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PubMed2004

Testicular lymphoma: organ-specific treatment did not improve outcome.

OBJECTIVES: To assess whether the use of an organ-specific treatment could improve event-free survival (EFS) and overall survival as endpoints in testicular lymphoma in the early stage: IE and IIE. METHODS: Thirty-four patients were selected to be treated with orchiectomy following six cycles of anthracycline-based combined chemotherapy and radiotherapy (scrotum and contralateral testis in stage IE, contralateral testis and lymph nodes in stage IIE). Prophylaxis to the central nervous system was administered with four monthly cycles of a high dose of methotrexate: 6 g/m2. RESULTS: Complete response was achieved in 33 cases (97%). However, relapses continue to be the rule; at a median follow-up of 74 months (range 61-120), 21 patients relapsed. Thus, actuarial curves at 5 years were 32% for EFS and 30% for overall survival, because all patients with failure and relapse died of tumor progression. Relapses were observed in uncommon sites: lung, bone marrow and as disseminate disease; no relapses were observed in irradiated sites of the central nervous system. CONCLUSIONS: Testicular lymphomas remain a problem as regards defining the optimal treatment. The use of a specific treatment based on organ-involved sites did not show any improvement in outcome. It is evident that more specific therapies need to be explored.

Actuarial Analysis↗
PubMed1995

Organ-specific cardiac autoantibodies in dilated cardiomyopathy. Frequency and clinical correlates in Polish patients.

Organ- and disease-specific cardiac autoantibodies are found in a third of dilated cardiomyopathy patients from the U.K. and Italy and represent markers of autoimmune involvement. The role of autoimmunity may vary in dilated cardiomyopathy patients from different countries due to differences in genetic susceptibility to autoimmune diseases. The aim of this study was to assess the frequency of organ-specific cardiac autoantibodies detected by immunofluorescence in a consecutive series of patients with dilated cardiomyopathy and in disease and normal control subjects from Poland. The study groups included 79 patients with idiopathic (WHO criteria) dilated cardiomyopathy, 55 patients with other cardiac disease and 60 normal subjects. Cardiac antibody tests were performed by indirect immunofluorescence on human heart; skeletal muscle was used to identify cross-reacting antibodies. The frequency of organ-specific cardiac autoantibodies was higher in patients with dilated cardiomyopathy (21/79, 27%) than in controls with other cardiac disease (1/55, 2% P < 0.001) or in normal subjects (7/60, 12% P < 0.02). Conversely, cross-reactive antibodies were detected in similar proportions in patients with dilated cardiomyopathy (5/79, 6%), disease controls (7/55, 13%) and normal subjects (6/60, 10%, P = ns). The organ-specific antibody was more common in patients with dilated cardiomyopathy with insidious onset of disease (17/34, 50%) compared to those who did not exhibit this feature (4/45, 9%, P < 0.0001). Organ- and disease-specific cardiac autoantibodies were found in 27% of Polish patients with dilated cardiomyopathy at diagnosis; this is evidence for autoimmune involvement in a subset of patients from our country, as seen in a previously reported series of Western European origin. The association of antibody status with insidious onset of symptoms is in keeping with the long latency period observed in other autoimmune disorders.

Adult↗
PubMed1997

Comparative study on organ-specificity of tumorigenicity, mutagenicity and cell proliferative activity induced by dimethylnitrosamine in Big Blue mice.

Recently, we have shown that dimethylnitrosamine (DMN) treatments increase lacI mutant frequency in the liver, kidney and lung but not in other organs, and also enhance cell proliferation only in the bronchial epithelia. In the present study, organ specificity of tumorigenicity induced by DMN was compared to those of lacI mutation and cell proliferation in Big Blue mice. Male 8-week-old Big Blue mice were treated with daily i.p. injections of 1 or 10 mg/kg DMN for 5 days, or a single i.p. injection of 5 or 10 mg/kg DMN. Except for the 10 mg/kg x 5 DMN group, all animals survived until 78 weeks after the first treatment of DMN. In the present study, the induction of cell proliferation in the bronchial epithelia was confirmed in a dose-dependent manner. At the termination of 78 weeks, it was histopathologically shown that the DMN-treated mice developed liver cell tumor in three out of seven (43%) of the 5 mg/kg group, renal tubule dysplasia in three out of seven (43%) of the 1 mg/kg x 5 group, and duodenal adenocarcinoma in one of seven (14%) of the 1 mg/kg x 5 group, although no neoplastic or preneoplastic lesions were found in the control mice. Because non-transgenic C57BL/6 mice are resistant to developing spontaneous liver cell and duodenal tumors, it was speculated that even these low doses of DMN could be sufficient to initiate target cells. Our results thus suggest that organ specificity of tumorigenicity by DMN is in favorable agreement with that of lacI mutation but not with possibly temporal cell proliferation induced by DMN.

Animals↗
PubMed1993

Developmental and organ-specific changes in DNA-protein interactions in the tomato rbcS1, rbcS2 and rbcS3A promoter regions.

DNase I footprinting assays were used to map sites of DNA-protein interaction in the promoter regions of three of the five genes encoding the small subunit of ribulose-1,5-bisphosphate carboxylase (rbcS) in tomato. Organ-specific differences in DNase I protection patterns were observed using nuclear extracts derived from cotyledons, leaves, young fruit, mature fruit, and roots of tomato, implying that organ-specific transcription of these genes is controlled at the level of DNA-protein interaction. The three genes, designated rbcS1, -2 and -3A are similarly expressed in cotyledons of dark-grown seedlings, in immature tomato fruit, and in leaves under conditions of water stress. These three genes share at least three DNA sequence motifs, including the G-box sequence, which are apparently not present in the other two tomato rbcS genes. We find protection of one or more of these sequences in the aforementioned organs, indicating that the corresponding DNA-binding proteins could function in directing differential expression of the genes, although functional studies would be required to establish this point. While most of the DNase I protections encompass previously identified conserved sequence motifs and their flanking sequence, we also observe protection of additional sequences, many of which occur in the region of the transcription start site.

Base Sequence↗
PubMed1989

Organ-specific metallothionein induction in mice by X irradiation.

Metallothioneins (MTs) are induced in cultured cells and experimental animal tissues by a variety of chemical agents. We report that whole-body X irradiation (1 to 80 Gy) induces MT-1 mRNA transcription and protein expression and accumulation in liver but not in kidney or spleen. The degree of induction was comparable to maximum levels achieved after treatment with metal salts, but the peak of MT-1 mRNA and protein accumulation was approximately 10 h later than with treatment with metal salts and remained high for an extended period. Because of the lack of induction of MT-1 by X rays in cultured cells, and the similarity of the tissue pattern of MT induction between X rays and other agents that also do not induce MT expression in cultured cells, it appears that these agents may act through the mediation of tissue-specific factors. The implications of radiation-induced metallothionein synthesis and organ-specific resistance to cellular damage are discussed.

Animals↗
PubMed1986

[Activity of various organ-specific liver enzymes in patients with myocardial infarction complicated by cardiogenic shock].

The activity of some organ specific enzymes of the liver subcellular structures in the blood serum was examined in 56 patients with cardiogenic shock. The correlation between the gravity of clinical signs of cardiogenic shock and blood enzyme degree was revealed. It was concluded that biochemical criteria could be used in the diagnosis of irreversible changes in the liver in cardiogenic shock.

Acid Phosphatase↗
PubMed1988

Neonatal thymus provides all the information required for tolerance induction against all the non-thymic organ-specific minor histocompatibility antigens.

Using our original "in vivo MLR" technique, we demonstrated that B10.D2 cells grafted into irradiated (DBA/2 x B10.D2)F1 mice (H-2d/H-2d) were stimulated to divide by the whole non-H-2 minor histocompatibility antigens (MiHA) of the DBA/2 background in each organ where these MiHA are expressed. When B10.D2 cells were grafted into N7 mice (generation descending from six successive backcrosses with B10.D2 after an initial cross DBA/2 x B10.D2) which had kept 1/64 of the DBA/2 genetic background, a lack of correlation between the levels of stimulation in the different organs of the same mouse was demonstrated. We established that the number of expressed MiHA lies between 7 and more than 100, depending on the organ, and that the organ specificity is a feature of the expression of these MiHA. Furthermore, using a different technique, we demonstrated that B10.D2 T cells can acquire a specific tolerance state towards the whole DBA/2 antigen background throughout maturation and differentiation in a fully syngeneic environment with the exception of a neonate-(DBA/2 x B10.D2)F1 grafted thymus. We concluded, therefore, that all information corresponding to the adult- and organ-specific MiHA is available in the neonatal thymus. Three working hypotheses are proposed to reconcile the two lines of results.

Animals↗
PubMed2003

Organ-specificity in a plant disease is determined independently of R gene signaling.

The molecular basis of organ specificity in plant diseases is little characterized. Downy mildew of Arabidopsis caused by the oomycete Hyaloperonospora parasitica (formerly Peronospora parasitica) is characteristically a leaf disease. Resistant host genotypes recognize the pathogen in a gene-for-gene dependent manner and respond with the production of H2O2 and the execution of a genetically programmed hypersensitive cell death (HR). We inoculated the roots of Arabidopsis genotypes Col-0, Ws-0, and Wei-0 with the NOCO and WELA races of the pathogen and compared the responses with those observed in leaves. Combinations of incompatible genotypes of host and pathogen showed the expected responses of an oxidative burst and the HR in leaves, but surprisingly, roots showed no signs of active defense and appeared completely susceptible to all the H. parasitica isolates tested. Reverse transcriptase-polymerase chain reaction showed that the R gene RPP1, which mediates resistance in leaves of accession Ws-0 to the H. parasitica isolate NOCO, was expressed in leaves as well as in roots. Similarly, NDR1 and EDS1, two components of R gene-mediated signaling pathways, are also expressed in both tissues. To our knowledge, it has not been previously demonstrated that expression of R genes and downstream components of the signaling cascade are not sufficient for the induction of avirulence gene-mediated defense mechanisms in roots.

Apoptosis↗
PubMed2002

The number of markers of pancreatic autoimmunity is proportional to the risk for type 1 diabetes mellitus in Italian and English patients with organ-specific autoimmune diseases.

An 11-year prospective study was carried out in 226 patients with organ-specific autoimmune disease (OSAD) coming from northern Italy and southern England. Patients were investigated for diabetes-related autoantibodies (ICAs, GADAbs, and IA2Abs) in order to evaluate the best immunological combination in predicting type 1 DM. One hundred twenty-eight patients were ICA positive (77 Italian and 51 English), and 98 were ICA negative. ICAs were detected by immunofluorescence technique on human pancreas, whereas GADAbs and IA2Abs were found by immunoprecipitation assay. During follow-up, 33 of 128 (25.8%) ICA(+) (26% of Italian and 25.5% of English) and 2 of 98 (2%) ICA(-) patients developed type 1 DM (17 with acute-onset, and 18 with non-acute-onset disease). Among ICA(+) patients, three subgroups were considered: ICA(+) alone; ICA and GADAb(+); ICA, GADAb, and IA2Ab(+). Patients who were only ICA(+) had a predictive value for type 1 DM of 4.7%, with an annual incidence of 0.7%, and a cumulative risk of 6%. ICA and GADAb(+) patients had a predictive value of 17.5%, with an annual incidence of 2%, and a cumulative risk of 20%. ICA, GADAb, and IA2Ab(+) patients had a predictive value of 72, with an annual incidence of 13%, and a cumulative risk of 87%. Patients having three immunological markers revealed a prevalence increased in HLA-DR3 and/or -DR4, but reduced in HLA-DR2 haplotypes. The risk for type 1 DM increased proportionally with the number of diabetes-related antibodies, which were also related to the presence of genetic markers of disease susceptibility.

Adult↗
PubMed1987

Islet cell and insulin autoantibodies in organ-specific autoimmune patients. Their behaviour and predictive value for the development of type 1 (insulin-dependent) diabetes mellitus. A 10-year follow-up study.

To evaluate the behaviour and predictive value of islet cell and insulin autoantibodies in patients with organ-specific autoimmune diseases, we followed 21 non-diabetic subjects for a mean period of 84 +/- 27 months. Ten patients were persistently seropositive for complement-fixing islet cell antibodies and high titres of immunoglobulin G islet cell antibodies (greater than or equal to 1:8). The prevalence of persistent insulin autoantibodies in this group was 67%. Seven patients (70%) developed Type 1 (insulin-dependent) diabetes mellitus after a latency period of 2-60 months. The predictive value of complement-fixing islet cell antibodies was 65%, and in the presence of both complement-fixing islet cell and insulin autoantibodies the predictive value rose to 76%. Eleven patients were seronegative for complement-fixing islet cell antibodies and had low immunoglobulin G islet cell antibodies titres (less than 1:8) that were either persistent or transient, or that fluctuated during follow-up. The prevalence of persistent insulin autoantibodies in this group was 45%; only one subject developed Type 1 diabetes. The predictive value of persistent islet cell antibodies (complement-fixing positive/negative) was 54%, and it rose to 70% when both islet cell and insulin autoantibodies were present. Individuals with only insulin autoantibodies or immunoglobulin G islet cell antibodies did not develop diabetes mellitus. A high frequency of HLA-DR3 and/or DR4 was found in patients who developed diabetes mellitus. Thus, the presence of both islet cell and insulin autoantibodies in patients with organ-specific autoimmune disease appears to confer the highest risk of progression toward Type 1 diabetes.

Adolescent↗
PubMed2000

Organ-specific immune responses associated with infectious disease.

The immune response to infection can vary markedly in different organs of the same animal. In some organs, the infection can resolve with subsequent immunity to re-infection, whereas in other organs, pathogens can persist. Here, Christian Engwerda and Paul Kaye highlight the importance of defining organ-specific immune mechanisms for developing strategies that deal effectively with infectious diseases and their associated pathologies.

Animals↗
PubMed2005

Levels of angiogenesis and expression of angiogenesis-related genes are prognostic for organ-specific metastasis of renal cell carcinoma.

BACKGROUND: To identify organ-specific, metastasis-related factors that can be used to predict the development and location of metastasis of clear cell renal cell carcinoma (CRCC), the authors assessed the angiogenesis and the expression of angiogenesis-related genes in primary and metastatic tumors. METHODS: They evaluated intratumoral microvessel density (MVD) by immunohistochemical staining, assessed the expression of angiogenesis-related genes by mRNA in situ hybridization, and determined the clinicopathologic characteristics of 92 archival specimens of primary and metastatic CRCCs from 54 patients. All 38 metastatic tumor specimens were resected from 24 patients. RESULTS: The pathologic stage (P=0.026) of the primary tumor specimen was an important predictor for metastasis, as were MVD (P=0.000025) and the ratio of matrix metalloproteinases (MMPs) to E-cadherin (M/E ratio; P=0.000041). In addition, primary tumor specimens resected from patients with metastatic CRCCs had high MVD, high levels of MMP-2 expression, and a high M/E ratio (P <0.05). Relative to the primary tumors, the metastatic tumors also had high MVD, overexpression of basic fibroblast growth factor, vascular endothelial growth factor, interleukin-8, MMPs, and a high M/E ratio (P <0.05). Multivariate analysis revealed that MVD and the M/E ratio in the primary tumor were independent prognostic factors for metastasis (P=0.049 and P=0.001, respectively). Furthermore, the M/E ratio in metastatic tumor specimens resected from the lung and lymph node was an independent prognostic factor for metastasis (P=0.01823 and P=0.03950, respectively). CONCLUSIONS: The current study indicated that angiogenesis and M/E ratio were specific predictors for metastases of RCC, especially to the lung or lymph node. Therefore, MMPs and E-cadherin could be relevant targets for novel therapeutic strategies to control or prevent the metastasis of RCC.

Aged↗
PubMed1999

Premenarchal and postmenarchal girls with insulin-dependent diabetes mellitus: ovarian and other organ-specific autoantibodies, menstrual cycle.

STUDY OBJECTIVE: To estimate various organ-specific autoantibodies and detect other endocrine autoimmune disorders and menstrual cycle characteristics in girls with Type 1 insulin dependent diabetes mellitus (IDDM). DESIGN: Prospective cohort study from 1993 to 1998, duration 4.5 years. SETTING: Diabetes & Endocrine Clinic of the University Hospital, Motol, Prague. PATIENTS: 53 IDDM girls (group A--43 postmenarchal, group B--10 premenarchal), 15.5 +/- 2.5 (8-19) years old, 6.2 +/- 4.3 years after IDDM onset. MAIN OUTCOME MEASURES: Ovarian autoantibodies directed to ooplasm, zona pellucida, membrana granulosa, theca folliculi interna, and lutein cells, insulin autoantibodies, thyroid peroxidase and thyroglobulin autoantibodies. Menstrual cycle character, endocrine glands disturbance. Diabetes control, body mass index, duration of IDDM. RESULTS: Ovarian autoantibodies in at least one of the followed structures were found in 67.9% of the IDDM girls. In the control group of 21 healthy girls of corresponding age, the positive findings in lutein cells were found in only 4.8% of the girls (P < 0.01 versus IDDM girls). The lutein cells commonly associated with theca folliculi interna cells were the most frequent immunopositive structures in diabetic girls (P < 0.05 versus another positive ovarian autoimmune structure). Autoantibodies directed to ovarian steroid producing cells were frequent in IDDM patients with both irregular and normal menstrual cycles. Irregular menstrual cycles were diagnosed in 27.9% of IDDM girls, polymenorrhea in half of them, and oligomenorrhea in the remainder. Diabetes control in our patients (glycosylated hemoglobin HbA1c in postmenarchal girls 10.1 +/- 2.0%) did not differ between those with regular and those with irregular menstrual cycles. Over a follow-up period one-third of the girls with oligomenorrhea and a long-term noncompliance (HbA1c 13.5%) developed secondary amenorrhea. Insulin autoantibodies were found in 67.8%, thyroid peroxidase autoantibodies in 12.5%, and thyroglobulin autoantibodies in 10.4% of the IDDM girls. Autoimmune thyroiditis was diagnosed in 5 IDDM patients (9.4%); hypothyroidism developed in 3 of them. Menstrual cycle was irregular in 4 of the 5 girls with autoimmune thyroiditis (polymenorrhea in 1, oligomenorrhea in another 3 girls). CONCLUSIONS: An increased incidence of various circulating autoantibodies may be markedly demonstrated in IDDM girls. Their reproductive function might have an important relationship to an evidence of ovarian autoantibodies. Menstrual cycle disturbances could be linked to the poor diabetes control, to the presence of ovarian and other autoantibodies, and also to other autoimmune disease.

Adolescent↗
PubMed2002

The neuropeptides GnRH-II and GnRH-I are produced by human T cells and trigger laminin receptor gene expression, adhesion, chemotaxis and homing to specific organs.

Can T cells be directly activated to de novo gene expression by gonadotropin-releasing hormone-II (GnRH-II), a unique 10-amino-acid neuropeptide conserved through 500 million years of evolution? GnRH-II, which has been identified in mammals, shares 70% homology with the mammalian hypothalamic neurohormone GnRH (GnRH-I), the primary regulator of reproduction, but is encoded by a different gene. Although both neuropeptides are produced mainly in brain, their localization and promoter regulation differ, suggestive of distinct functions. Indeed, GnRH-II barely affects reproduction and its role in mammalian physiology is unknown. We find here that human normal and leukemic T cells produce GnRH-II and GnRH-I. Further, exposure of normal or cancerous human or mouse T cells to GnRH-II or GnRH-I triggered de novo gene transcription and cell-surface expression of a 67-kD non-integrin laminin receptor that is involved in cellular adhesion and migration and in tumor invasion and metastasis. GnRH-II or GnRH-I also induced adhesion to laminin and chemotaxis toward SDF-1alpha, and augmented entry in vivo of metastatic T-lymphoma into the spleen and bone marrow. Homing of normal T cells into specific organs was reduced in mice lacking GnRH-I. A specific GnRH-I-receptor antagonist blocked GnRH-I- but not GnRH-II-induced effects, which is suggestive of signaling through distinct receptors. We suggest that GnRH-II and GnRH-I, secreted from nerves or autocrine or paracrine sources, interact directly with T cells and trigger gene transcription, adhesion, chemotaxis and homing to specific organs, which may be of clinical relevance.

Animals↗
PubMedDate not supplied

Effect of intravenous gammaglobulin on organ specific antibodies and lymphocyte subsets.

OBJECTIVE: The intravenous (i.v.) administration of immunoglobulins (Ig) has resulted in clinical improvement and decreased autoantibody titers in a large number of autoimmune diseases. In this study, the in vivo effects of polyvalent Ig for i.v. use (IVIG) on the level and course of organ-specific antibodies and lymphocyte subsets in patients with autoimmune thyroid disease (ATD) were assessed. METHODS: 19 patients were treated with prednisolone (P) while 21 patients received IVIG. Thyroid microsomal, thyroglobulin- and thyrotropin-receptor autoantibodies (Abs), as well as the lymphocyte ratio CD4/CD8, were measured before and at the end of immunosuppressive therapy. RESULTS: Among the patients treated with IVIG, there was a marked decrease (p < 0.0001) in the microsomal, thyroglobulin and TSH-receptor Abs titers. Significant changes in the titers were also observed after P therapy. The lymphocyte ratio dropped markedly in both groups (p < 0.0005). CONCLUSION: The significant decrease in organ specific Abs in the IVIG group may be explained in terms of a direct and local immunosuppressive effect of the drug on the intrathyroid lymphocytes.

Antibody Formation↗
PubMed1996

Characterization of three potato lipoxygenases with distinct enzymatic activities and different organ-specific and wound-regulated expression patterns.

Lipoxygenases are ubiquitous enzymes in eukaryotes. In plants, lipoxygenases are involved in the synthesis of the hormone jasmonic acid that regulates plant responses to wounding and, in addition, is an inducer of tuberization in potato. We have isolated potato lipoxygenase cDNA clones. From their deduced amino acid sequences, three distinct classes are defined (Lox1, Lox2, and Lox3). They are encoded in gene families that display organ-specific expression, lox1 being expressed mostly in tubers and roots, lox2 in leaves, and lox3 in leaves and roots. Consistent with their organ-specific expression pattern, Lox1 expressed in bacteria preferentially uses as substrate linoleic acid, abundant in membrane lipids of tubers, whereas linolenic acid, prevalent in leaves, is the preferred substrate for the other two classes of lipoxygenase. Analyses on reaction products of the enzymes expressed in bacteria reveal that Lox1 primarily produces 9- hydroperoxides. In contrast, the jasmonic acid precursor, 13-hydroperoxylinolenic acid, is the major product of the action of Lox2 and Lox3 on linolenic acid. Upon wounding, the levels of Lox2 and Lox3 transcripts rise markedly in leaves. While Lox3 mRNA accumulation peaks as early as 30 min after wounding, Lox2 shows a steady increase over a 24-h time course, suggesting different roles for these lipoxygenase isoforms in the synthesis of the plant hormone jasmonic acid.

Amino Acid Sequence↗
PubMed1992

Organ-specific DNA damage of tris(2,3-dibromopropyl)-phosphate and its diester metabolite in the rat.

The organ specificity of tris(2,3-dibromopropyl)phosphate(Tris-BP)-induced DNA damage was investigated in the rat 2 h after a single i.p. injection of 350 mumol/kg. Extensive DNA damage, measured with the alkaline elution method, was found in the kidney, liver and small intestine. Less, but significant DNA damage was detected in the brain, lung, spleen, large intestine and testis. The role of different pathways in the activation of Tris-BP to DNA damaging products was studied in isolated liver and testicular cells. Concentrations as low as 2.5-5 microM Tris-BP caused DNA damage in the hepatocytes, whereas an approximately 10-fold higher concentration was needed in testicular cells to produce a similar amount of DNA damage. Depletion of GSH by diethyl maleate (DEM) did not affect the extent of DNA damage caused by Tris-BP in the liver cells, but blocked the genotoxic effect in testicular cells. Two specifically deuterated Tris-BP analogs, C3D2-Tris-BP and C2D1-Tris-BP, were significantly less potent in causing DNA damage than the protio compound in isolated liver cells and were somewhat less potent in testicular cells. The major urinary metabolite of Tris-BP, bis(2,3-dibromopropyl)phosphate (Bis-BP), was less potent than Tris-BP in causing kidney DNA damage after in vivo exposure. Furthermore, Bis-BP induced substantially less DNA damage in isolated liver and testicular cells. Similar to the effect of DEM on the DNA damage caused by Tris-BP, the DNA damage caused by Bis-BP could be decreased by DEM-pretreatment in testicular cells but not in liver cells. The present study shows that Tris-BP is a potent multiorgan genotoxic agent in vivo. The in vitro data indicate that P-450 mediated metabolism of Tris-BP is more important than activation by glutathione S-transferases of Tris-BP in liver cells, whereas the latter activation pathway seems to be most important in testicular cells.

Animals↗
PubMed1997

Organ-specific transcription of the rrn operon in spinach plastids.

The spinach rrn operon is used as a model system to study transcriptional regulation in higher plant photosynthetic and non-photosynthetic plastids. We performed capping experiments to determine whether P1, PC, or P2 promoters are employed for rrn transcription start sites in cotyledon and root tissues. By using a new method of analysis of capped RNA we demonstrate for the first time that 1) in both organs the rrn operon is expressed in a constitutive manner by cotranscription with the preceding tRNA(GAC)Val gene, and 2) the PC transcription start site is used only in cotyledons and leaves, i.e. we demonstrate the organ-specific usage of a plastid promoter. Both start sites, PC and that of the tRNA(GAC)Val cotranscript, lack Escherichia coli-like consensus sequences. The cotranscript is initiated 457 base pairs upstream of the tRNA(GAC)Val gene. The PC-specific DNA-binding factor, CDF2, is not detectable in root tissues confirming its regulatory role in PC-initiated rrn expression and the organ specificity of PC expression. Furthermore, our results show that rrn operon expression patterns differ in spinach and tobacco indicating species-specific transcriptional regulation of plant plastid gene expression.

Base Sequence↗