxyoctadecadienoic acids and H(2)O(2) to increase IGF-1R expression, suggesting that oxidative stress may be an early event in the angiotensin II signaling cascade. Furthermore, calcium chelation inhibited the angiotensin II effect. Transient transfection assays revealed that a (-2350)+640 IGF-1R promoter/luciferase construct was fully responsive to angiotensin II stimulation (127+/-20% increase). Ten millimoles per liter hydroperoxyoctadecadienoic acids and 0.2 mmol/L H(2)O(2) increased luciferase activity by 79+/-8.5% and 63+/-12%, respectively, and 5 mmol/L N-acetyl-L-cysteine blocked the angiotensin II-induced upregulation of luciferase activity by 70%. These data suggest that angiotensin II stimulates IGF-1R gene transcription via calcium-dependent activation of protein tyrosine kinase activity that lies downstream from an oxidant stimulus. These findings provide key insights into the signaling mechanisms whereby angiotensin II exerts its growth-promoting effects on the vasculature.

Acetylcysteine↗

PubMed1999

An essential role for macrophage migration inhibitory factor (MIF) in angiogenesis and the growth of a murine lymphoma.

BACKGROUND: Macrophage migration inhibitory factor (MIF) has been shown to counterregulate glucocorticoid action and to play an essential role in the activation of macrophages and T cells in vivo. MIF also may function as an autocrine growth factor in certain cell systems. We have explored the role of MIF in the growth of the 38C13 B cell lymphoma in C3H/HeN mice, a well-characterized syngeneic model for the study of solid tumor biology. MATERIALS AND METHODS: Tumor-bearing mice were treated with a neutralizing anti-MIF monoclonal antibody and the tumor response assessed grossly and histologically. Tumor capillaries were enumerated by immunohistochemistry and analyzed for MIF expression. The effect of MIF on endothelial cell proliferation was studied in vitro, utilizing both specific antibody and antisense oligonucleotide constructs. The role of MIF in angiogenesis also was examined in a standard Matrigel model of new blood vessel formation in vivo. RESULTS: The administration of anti-MIF monoclonal antibodies to mice was found to reduce significantly the growth and the vascularization of the 38C13 B cell lymphoma. By immunohistochemistry, MIF was expressed predominantly within the tumor-associated neovasculature. Cultured microvascular endothelial cells, but not 38C13 B cells, produced MIF protein and required its activity for proliferation in vitro. Anti-MIF monoclonal antibody also was found to markedly inhibit the neovascularization response elicited by Matrigel implantation. CONCLUSION: These data significantly expand the role of MIF in host responses, and suggest a new target for the development of anti-neoplastic agents that inhibit tumor neovascularization.

Animals↗

PubMed1999

Relationship between remodeling and function of left ventricle and angiotensin II AT1 receptor expression after myocardial infarction in rats.

OBJECTIVE: To determine the relationship between remodeling and dysfunction of left ventricle (LV) and the expression of the angiotensin II AT1 receptor mRNA after myocardial infarction (MI) in rats. METHODS: Nine MI rats (Group A) and 8 sham-operated rats (Group B) were studied by both Doppler echocardiography and Dot blot using Digoxingenin-labelled cDNA probes. RESULTS: Compared with Group B, Group A showed the increase in LV internal diastolic diameter (0.87 +/- 0.06 mm vs 0.66 +/- 0.03 mm, respectively, P < 0.01) and volume (0.73 +/- 0.09 ml vs 0.51 +/- 0.05 ml, P < 0.01). In addition, thinning of anterior wall, thickening of posterior wall, increasing of peak early filling velocity (peak E), decreasing of late filling velocity (peak A) and increasing of the E/A were demonstrated in MI rats 7 weeks after MI. The levels of the cardiac angiotensin II AT1 receptor mRNA in Group A were higher than those of Group B (2.2-fold). CONCLUSIONS: Seven weeks after MI in rats, character of LV remodeling and dysfunction were developed and the expression of cardiac angiotensin II AT1 receptor mRNA was increased.

Animals↗

PubMed1999

[Determination of impurities in osmium powder by ICP-AES using matrix separation].

An inductively coupled plasma-atomic emission spectrometry method has been developed for the determination of impurities in osmium powder. The sample was dissolved in nitric acid at 150-200 degrees C. Osmium was oxided and its oxide vapour was absorbed by NaOH. The residual solution was then analyzed by ICP-AES. The determination limit of the method is 0.005-0.134 microg x mL(-1). The recovery range of the method is 91%-112%. The precision of the method is less than 3%. This method can be used to determine 18 elements simultaneously. It is simple, rapid and precise.

English Abstract↗

PubMed1998

Functional and morphologic evidence of the presence of tissue-plasminogen activator in vascular nerves: implications for a neurologic control of vessel wall fibrinolysis and rigidity.

Tissue plasminogen activator (t-PA) is expressed by hypothalamic and peripheral sympathetic neurons. The sympathetic axons that permeate artery walls have not been investigated as possible sources of intramural t-PA. The plasmin produced by such a system would locally activate both fibrinolysis and matrix metalloproteinases that regulate arterial collagen turnover. To assess this neural t-PA production, we investigated the capacity of rat cervical sympathetic ganglion neurons to synthesize and release t-PA, and the expression of the enzyme in carotid artery and the iris-choroid microvascular tissues that receive the ganglion axon distribution. Functional studies confirmed that (i) the ganglion neuron cell bodies synthesize t-PA mRNA, (ii) cultured ganglion carotid artery and iris-choroid microvascular explants predominantly release t-PA rather than urokinase, (iii) microvascular tissues release approximately 20 times more t-PA per milligram than carotid explants (which accords with the higher innervation density of small vessels), and (iv) removal of the endothelium did not cause major reductions in the t-PA release from carotid and microvascular explants. Immunolocalization studies then confirmed a strong expression of the enzyme within the ganglion axons, the carotid adventitia that receives these axons, and the predominantly sympathetic axon terminals in the iris-choroid microvasculature. These data indicate the existence of a previously undescribed system for the delivery of neural t-PA to vessel walls. The intramural production of plasmin induced by this system represents a novel principle for the regulation of arterial matrix flexibility, especially in the media of densely innervated small arteries and resistance arterioles involved in the pathogenesis of stroke, hypertension, and vascular aging. Thus, the data suggest an important new interface between neuroscience and vascular biology that merits further exploration.

Aging↗

PubMed1998

Human chondroitin 6-sulfotransferase: cloning, gene structure, and chromosomal localization.

Chondroitin 6-sulfotransferase (C6ST) is the key enzyme in the biosynthesis of chondroitin 6-sulfate, a glycosaminoglycan implicated in chondrogenesis, neoplasia, atherosclerosis, and other processes. C6ST catalyzes the transfer of sulfate from 3'-phosphoadenosine 5'-phosphosulfate to carbon 6 of the N-acetylgalactosamine residues of chondroitin. Based on the previously published avian sequence, we searched the database of expressed sequence tags (dbEST) and obtained partial-length cDNAs that we completed by 5'-RACE using human chondrosarcoma and endothelial-cell RNA as template. Stable transfection of our full-length expression construct into CHO-K1 cells resulted in marked increases in C6ST and keratan sulfate sulfotransferase (KSST) enzymatic activities in cell homogenates. The predicted 411 amino acid sequence of human C6ST contains an N-terminal hydrophobic domain consistent with membrane insertion, four potential sites for N-linked glycosylation, several consensus sequences for protein phosphorylation, and one RGD sequence. The human and chick C6ST cDNA share 51% nucleotide identity, 40% amino acyl identity, and 75% amino acyl conservation. The human C6ST gene structure has been elucidated and exhibits an intron-less coding region, and the gene has been mapped to human chromosome 11 by radiation hybrid panel mapping.

Acetylgalactosamine↗

PubMed1998

Involvement of macrophage migration inhibitory factor in the evolution of rat adjuvant arthritis.

OBJECTIVE: Recent studies have established an essential role for macrophage migration inhibitory factor (MIF) in T cell and macrophage activation, both of which are characteristics of rat adjuvant arthritis. This study investigated the role of MIF in early adjuvant arthritis. METHODS: MIF was detected in rat synovium by immunohistochemistry and enzyme-linked immunosorbent assay using specific monoclonal antibodies (MAb). Anti-MIF MAb treatment was administered, and the effects on clinical aspects of adjuvant arthritis were assessed. RESULTS: MIF was absent from normal rat synovium prior to adjuvant injection, but was detectable on day 4 after injection (6 days before the onset of clinical disease) and was colocalized with ED-1+ macrophages throughout the evolution of the disease. Levels of MIF were increased in established adjuvant arthritis sera, and adjuvant arthritis synovial macrophages released MIF at a mean +/- SEM concentration of 607.9 +/- 201.5 pg/ml. Anti-MIF treatment led to profound, dose-dependent inhibition of the adjuvant arthritis clinical score, paw swelling, and synovial lavage leukocyte numbers (P < 0.001), and also resulted in reduced synovial macrophage and T cell accumulation. CONCLUSION: These findings demonstrate an important role for MIF in the evolution of rat adjuvant arthritis.

Animals↗

PubMed1998

Impaired growth and risk of fetal death: is the tenth percentile the appropriate standard?

OBJECTIVE: Our purpose was to determine whether the 10th percentile of birth weight for gestational age is appropriate to identify fetuses at risk of death associated with impaired growth. STUDY DESIGN: All live births recorded in Virginia from Jan. 1, 1991, through Dec. 31, 1993, were examined. Percentile growth curves were constructed, and fetal, neonatal, and perinatal mortality rates were calculated for births within various percentile intervals. RESULTS: Significantly elevated fetal mortality was found for birth weights through the 15th percentile. The odds ratio for fetal mortality relative to the baseline for births < or = 5th percentile was 5.6, for the 5th through the 10th percentile 2.8, and for the 10th through the 15th percentile 1.9. These were all significant. CONCLUSION: Fetuses with birth weights between the 10th and 15th percentiles are at a significantly increased risk for fetal death. Therefore the use of the 15th percentile as a diagnostic threshold for the identification of the fetus at increased risk associated with impaired growth is recommended.

Birth Weight↗

PubMed1998

The gH-gL complex of herpes simplex virus (HSV) stimulates neutralizing antibody and protects mice against HSV type 1 challenge.

The herpes simplex virus type 1 (HSV-1) gH-gL complex which is found in the virion envelope is essential for virus infectivity and is a major antigen for the host immune system. However, little is known about the precise role of gH-gL in virus entry, and attempts to demonstrate the immunologic or vaccine efficacy of gH and gL separately or as the gH-gL complex have not succeeded. We constructed a recombinant mammalian cell line (HL-7) which secretes a soluble gH-gL complex, consisting of gH truncated at amino acid 792 (gHt) and full-length gL. Purified gHt-gL reacted with gH- and gL-specific monoclonal antibodies, including LP11, which indicates that it retains its proper antigenic structure. Soluble forms of gD (gDt) block HSV infection by interacting with specific cellular receptors. Unlike soluble gD, gHt-gL did not block HSV-1 entry into cells, nor did it enhance the blocking capacity of gD. However, polyclonal antibodies to the complex did block entry even when added after virus attachment. In addition, these antibodies exhibited high titers of complement-independent neutralizing activity against HSV-1. These sera also cross-neutralized HSV-2, albeit at low titers, and cross-reacted with gH-2 present in extracts of HSV-2-infected cells. To test the potential for gHt-gL to function as a vaccine, BALB/c mice were immunized with the complex. As controls, other mice were immunized with gD purified from HSV-infected cells or were sham immunized. Sera from the gD- or gHt-gL-immunized mice exhibited high titers of virus neutralizing activity. Using a zosteriform model of infection, we challenged mice with HSV-1. All animals showed some evidence of infection at the site of virus challenge. Mice immunized with either gD or gHt-gL showed reduced primary lesions and exhibited no secondary zosteriform lesions. The sham-immunized control animals exhibited extensive secondary lesions. Furthermore, mice immunized with either gD or gHt-gL survived virus challenge, while many control animals died. These results suggest that gHt-gL is biologically active and may be a candidate for use as a subunit vaccine.

Animals↗

PubMed1998

The PK domain of the large subunit of herpes simplex virus type 2 ribonucleotide reductase (ICP10) is required for immediate-early gene expression and virus growth.

The large subunit of herpes simplex virus (HSV) ribonucleotide reductase (RR), RR1, contains a unique amino-terminal domain which has serine/threonine protein kinase (PK) activity. To examine the role of the PK activity in virus replication, we studied an HSV type 2 (HSV-2) mutant with a deletion in the RR1 PK domain (ICP10DeltaPK). ICP10DeltaPK expressed a 95-kDa RR1 protein (p95) which was PK negative but retained the ability to complex with the small RR subunit, RR2. Its RR activity was similar to that of HSV-2. In dividing cells, onset of virus growth was delayed, with replication initiating at 10 to 15 h postinfection, depending on the multiplicity of infection. In addition to the delayed growth onset, virus replication was significantly impaired (1,000-fold lower titers) in nondividing cells, and plaque-forming ability was severely compromised. The RR1 protein expressed by a revertant virus [HSV-2(R)] was structurally and functionally similar to the wild-type protein, and the virus had wild-type growth and plaque-forming properties. The growth of the ICP10DeltaPK virus and its plaque-forming potential were restored to wild-type levels in cells that constitutively express ICP10. Immediate-early (IE) genes for ICP4, ICP27, and ICP22 were not expressed in Vero cells infected with ICP10DeltaPK early in infection or in the presence of cycloheximide, and the levels of ICP0 and p95 were significantly (three- to sevenfold) lower than those in HSV-2- or HSV-2(R)-infected cells. IE gene expression was similar to that of the wild-type virus in cells that constitutively express ICP10. The data indicate that ICP10 PK is required for early expression of the viral regulatory IE genes and, consequently, for timely initiation of the protein cascade and HSV-2 growth in cultured cells.

Animals↗

PubMed1998

Structural and antigenic analysis of a truncated form of the herpes simplex virus glycoprotein gH-gL complex.

The herpes simplex virus (HSV) gH-gL complex is essential for virus infectivity and is a major antigen for the host immune system. The association of gH with gL is required for correct folding, cell surface trafficking, and membrane presentation of the complex. Previously, a mammalian cell line was constructed which produces a secreted form of gHt-gL complex lacking the transmembrane and cytoplasmic tail regions of gH. gHt-gL retains a conformation similar to that of its full-length counterpart in HSV-infected cells. Here, we examined the structural and antigenic properties of gHt-gL. We first determined its stoichiometry and carbohydrate composition. We found that the complex consists of one molecule each of gH and gL. The N-linked carbohydrate (N-CHO) site on gL and most of the N-CHO sites on gH are utilized, and both proteins also contain O-linked carbohydrate and sialic acid. These results suggest that the complex is processed to the mature form via the Golgi network prior to secretion. To determine the antigenically active sites of gH and gL, we mapped the epitopes of a panel of gH and gL monoclonal antibodies (MAbs), using a series of gH and gL C-terminal truncation variant proteins produced in transiently transfected mammalian cells. Sixteen gH MAbs (including H6 and 37S) reacted with the N-terminal portion of gH between amino acids 19 and 276. One of the gH MAbs, H12, reacted with the middle portion of gH (residues 476 to 678). Nine gL MAbs (including 8H4 and VIII 62) reacted with continuous epitopes within the C-terminal portion of gL, and this region was further mapped within amino acids 168 to 178 with overlapping synthetic peptides. Finally, plasmids expressing the gH and gL truncations were employed in cotransfection assays to define the minimal regions of both gH and gL required for complex formation and secretion. The first 323 amino acids of gH and the first 161 amino acids of gL can form a stable secreted hetero-oligomer with gL and gH792, respectively, while gH323-gL168 is the smallest secreted hetero-oligomer. The first 648 amino acids of gH are required for reactivity with MAbs LP11 and 53S, indicating that a complex of gH648-gL oligomerizes into the correct conformation. The data suggest that both antigenic activity and oligomeric structure require the amino-terminal portions of gH and gL.

Amino Acid Sequence↗

PubMed1998

[Gastroenteric absorptive kinetic study on strychine in Jiufensan].

After P. O. Jiufensan, the rest curve of strychine in stomach and intestines of mice per kg was determined by TLC scanning. And the gastroenteric absorptive kinetic rule of strychine in rivo was studied, As a result, the strychine in stomach and intestine of mice accorded with pharmacokinetic model of one room. Also the main pharmacokinetic parameters of this preparation were examined.

Animals↗

PubMed1998

[Direct determination of trace elements in tungsten products with ICP-AES].

A direct determination of Al, As, Ca, Cd, Co, Cr, Cu, Fe, Mg, Mn, Mo, Ni, Sn, Ti and V in tungsten products with ICP-AES is presented. The influence of tungsten matrix is studied. Based on the selected optimum operating parameters, the feasibility of the proposed method is evaluated by analyzing three WO3 National References. The results are satisfactory.

English Abstract↗

PubMed1997

Biochemical and mutational investigations of the enzymatic activity of macrophage migration inhibitory factor.

The protein mediator MIF has been identified as being released from immune cells by glucocorticoid stimulation and to counter-regulate glucocorticoid action. MIF also has been described recently to exhibit dopachrome tautomerase activity and to be structurally homologous to the bacterial enzymes 4-oxalocrotonate tautomerase (4-OT) and 5-carboxymethyl-2-hydroxymuconate isomerase (CHMI). We performed site-directed mutagenesis and biochemical analyses of mouse MIF in order to identify amino acid residues and protein domains that are essential for enzymatic reactivity. Mutant proteins which lacked a free N-terminal proline residue were enzymatically inactive, as was a preparation of native MIF modified covalently at its N terminus by 3-bromopyruvate, suggesting that this proline has a catalytic function. Substitutions of the internal histidine residues 42 and 63 did not affect enzymatic activity, indicating that these basic residues are not involved in dopachrome tautomerization. Carboxy-truncated forms of MIF (residues 1-110 and 1-104) also were inactive, affirming the role of the carboxy terminus in stable trimer formation and the importance of the trimer for enzymatic activity. Additional evidence for the homotrimeric structure of MIF under native solution conditions was obtained by SDS-PAGE analysis of MIF after chemical cross-linking at low protein concentrations. The enzymatic activity of MIF was found to be reversibly inhibited by micromolar concentrations of fatty acids with chain lengths of at least 16 carbon atoms. Of note, molecular modeling of the substrate L-dopachrome methyl ester into the active site of MIF suggests an acid-catalyzed enzymatic mechanism that is different from that deduced from studies of the enzymes 4-OT and CHMI. Finally, in vitro analysis of an enzymatically inactive MIF species (P2 --> S) indicates that the glucocorticoid counter-regulatory activity of MIF can be functionally dissociated from its tautomerization activity.

Amino Acid Sequence↗

PubMed1997

Undifferentiated U937 cells transfected with chemoattractant receptors: a model system to investigate chemotactic mechanisms and receptor structure/function relationships.

Transfection of either the C5a receptor or the formyl peptide receptor into undifferentiated U937 cells generated continuously growing cell lines that stably expressed these receptors. The transfected cells displayed significant numbers of cell surface receptors that had ligand binding properties similar to fully differentiated U937 cells. Undifferentiated transfected U937 cells were capable of a ligand-specific calcium flux and showed migratory responses that were qualitatively and quantitatively similar to differentiated cells and were specific for each chemoattractant. Moreover, the chemotactic response could be desensitized by preincubating the cells in a high concentration of ligand and could be blocked by pertussis toxin. These results demonstrate that undifferentiated U937 cells possess the subcellular signaling apparatus and machinery necessary to generate a motile response and that the only missing component for chemotaxis is expression of a chemoattractant receptor. In addition, the results demonstrate that undifferentiated U937 cells transfected with chemoattractant receptors provide a defined model system to study receptor structure/function relationships and may be used to investigate receptor-mediated chemotactic responses in a relevant human myeloid cell.

Antigens, CD↗

PubMed1997

An enzyme similar to animal type II photolyases mediates photoreactivation in Arabidopsis.

The important issue of photoreactivation DNA repair in plants has become even more interesting in recent years because a family of genes that are highly homologous to photoreactivating DNA repair enzymes but that function as blue light photoreceptors has been isolated. Here, we report the isolation of a novel photolyase-like sequence from Arabidopsis designated PHR1 (for photoreactivating enzyme). It shares little sequence similarity with either type I photolyases or the cryptochrome family of blue light photoreceptors. Instead, the PHR1 gene encodes an amino acid sequence with significant homology to the recently characterized type II photolyases identified in a number of prokaryotic and animal systems. PHR1 is a single-copy gene and is not expressed in dark-grown etiolated seedlings: the message is light inducible, which is similar to the expression profile for photoreactivation activity in plants. The PHR1 protein complements a photolyase-deficient mutant of Escherichia coli and thus confers photoreactivation activity. In addition, an Arabidopsis mutant that is entirely lacking in photolyase activity has been found to contain a lesion within this Arabidopsis type II photolyase sequence. We conclude that PHR1 represents a genuine plant photolyase gene and that the plant genes with homology to type I photolyases (the cryptochrome family of blue light photoreceptors) do not contribute to photoreactivation repair, at least in the case of Arabidopsis.

Amino Acid Sequence↗