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The soil-borne bacterial pathogen Ralstonia solanacearum invades a broad range of plants through their roots, resulting in wilting of the plant, but no effective protection against this disease has been developed. Two bacterial wilt disease-inhibiting compounds were biochemically isolated from tobacco and identified as sclareol and cis-abienol, labdane-type diterpenes. When exogenously applied to their roots, sclareol and cis-abienol inhibited wilt disease in tobacco, tomato and Arabidopsis plants without exhibiting any antibacterial activity. Microarray analysis identified many sclareol-responsive genes in Arabidopsis roots, including genes encoding or with a role in ATP-binding cassette (ABC) transporters, and biosynthesis and signaling of defense-related molecules and mitogen-activated protein kinase (MAPK) cascade components. Inhibition of wilt disease by sclareol was attenuated in Arabidopsis mutants defective in the ABC transporter AtPDR12, the MAPK MPK3, and ethylene and abscisic acid signaling pathways, and also in transgenic tobacco plants with reduced expression of NtPDR1, a tobacco homolog of AtPDR12. These results suggest that multiple host factors are involved in the inhibition of bacterial wilt disease by sclareol-related compounds. [ABSTRACT FROM AUTHOR]

The TEIL (Tobacco EIN3-Like) gene is a tobacco homologue of arabidopsis Ethylene Insensitive 3 (EIN3), and the gene product binds an 8 bp sequence in the tobacco PR1a promoter in a sequence specific manner. It was found here that accumulation of TEIL transcript was induced by wounding and preceded basic PR gene expression. To study the downstream signalling pathway of TEIL, TEIL was overexpressed under the control of the constitutive 35S promoter in tobacco plants. In 35S::TEIL lines, basic PR genes, which are wound-, jasmonate-, and ethylene-inducible, were expressed constitutively. Next, the conserved 781 bp sequence among tobacco EIN3-like (EIL) protein genes was introduced as an inverted-repeat (IR) into tobacco to suppress expression of these genes. In two independent IRTEIL lines, the TEIL transcript was not found and transcripts of other tobacco EILs, NtEIL3, and NtEIL5, were reduced. In IRTEIL plants, wound-, jasmonate-, and ACC-induced accumulation of basic PR gene transcripts was significantly inhibited. These results indicate that TEIL functions upstream of tobacco basic PR genes in wound signalling via not only ethylene but also jasmonate. In 35S::TEIL plants, the pistil length of the flower was longer with a slight protrusion of the stigma compared with the control. In IRTEIL plants, the length of the stamens was shorter than the control with significant protrusion of the stigma in the flower. These observations indicate the involvement of tobacco EILs in flower development. [ABSTRACT FROM PUBLISHER]

The vascular system-specific and wound-responsive cis-element (VWRE) has been identified as a novel cis-element for wound-induced and vascular system-specific expression of the tobacco peroxidase gene, tpoxN1. Here we isolated two independent clones that encode VWRE binding proteins by yeast one-hybrid screening. As the gene products have an AP2/ERF (APETALA2/ethylene-responsive factor) domain, and the transcripts were accumulated transiently after wounding, we named them wound-responsive AP2/ERF-like factor 1 (WRAF1) and WRAF2. The AP2/ERF domains of the two WRAFs share 97% homology, and are classified into the ERF subfamily B-4. Gel mobility shift analysis indicated that WRAFs specifically bind VWRE, which contains no known cis-elements for other AP2/ERF proteins. The binding activity of the WRAFs was found to be localized in the AP2/ERF domain. The WRAFs transactivated a promoter containing four tandem repeats of the VWRE, but not that of the mutated VWRE. Overexpression of the WRAF genes led to constitutive expression of the potential target gene, tpoxN1, in unwounded transgenic plants. These results indicate that the novel transcription factors WRAF1 and WRAF2 bind the VWRE as positive regulators for the expression of the tpoxN1 gene. [ABSTRACT FROM AUTHOR]

In tobacco ( Nicotiana tabacum), wounding causes rapid activation of two mitogen-activated protein kinases (MAPKs), wound-induced protein kinase (WIPK) and salicylic acid (SA)-induced protein kinase (SIPK), and the subsequent accumulation of jasmonic acid (JA). Our previous studies suggested that activation of WIPK is required for the production of wound-induced JA. However, the exact role of WIPK remains unresolved. We generated transgenic tobacco plants in which either WIPK or SIPK were silenced using RNA interference to define the roles of WIPK and SIPK in the wound response. In addition, transgenic tobacco plants were generated in which both WIPK and SIPK were silenced to examine the possibility that they have redundant roles. Wound-induced JA production was reduced compared with non-silenced plants in all of the WIPK-, SIPK- and WIPK/SIPK-silenced plants. Transgenic plants over-expressing NtMKP1, a gene encoding tobacco MAPK phosphatase, which inactivates WIPK and SIPK, also exhibited reduced JA production in response to wounding. In both WIPK/SIPK-silenced and NtMKP1-over-expressing plants, wounding resulted in an abnormal accumulation of both SA and transcripts for SA-responsive genes. These results suggest that WIPK and SIPK play an important role in JA production in response to wounding, and that they function cooperatively to control SA biosynthesis. [ABSTRACT FROM AUTHOR]

The mitogen-activated protein kinase (MAPK) cascade is involved in responses to biotic and abiotic stress in plants. In this study, we isolated a new MAPK, NtMPK4, which is a tobacco homolog of Arabidopsis MPK4 (AtMPK4). NtMPK4 was activated by wounding along with two other wound-responsive tobacco MAPKs, WIPK and SIPK. We found that NtMPK4 was activated by salicylic acid-induced protein kinase kinase (SIPKK), which has been isolated as an SIPK-interacting MAPK kinase. In NtMPK4 activity-suppressed tobacco, wound-induced expression of jasmonic acid (JA)-responsive genes was inhibited. NtMPK4-silenced plants showed enhanced sensitivity to ozone. Inversely, transgenic tobacco plants, in which SIPKK or the constitutively active type SIPKKEE was overexpressed, exhibited greater responsiveness to wounding with enhanced resistance to ozone. We further found that NtMPK4 was expressed preferentially in epidermis, and the enhanced sensitivity to ozone in NtMPK4-silenced plants was caused by an abnormal regulation of stomatal closure in an ABA-independent manner. These results suggest that NtMPK4 is involved in JA signaling and in stomatal movement. [ABSTRACT FROM AUTHOR]

We previously reported that three types of tobacco calmodulin (CaM) isoforms originated from 13 genes are differently regulated at the transcript and protein levels in response to wounding and tobacco mosaic virus-induced hypersensitive reaction (HR); wound-inducible type I and HR-inducible type III levels increased after wounding and HR, respectively, while type II, whose expression is constitutive and wound responsible, remained unchanged. Here, we show that these CaMs differentially activate target enzymes; rat NO synthase was activated most effectively by type III, moderately by type I and weakly by type II, and plant NAD kinase (NADK) was activated in the inverse order. Furthermore, we found that a suitable Ca2+ concentration differs by type; type II activated NADK at lower Ca2+ of around 0.1 µM, which is the cytosolic concentration in unstimulated cells, type I did so at 1–5 µM, which is the increased Ca2+ concentration in stimulated cells, while type III did not at any Ca2+ level. NADK activation was highest over a pH range of 7.1–6.8 for which the cytosolic pH reportedly changed from 7.5 after being stimulated. Thus, tobacco CaMs, especially type I, effectively activate NADK in stimuli-induced conditions. [ABSTRACT FROM AUTHOR]

Polyamines (PAs) play important roles in cell proliferation, growth and environmental stress responses of all living organisms. In this study, we examine whether these compounds act as signal mediators. Spermine (Spm) specifically activated protein kinases of tobacco leaves, which were identified as salicylic acid (SA)-induced protein kinase (SIPK) and wound-induced protein kinase (WIPK), using specific antibodies. Upon Spm treatment, upregulation of WIPK, but not SIPK, was observed. Spm-induced mitogen-activated protein kinases (MAPKs) activation and WIPK upregulation were prevented upon pre-treatment with antioxidants and Ca2+ channel blockers. Additionally, Spm specifically stimulated expression of the alternative oxidase ( AOX) gene, which was disrupted by these antioxidants and Ca2+ channel blockers. Bongkrekic acid (BK), an inhibitor of the opening of mitochondrial permeability transition (PT) pores, suppressed MAPKs activation and accumulation of WIPK and AOX mRNA. Our data collectively suggest that Spm causes mitochondrial dysfunction via a signalling pathway in which reactive oxygen species and Ca2+ influx are involved. As a result, the phosphorylation activities of the two MAPK enzymes SIPK and WIPK are stimulated. [ABSTRACT FROM AUTHOR]

The E2F family plays a pivotal role in cell cycle control and is conserved among plants and animals, but not in fungi. This provides for the possibility that the E2F family was integrated during the development of higher organisms, but little is known about this. We examined the effect of E2F ectopically expressed in transgenic tobacco (Nicotiana tabacum) plants on growth and development using E2Fa (AtE2F3) and DPa from Arabidopsis. E2Fa-DPa double transgenic lines exhibited altered phenotypes with curled leaves, round shaped petals, and shortened pistils. In mature but not immature leaves of the double transgenic lines, there were enlarged nuclei with increasing ploidy levels accompanied by the ectopic expression of S phase — but not M phase-specific genes. This indicates that a high expression of E2F promotes endoreduplication by accelerating S phase entry in terminally differentiated cells with limited mitotic activity. Furthermore, mature leaves of the transgenic plants contained increased numbers of small cells, especially on the palisade (adaxial) side of the outer region toward the edge, and the leaf strips exhibited hormone-independent callus formation when cultured in vitro. These observations suggest that an enhanced E2F activity modulates cell cycle in a cell type-specific manner and affects plant morphology depending on a balance between activities for committing to S phase and M phase, which likely differ between organs or tissues. [ABSTRACT FROM AUTHOR]

Examines the isolation and chemical identification of a wound-induced protein kinase (WIPK)-activating substance from tobacco leaves. Response to tobacco mosaic virus; Treatment of leaves with WAF-1; Role in the induction of WIPK and wound- and pathogen-inducible pathogenesis-related genes in wounded tobacco plants.

Overproduction of animal cell death suppressors Bcl-xL and Ced-9 conferred enhanced resistance to UV-B and paraquat treatment in tobacco plants [Mitsuhara et al. (1999) Curr. Biol. 9: 775]. We report here that the progeny could germinate in 0.2 M NaCl or at 10°C under light, while control plants could not. Suspension-cultured Bcl cells resisted NaCl treatment maintaining an active mitochondrial membrane potential for longer than control cells. When intracellular pH was determined by in vivo 31P-NMR, immediate cytoplasmic acidification by 0.3 M NaCl treatment in control cells was found to be suppressed in transgenic cells. Monitoring of cytoplasmic and vacuolar pHs in control cells indicated the vacuole was disrupted 40 min after 0.5 M NaCl treatment, while the compartment between the cytoplasm and vacuole was likely to remain intact in Bcl cells for 100 min. Enhanced shoot regeneration from cut leaf pieces and more vigorous rooting from cut stem ends were found in transgenic plants. The Bcl protein was abundant in all subcellular fractions. Based on the results in transgenic plants carrying a mutant bcl-xL gene, Bcl-xL is thought to suppress cell death and enhance the viability of plants in stressful environments by contributing to the maintenance of the homeostasis of organella. [ABSTRACT FROM PUBLISHER]

A gene encoding a receptor-like protein kinase was isolated as the gene induced in the early period of N gene-dependent hypersensitive cell death in tobacco leaves. The kinase domain expressed as a glutathione S-transferase fusion protein was capable of autophosphorylation, indicating that this gene encodes an active protein kinase. A high level of the transcript accumulated before necrotic lesion formation in tobacco mosaic virus (TMV)-inoculated tobacco leaves carrying the N gene but it was low in a tobacco cultivar lacking the N gene. A small but reproducible increase in the transcript was found 1–2 h after a temperature shift from 30°C to 20°C even in healthy leaves, suggesting the gene expression is temperature sensitive. The gene was named WRK for wound-induced receptor-like protein kinase, because the transcript increased to a maximum within 15–30 min of wounding. In suspension cultured tobacco cells, an increase in the transcript was found 15 min after transfer to a new medium, but it was suppressed under high osmotic pressures. The wound-induced WRK accumulation was enhanced by cycloheximide treatment, but not by known defense signal compounds (salicylic acid, jasmonic acid, 1-aminocyclopropan-1-carboxylic acid and abscisic acid) and some plant hormones. Thus, WRK is a wound-inducible and temperature-sensitive protein kinase gene induced before hypersensitive cell death probably through unknown signaling pathways. [ABSTRACT FROM PUBLISHER]

SummaryPlants have recently been found to have E2F-like and Rb-like proteins, regulators responsible for the G1 (G0 )-S phase transition of the cell cycle in animals. Here we show that E2F is involved in transcription of plant genes for proliferating cell nuclear antigen (PCNA), which is required for DNA replication. Potential E2F binding sites found in the rice PCNA promoters mediated transcriptional activation in actively dividing cells and tissues of tobacco, but not transcriptional repression in terminally differentiated tissues, as also observed for the PCF binding sites previously found in the rice promoter. Similar results were obtained from analyses for a PCNA promoter isolated from tobacco, which contained two E2F-like sites, each with a different degree of contribution to the promoter activation. These E2F-like sites except for a rice site were indeed bound specifically by recombinant proteins of rice E2F, OsE2F1 and OsE2F2, and complexes of OsE2F1 with Arabidopsis DP proteins. Furthermore, OsE2F1 had the ability to transactivate an E2F-reporter gene containing the tobacco E2F site on co-expression with an Arabidopsis DP, and the transactivation was greatly enhanced by tagging a canonical nuclear localization signal to OsE2F1, suggesting a nuclear import-mediated regulation of the OsE2F1 function. In addition, we found that a large number of replication- and mismatch repair-associated genes in Arabidopsis contain E2F binding sequences conserved in their predicted promoter regions. [ABSTRACT FROM AUTHOR]

A tobacco peroxidase gene tpoxN1 was reported to be expressed within 1 h after wounding in leaves [Hiraga et al. (2000a) Plant Cell Physiol. 41: 165]. We describe here further results on the wound-induced tpoxN1 expression. The quick tpoxN1 induction occurred preferentially in stems and petioles, but was negligible in leaf blades even 8 h after wounding. Induced GUS activity was also detected rapidly after wounding in the stem of transgenic tobacco plants carrying the tpoxN1 promoter::GUS fusion gene, localized mainly in the vascular systems where it was maintained this level for 14 d or more. Strong GUS activity was also found in the petiole and veinlet as well as the epidermal tissue in the stem. Treatment of known inducers for wound-responsive genes such as jasmonate, 1-aminocyclopropane-1-carboxylate, spermine, phytohormones and other stress treatments did not enhance wound-induced tpoxN1 gene expression in stems at all, but rather repressed it in some cases. Studies using metabolic inhibitors suggested that phosphorylation and dephosphorylation of proteins together with de novo protein synthesis are likely to be involved in the wound-induced tpoxN1 expression as well as some other wound-responsive genes. Thus, tpoxN1 is a unique wound-inducible and possible wound-healing gene which is rapidly expressed being maintained for a long time in veins via an unknown wound-signaling pathway(s). [ABSTRACT FROM PUBLISHER]

We isolated 13 tobacco calmodulin (CaM) genes, NtCaM1–13, and analyzed their expression profile in response to pathogen infection and wounding using specific DNA probes for individual CaM genes and specific antibodies for CaM proteins in groups I (NtCaM1/2), II (NtCaM3/4/5/6/7/8/11/12 and 9/10) and III (NtCaM13), respectively. Synchronous cell death in tobacco mosaic virus (TMV)-infected N-gene-containing tobacco leaves accompanied a predominant accumulation of NtCaM1, 2 and 13 transcripts and NtCaM13-type protein, which is a possible ortholog of soybean defense-involved CaM (SCaM-4), preceding induction of PR-1 and PR-3 defense genes. Accumulation of NtCaM1, 2, 3 and 4 transcripts was induced within 30 min after wounding and NtCaM1-type protein accumulated transiently after wounding. NtCaM13-type protein, which was found at a low level in healthy leaves, decreased instantly after wounding. The treatment with a proteasome inhibitor, lactacystin, enhanced wound-induced accumulation of NtCaM1-type protein and inhibited wound-induced decrease of NtCaM13-type protein, suggesting that proteasome activity is involved in the degradation of these CaMs. Thus, our results indicate that levels of individual CaM proteins are differentially regulated both transcriptionally and post-transcriptionally in tobacco plants that are exposed to stresses such as pathogen-induced hypersensitive cell death and wounding. [ABSTRACT FROM AUTHOR]

L. (cv. Petit Havana SR1) were grown under ultraviolet-B (UV-B, 290–320 nm) irradiation, and soluble proteins were extracted from the leaves. Two-dimensional electrophoresis revealed that a minimum of 12 polypeptides were induced by UV-B. Polypeptides which were so abundant as to be detectable by Coomassie brilliant blue staining were then subjected to N-terminal amino acid sequence analyses. Two of the polypeptides were identified as a 23 kDa protein of PS II and 6 as a pathogenesis-related protein 5 (PR-5). Immunoblotting demonstrated that other PR proteins, PR-1 and PR-3 were also induced by UV-B. Salicylic acid (SA), which is an important component of signal transduction that leads to the expression of PR proteins and exhibition of acquired resistance to pathogens, increased in response to exposure to UV-B. In addition, the activity of phenylalanine ammonialyase, which catalyzes the synthesis from phenylalanine of trans-cinnamic acid, the endogenous precursor of SA, was transiently increased by UV-B irradiation. These results suggest that UV-B activates the signal transduction pathway, which is a common step in pathogen infection. [ABSTRACT FROM AUTHOR]

In tobacco plants, wounding induces production of a set of defense-related proteins such as basic pathogenesisrelated (PR) proteins and proteinase inhibitors (PIs) via the jasmonate/ethylene pathway. Although class III plant peroxidase (POX) is also wound-inducible, the regulatory mechanism for its wound-induced expression is not fully understood. Here, we describe that a tobacco POX gene (tpoxN1), which is constitutively expressed in roots, is induced locally 30 min after wounding and then systemically in tobacco plants. Infection of necrotizing virus also induced tpoxN1 gene. The wound-induced expression was not enhanced by known wound-signal compounds such as methyl jasmonate (MeJA) and ethephon in contrast to other wound-inducible genes such as basic PR-1 and PI-II genes. And treatment with MeJA and coronatine, biological analogs of jasmonate, rather suppressed the tpoxN1 expression. Salicylic acid, an antagonist of jasmonatebased wound signaling, did not suppress the wound-induced expression of tpoxNl. Only spermine, which is reported as an endogenous inducer for acidic PR genes in tobacco mosaic virus-infected tobacco leaves, could induce tpoxN1 gene expression. These results suggest that woundinduced expression of the tpoxN1 gene is regulated differently from that of the basic PR and PI-II genes. [ABSTRACT FROM AUTHOR]

Treatment of wounded tobacco leaves with a proteasome-specific inhibitor lactacystin resulted in; (1) enhanced expression of proteasome subunit genes, (2) suppressed expression of proteasome activity, (3) induced accumulation of Ub-conjugated proteins, and (4) suppressed expression of wound-inducible genes, indicating that the Ub-proteasome system is involved in wound-signaling in plants. [ABSTRACT FROM AUTHOR]

Sarcotoxin IA is a bactericidal peptide of 39 amino acids found in the common flesh fly, Sarcophaga peregrina. Many agronomically important bacteria in Japan are killed by this peptide at sab-micro molar levels, and the growth of tobacco and rice suspension cultured cells is not inhibited with less than 25 µM. Transgenic tobacco plants which overexpress the peptide, i.e. over 250 pmol per gram of fresh leaf, under the control of a high expression constitutive promoter showed enhanced resistance to the pathogens for wild fire disease (Pseudomonas syringae pv. tabaci) and bacterial soft rot disease (Erwinia carotovora subsp. carotovora). [ABSTRACT FROM PUBLISHER]

Salicylic acid (SA) and jasmonic acid (JA) are essential compounds in the pathogen- and wound-signaling pathways accompanying induced expression of acidic and basic pathogenesis-related (PR) protein genes, respectively. However, on the effect of exogenously supplied SA and JA in induction of PR gene expression, conflicting results have been obtained using various plant materials at different developmental stages. There is no clear evidence on these effects in the presence of both signals at the same time. We analyzed the effect of SA on wound- and JA-induced basic PR gene expression and that of JA on SA-induced acidic Pi? gene expression in mature tobacco leaves. Wound-induced accumulation of transcripts for all 4 basic PR genes tested was enhanced in the presence of MeJA, and inhibited in the presence of SA. On the other hand, expression of all 3 acidic PR genes tested was induced by SA and was inhibited by MeJA. Using antibodies raised against acidic PR-1 and PR-2 proteins, these effects were confirmed at the protein level. These results indicated that JA works as an inducer of basic PR genes, and also as an inhibitor for acidic PR genes, while SA does the opposite. [ABSTRACT FROM AUTHOR]

To enhance the disease resistance of plants expressing a foreign peptide, the gene for sarcotoxin IA, which is an antimicrobial peptide from an insect consisting of 39 amino acid residues, was introduced into tobacco (Nicotiana tabacum) under the control of a high expression promoter via Agrobacterium-mediated transformation. In transgenic plants, sarcotoxin IA mRNA accumulated to detectable levels, however, the amount of the peptide produced was so small that we could scarcely detect it by protein gel blot analysis, probably because of the instability of short peptides in plant cells. To improve the expression efficiency, genes for four types of amino-terminal and carboxyl-terminal translational fusions of sarcotoxin IA together with the GUS gene were introduced into tobacco. In all four types of transgenic tobacco plants, high level transcripts similar to that in the direct expression sarcotoxin IA construct were found. Protein gel blot analysis with both anti-sarcotoxin IA and GUS antibodies showed production of high levels of fusion protein in all transgenic plants. Among them, three types had abnormal membranes and phenotypes, although no such abnormalities were found in transgenic plants in which only sarcotoxin IA was expressed in a secretable form. All together, these results indicated that, for stable and effective expression of a foreign short peptide in transgenic plants, expression as a fusion protein is useful and that secretion of sarcotoxin IA outside of cells is necessary for generation of useful antimicrobial transgenic plants. [ABSTRACT FROM AUTHOR]

Plants respond differentially to wounding and pathogens using distinct signaling pathways, so that wound signals are transmitted to jasmonic acid (JA) which induces basic pathogenesis-related (PR) proteins, whereas pathogenic signals cause, in addition to JA, accumulation of salicylic acid (SA) which stimulates production of acidic PR proteins. Transgenic tobacco plants expressing a gene for a small GTP binding protein respond abnormally to mechanical wounding to produce SA and consequently acidic PR proteins, suggesting that wound signals cross with pathogen signaling pathways [Sano et al. (1994) Proc. Natl. Acad. Sci. USA 91: 10556]. This unusual signal crossing is associated with a highly sensitive wound-response of transgenic plants which, upon wounding, produce JA at least eighteen hours earlier than wild-type plants. When wildtype plants are wounded in the presence of the synthetic cytokinin, benzylaminopurine, production of JA begins six hours earlier than in untreated samples, and also SA begins to accumulate. The cytokinin antagonist, 2-chloro-4-cyclohexylamino-6-ethylamino-s-triazine, erases these effects. Because transgenic plants constitutively produce four-to six-fold higher amounts of endogenous cytokinins than wild-type plants, it is concluded that cytokinins are indispensable for control of endogenous levels of SA and JA. [ABSTRACT FROM AUTHOR]

A series of chimeric promoters for higher-level expression of foreign genes in plants was constructed as fusions of a gene for rβ-glucuronidase (GUS) with the terminator of a gene for nopaline synthase (nos) or of the cauliflower mosaic virus (CaMV) 35S transcript, and the strength of these promoters was assayed in transient and stable expression systems in tobacco and rice. As parts of these promoters, the CaMV 35S core promoter, three different 5′-upstream sequences of the 35S promoter, the first intron of a gene for phaseolin, and a 5′-untranslated sequence (Ω sequence) of tobacco mosaic virus were used in various combinations. In tobacco and rice protoplasts, all three fragments of the 35S promoter (–419 to –90, –390 to –90 and –290 to –90, relative to the site of initiation of transcription), the intron, and the Ω sequence effectively enhanced GUS activity. Some chimeric promoters allowed levels of GUS activity that were 20- to 70-fold higher than those obtained with the 35S promoter in pBI221. In tobacco protoplasts, the two longer fragments of the 35S promoter were more effective than the shortest fragment. In rice cells, by contrast, the shortest fragment was as effective as the two longer ones. The terminator of the 35S transcript was more effective than that of the nos gene for gene expression. In transgenic tobacco plants, a representative powerful promoter, as compared to the 35S promoter, allowed 10- and 50-fold higher levels of expression on average and at most, respectively, with no clear qualitative differences in tissue- and organ-specific patterns of expression. When the representative promoter was introduced into tobacco with a gene for luciferase, the autofluorescence of detached leaves after a supply of luciferin to petioles was great and was easily detectable by the naked eye in a dark room. [ABSTRACT FROM AUTHOR]

Discusses the release from post-transcriptional gene silencing by cell proliferation in transgenic tobacco plants. Transgene silencing in tobacco plants overproducing a firefly luciferase gene; Biochemical analysis.