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PubMed1994

The X-gene of human hepatitis B virus transactivates the c-jun and alpha-fetoprotein genes.

The X-gene product of human hepatitis B virus is a transacting transcriptional factor which activates a variety of heterologous viral and host promoters/enhancers. We have found that the X-gene product can significantly transactivate the regulatory sequences located at the 5'-upstream of the c-jun oncogene when a reporter plasmid containing the sequences was co-transfected to HepG2 cells with an X-gene expression plasmid. The results of mutational analysis indicate that the X-gene activation requires the AP-1 sequence of the c-jun gene. Furthermore, we also found that the X-gene is capable of activating the 5'-upstream sequence of the alpha-fetoprotein gene. There are at least two elements that respond to the X-gene transactivation. One is located in the sequences between -5,100 and -2,900, and the other is at the C/EBP site. Therefore, the X-gene activates the c-jun and alpha-fetoprotein genes through different host factors, namely AP-1 and C/EBP, respectively. The results of c-jun activation by the X-gene strongly support the previous hypothesis that the X-gene may play a critical role in the development of hepatocellular carcinoma.

Base Sequence↗

PubMed2005

Stimulation of group I metabotropic glutamate receptors evokes calcium signals and c-jun and c-fos gene expression in human T cells.

To study if the activation of group I mGlu receptors in human T cells modifies intracellular Ca2+ concentration ([Ca2+](i)) and cell function, we measured [Ca2+](i) on cell suspensions (spectrofluorimetric method) or single cell (digital Ca2+ imaging system) using fura-2 as indicator. Early-inducible gene (c-jun and c-fos) expression was studied by reverse transcriptase-polymerase chain reaction assay as representative of Ca(2+)-sensitive gene expression. (1S,3R)-ACPD (100 microM), the selective mGlu receptor agonist, evoked a significant increase (34.1+/-4.9%) of [Ca2+](i), pharmacologically characterized as mediated by group I mGlu receptors, since both (S)-3,5-DHPG (100 microM), a selective group I mGlu receptor agonist and CHPG (1mM), the specific mGlu5 receptor agonist, reproduced the effects, that were abolished by AIDA (1mM), a selective group I mGlu receptor antagonist. (S)-3,5-DHPG-induced a rapid [Ca2+](i) rise (initial phase) followed by a slow decrease (second phase) to the baseline. Both extracellular Ca2+ and Ca2+ released from intracellular stores contribute to the [Ca2+](i) increase which depend on PLC activation. In a Ca(2+)-free buffer, the second phase rapidly return to the baseline; LaCl3 (1-10 microM), an inhibitor of extracellular Ca2+ influx, significantly reduced the second phase only; thapsigargin (1microM), by discharging intracellular Ca2+ stores, U 73122 (10 microM) and D609 (300 microM), by inhibiting PLC activity, prevented both phases. In our system, PTX pre-treatment increased (S)-3,5-DHPG effects, demonstrating that PXT-sensitive G(i/o) proteins are involved. Finally, specific stimulation of these receptors in Jurkat cells upregulates c-jun and c-fos gene expression, thus activating multiple downstream signalling regulating important T cell functions.

Calcium Signaling↗

PubMed1990

Immediate-early gene expression differs between regenerating liver, insulin-stimulated H-35 cells, and mitogen-stimulated Balb/c 3T3 cells. Liver-specific induction patterns of gene 33, phosphoenolpyruvate carboxykinase, and the jun, fos, and egr families.

Immediate-early genes, whose expression increases independent of de novo protein synthesis during the transition from quiescence to proliferation, are postulated to play important regulatory roles in the growth response. The complement of immediate-early genes expressed must depend on the milieu of preexisting transcription factors in the quiescent cell as well as the type of mitogenic stimulation and, thus, may differ between cell types. We have begun characterizing the immediate-early response in regenerating liver and insulin-stimulated Reuber H-35 hepatoma cells in comparison with previously published results from mitogen-stimulated Balb/c 3T3 fibroblasts. The proliferating H-35 and regenerating liver cells maintain their similarity to quiescent liver as demonstrated by their continued production of the liver-specific albumin, CCAAT/enhancer binding protein, and phosphoenolpyruvate carboxykinase messenger RNAs (mRNA). Surprisingly, the phosphoenolpyruvate carboxykinase gene, which undergoes down-regulation in insulin-treated H-35 cells, was cloned by differential screening of a subtraction-enriched regenerating liver cDNA library and is an immediate-early gene in regenerating liver. H-35 cells treated with either insulin or phorbol 12-myristate 13-acetate express elevated levels of the jun genes, and phorbol 12-myristate 13-acetate pretreatment fails to abolish the insulin response, indicating that it does not depend on protein kinase C. jun family gene expression in regenerating liver differs from that in mitogen-treated fibroblasts in that the time course of expression of c-jun and junB is prolonged, and junD mRNA levels distinctly increase. Additionally, although c-fos and egr-1 mRNAs are expressed at elevated levels in stimulated liver cells, fos-B, fra-1, and egr-2 are not, which suggests that factors in addition to the serum response factor participate in the regulation of immediate-early gene induction. Interestingly, gene 33, which was cloned from a regenerating liver cDNA library by differential screening and lacks a recognizable serum response element, functions as an immediate-early gene in regenerating liver and in mitogen-treated H-35 and Balb/c 3T3 cells. These results suggest that gene 33 participates in the transition from quiescence to proliferation in many mitogen-treated cells in addition to its previously reported involvement in hormone responses. Overall, the results presented here suggest that the immediate-early response varies considerably between regenerating liver and mitogen-stimulated fibroblasts and could involve multiple, preexisting, tissue-specific, transcription-activating proteins.

Animals↗

PubMed2003

[Protective effects of c-jun anti-sense gene recombinant transfection on rat cardiomyocytes inflicted by hypoxia and burn serum].

OBJECTIVE: To investigate the protective effects of c-jun antisense gene recombinant transfection on rat cardiomyocytes inflicted by hypoxia and burn serum. METHODS: Cardiomyocytes from Wistar rat were isolated and cultured before being divided into normal control (C), transfection (T) and non-transfection (NT) groups. C-jun antisense gene recombinant was constructed and transfected into cardiomyocytes, which were then treated by hypoxia and burn serum in T group, while those in NT group were simply treated by hypoxia and burn serum. The changes in the c-jun mRNA expression were determined by RT-PCR at 1, 3 and 7 hours after the cardiomyocytes being stimulated, and the changes in the expressions of c-jun protein, troponin-T (TnT) and beta-tubulin were assayed by Western blot. The morphological changes in the cardiomyocytes were observed by LM and EM. RESULTS: 1) The expressions of c-jun mRNA and protein in the NT group were increased evidently when compared with those in C and T groups. 2) The expressions of TnT and beta-tubulin in NT group were decreased evidently in contrast to those in C and T groups. In addition, there exhibited evident structural derangement, dissolution and fragmentation to granules of cardiomyocytes in NT group, while the myocardial cytoskeletal structure was well preserved with scarce fragmentation and dissolution in T group. CONCLUSION: Increased expression of c-jun in rat cardiomyocytes resulting in myocardial injury could be induced by combined treatment of hypoxia and burn serum, while c-jun antisense gene recombinant transfection might protect rat cardiomyocytes from injury.

Animals↗

PubMed1996

Differential and antagonistic effects of v-Jun and c-Jun.

We compared the ability of cellular and viral Jun (c-Jun and v-Jun) to transactivate target genes. c-Jun and v-Jun bind specifically to 12-O-tetradecanoylphorbol-13-acetate responsive elements [TREs, also called activator protein 1 (AP-1) motifs]. However, whereas c-Jun activates TRE-controlled promoters, v-Jun represses them. Cotransfection of the two Jun proteins reduces c-Jun-dependent transactivation. The expression of the endogenous c-jun gene, regulated through a promoter-proximal AP-1-binding site, is repressed in v-Jun-transformed chicken embryo fibroblasts. It is suggested that an M(r) 18,000 v-Jun peptide prominent in v-Jun-transformed cells acts as a transdominant-negative regulator of AP-1 activity and of c-jun expression. In contrast to the results with TRE sites, both v-Jun and c-Jun activate transcription through the human T-cell leukemia virus type I 21-bp repeat which contains a sequence homologous to the cyclic AMP responsive element. However, full-length Jun proteins bind to this site only with low affinity, and binding of the truncated v-Jun was barely detectable. These observations show that the oncogenic viral form of Jun differs from the cellular version in promoter preference and on certain promoters acts as an antagonist to c-Jun.

Animals↗

PubMed2004

HMG-I/Y is a c-Jun/activator protein-1 target gene and is necessary for c-Jun-induced anchorage-independent growth in Rat1a cells.

The transcription complex activator protein-1 (AP-1) plays a role in a diverse number of cellular processes including proliferation, differentiation, and apoptosis. To identify AP-1-responsive target genes, we used a doxycycline-inducible c-Jun system in Rat1a cells. The HMG-I/Y chromatin binding protein was found to be up-regulated by c-Jun. Following induction of c-Jun expression, Rat1a cells under nonadherent growth conditions have sustained HMG-I/Y mRNA expression and 2-fold higher protein than uninduced cells. HMG-I/Y promoter reporter assays show that HMG-I/Y promoter activity increases in the presence of c-Jun expression, and gel mobility shift assays demonstrate that induced c-Jun binds to an AP-1 consensus site at position -1,091 in the HMG-I/Y promoter. Suppression of HMG-I/Y expression by its antisense sequence significantly reduces the ability of c-Jun-overexpressing Rat1a cells to grow in an anchorage-independent fashion. HMG-I/Y transforms Rat1a cells (although the colonies are smaller than that observed for the cells overexpressing c-Jun). Taken together, these results suggest that HMG-I/Y is a direct transcriptional target of c-Jun necessary for c-Jun-induced anchorage-independent growth in Rat1a cells.

Animals↗

PubMed1993

Changes in Hox1.6, c-jun, and Oct-3 gene expressions are associated with teratocarcinoma F9 cell differentiation in three different ways of induction.

To obtain information on the mechanism of teratocarcinoma cell differentiation, the expression of genes having a specific role in gene regulation was examined using three different methods of inducing differentiation: drug treatments with retinoic acid (RA) and sodium butyrate, and a genetic approach using ts mutants. The RAR-beta and MK genes were induced specifically by RA treatment, which indicates that these two genes are solely RA responsive. By contrast, a change in c-jun, Hox1.6, and Oct-3 gene expression was observed in all three methods of F9 cell differentiation. These findings suggest that these three genes, whether down-or up-regulated, play an important and key role during teratocarcinoma cell differentiation.

Animals↗

PubMed1995

Induction of the immediate early gene c-jun in human spinal cord in amyotrophic lateral sclerosis with concomitant loss of NMDA receptor NR-1 and glycine transporter mRNA.

The aetiology of the sporadic form of amyotrophic lateral sclerosis (ALS) is poorly understood although abnormalities in glutamate and glycine transport have been implicated which both could contribute to a neurodegenerative process mediated through the N-methyl-D-aspartate (NMDA) receptor. In this study we have used in situ hybridization to investigate whether any changes in the expression of NMDA receptors, the glycine transporter or glutamate-mediated injury responses are detectable in ALS. Two immediate early genes were investigated as markers of neuronal injury responses, c-jun and zif-268, both constitutively expressed in the spinal cord. Levels of c-jun mRNA were most abundant in intermediate grey and layer IX of the ventral horn containing motor neurones. This pattern was markedly changed in ALS with large increases (2-3 fold) in c-jun mRNA occurring in dorsal and ventral horn. The marked increase in c-jun mRNA was also substantiated by slot blot analysis of tissue homogenates of spinal cord and a parallel induction of zif-268 mRNA was also seen. NMDA receptor NR-1 mRNA was widely distributed in control spinal cord with the highest concentrations occurring in layers IX, X, intermediate grey and dorsal horn. The ALS cases showed a selective decrease in the level of NR-1 mRNA in the ventral region (50%) whilst no significant decrease was detected in the dorsal region. Quantitation of tissue homogenates with dorsal and ventral regions combined also yielded a significant decrease of 40% which supports the analysis from in situ hybridization densitometry.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

ACTH increases expression of c-fos, c-jun and beta-actin genes in the dexamethasone-treated rat adrenals.

Our recent finding that ACTH increases c-fos mRNA in the adrenal gland of hypophysectomized rats indicates that the gene product FOS may play an important role(s) in mediating the action of ACTH. However, hypophysectomy employed in that study causes the disappearance of trophic hormones other than ACTH and may modify the effect of ACTH. Thus, in the present investigation, dexamethasone-treated rats were used. Since FOS functions only when it dimerizes with JUN (the product of c-jun gene), the changes in the levels of c-fos and c-jun mRNAs were studied together with that of beta-actin mRNA which is also affected by ACTH. Northern blot analysis was employed to determine the mRNA levels. It was demonstrated that ACTH increases the mRNAs coding c-fos and c-jun in the adrenal glands of dexamethasone-treated, ACTH-suppressed rats. The c-fos mRNA was not detectable before ACTH administration. After ACTH administration, the mRNA levels were transiently increased, the maximum level being observed at 30 min after ACTH. At 180 min post ACTH, the level returned to the unstimulated level. The mRNA coding c-jun was detectable before ACTH administration and it also increased rapidly after ACTH with maximal stimulation at 30 min. However, the mRNA level at 180 min post ACTH was still higher than the unstimulated level. The changes in beta-actin mRNA were approximately the same as those of c-jun mRNA. These results suggest that increased expression of c-fos, c-jun and beta-actin genes by ACTH may play an important role in mediating its action on the adrenals.

Actins↗

PubMed2004

[Effect of methylmercury on expression of immediate early gene c-jun mRNA in rat brain].

In order to probe into the early prediction molecular index and the signal transduction molecular mechanism of methyl mercury chloride (MMC) neurotoxicity, the expression of c-jun mRNA in rat brains induced by different concentration MMC for different times were observed by using reverse transcription polymerase chain reaction (RT-PCR) methods (the control group was physiological saline of 0.9%, the concentrations of expose groups were 0.05, 0.5, 5 mg x kg(-1) respectively, the sampling times were 20, 60, 240, 1440 min). The result showed the expression of c-jun mRNA in rat brains was prior to the accumulation of mercury, and the expression of c-jun mRNA in rat brains could early predict the neurotoxicity of MMC. IEG (c-jun) participated in the toxicity process of injury by MMC.

Animals↗

PubMed1990

Obligatory wounding requirement for tumorigenesis in v-jun transgenic mice.

Avian sarcoma virus 17 induces fibrosarcomas in chickens and can transform a number of avian cell types in vitro by the action of v-jun. This gene and the related cellular genes c-jun, jun B and jun D, encode transactivating (or repressing) DNA-binding proteins that form homo- or heterodimeric (Jun-Jun and Jun-Fos) complexes which recognize the AP-1 consensus sequence TGACTCA, a response element that confers sensitivity to the tumour-promoting phorbol ester TPA. We have produced several lines of transgenic mice carrying the v-jun oncogene, driven by the promoter of the widely expressed H-2KK major histocompatibility complex (MHC) class I antigen gene. Transgenic animals are initially phenotypically normal, but after full-thickness wounding they show abnormal wound repair, characterized by hyperplastic granulation tissue. Many of these lesions are slowly progressive because of continuing fibroblast proliferation, and over 2-5 months some give rise to dermal fibrosarcomas. This reproducible multistep transition through a proliferative but benign intermediate is associated with characteristic increments in v-jun expression. Moreover, hyperplastic wound repair and its progression are both related to transgene dosage, suggesting that there exists a quantitative requirement or threshold for v-jun action. Our results indicate that v-jun is not oncogenic in transgenic mice as a result of a 'single-hit' mechanism, but rather, in addition to an obligatory wound, that secondary genetic or epigenetic events (possibly conscripting normal constituents of wound repair) are necessary for tumour development and progression.

Animals↗

PubMed1999

Cadmium-induced apoptosis and changes in expression of p53, c-jun and MT-I genes in testes and ventral prostate of rats.

Apoptosis and a change in the expression of p53, c-jun and MT-I genes occurred in rats exposed to cadmium in a way known to cause carcinogenesis in testes and ventral prostate. In situ end labelling (ISEL), DNA electrophoresis, and RT-PCR methods were used in present study. Adult male Wistar rats were given a single (s.c.) injection of 0, 5, 10, or 20 micromol/kg CdCl2. Then 12, 48 or 96 h after administration of cadmium, animals were sacrificed. It was observed that cadmium markedly induced apoptosis in the testes at the dose of 5 micromol/kg while 10 and 20 micromol/kg cadmium caused more necrosis than apoptosis. Apoptosis in the ventral prostate was markedly induced by all the doses of cadmium and there was an obvious time- and dose-dependent relationship between apoptotic index (AI) and cadmium treatment. Far fewer apoptotic cells appeared in liver, compared to the testes and ventral prostate. p53 mRNA expression was clearly enhanced in the ventral prostate but clearly suppressed in the testes by cadmium exposure, and the time- and dose-effect was very clear. The expression level of p53 in the liver was not affected by cadmium treatment. Cadmium-induced overexpression of c-jun gene appeared at 12 h in the liver, but not until 96 h in the testes and ventral prostate. Although the MT-I gene was found to be expressed in all tissues, marked induction by cadmium of the expression of MT-I gene was only observed in the liver. These results indicate: (1) that apoptosis is an early mechanism of acute tissue damage by cadmium in the testes and ventral prostate; (2) that p53 and c-jun genes may be involved in cadmium-induced cytotoxicity (apoptosis) and related carcinogenicity in male reproductive tissues; and (3) that the enhanced expression of MT-I in the liver could protect this organ from cadmium-induced cytotoxicity (apoptosis) and carcinogenicity.

Animals↗

PubMed1992

Positive regulation of the skeletal alpha-actin gene by Fos and Jun in cardiac myocytes.

Transcription of the skeletal alpha-actin gene is selectively activated in rat myocardiocytes undergoing hypertrophy both in vivo and in vitro. In most of these models, transient expression of certain proto-oncogene transcription factors precedes hypertrophy and sarcomeric gene induction. Using expression vectors encoding Fos and Jun, the main constituents of transcriptional activator protein AP-1, we analyzed the role of these oncoproteins in mediating the transcriptional induction of skeletal alpha-actin by adrenergic stimulation. Both c-fos and c-jun were induced early after beta-adrenergic stimulation, with peak mRNA levels preceding skeletal alpha-actin induction by several hours. A second peak of c-jun mRNA coincided with skeletal alpha-actin induction. Co-transfection assays in cardiac myocytes and P19 teratocarcinoma cells demonstrated that over-expression of c-jun, or c-fos plus c-jun, transactivated the skeletal alpha-actin promoter by about 5-fold. Comparable activation was not seen for alpha-myosin heavy chain or cardiac alpha-actin promoters. Skeletal alpha-actin promoter sequences between -153 and -36 were required for maximal transactivation by c-fos/c-jun, and purified Fos and Jun were bound specifically within this region. A direct physiological role is suggested for the AP-1 transcription factor complex in regulating skeletal alpha-actin gene expression and alpha-actin isoform switching during the onset of signal-mediated cardiac myocyte hypertrophy.

Actins↗

PubMed2006

Comparative effects of direct cadmium contamination on gene expression in gills, liver, skeletal muscles and brain of the zebrafish (Danio rerio).

The effects of cadmium (Cd) on gene expression were examined in four organs (gills, liver, skeletal muscles and brain) of the zebrafish. Adult male fish were subjected to three different water contamination pressures over periods of 7 and 21 days: control medium (C(0): no Cd added) and two contaminated media (C(1): 1.9 +/- 0.6 microg Cd l(-1), and C(2): 9.6 +/- 2.9 microg Cd l(-1)). Fourteen genes involved in antioxidant defences, metal chelation, active efflux of organic compounds, mitochondrial metabolism, DNA repair and apoptosis were selected and their expression levels investigated by quantitative real-time PCR. Cadmium concentrations were determined in the four organs and metallothionein (MT) protein levels investigated in brain, liver and gills. Although skeletal muscle was a poor Cd-accumulating tissue, many genes were up-regulated at day 7: mt1, cyt, bax, gadd and rad51 genes. Three additional genes, c-jun, pyc and tap, were up-regulated in muscles at day 21 whereas bax, gadd and rad51 had returned to basal levels. Surprisingly, mt1 and c-jun were the only genes displaying a differential induction after 21 days in liver, although this organ accumulated the highest cadmium concentration. In brain, only mt1, mt2 and c-jun genes were up-regulated after 21 days. In gills, the highest response was observed after 7 days, featuring the differential expression of oxidative stress-response hsp70 and mitochondrial sod genes, along with genes involved in mitochondrial metabolism and metal detoxification. Then, after 21 days, the expression of almost every genes returned to basal levels while both mt1 and mt2 genes were up-regulated.

Animals↗

PubMed1997

Expressions of c-jun and jun-B proto-oncogenes in odontoblasts during development of bovine tooth germs.

c-jun and jun-B genes are among the nuclear proto-oncogenes induced by growth factors such as the TGF-beta superfamily and play important roles in cell differentiation. These gene products enhance expressions of proteins including osteocalcin, alkaline phosphatase, and collagens. On the other hand, it is well-known that the TGF-beta superfamily affects odontoblast differentiation, and that differentiated odontoblasts express extracellular and membrane proteins as described above. However, there are few reports of factors that participate in the transcriptional regulation of odontoblasts. Especially, little is known about the expression of c-jun and jun-B genes. In this study, we focused on the examination of expressions of c-jun and jun-B genes in dental papillae of bovine tooth germs. Using in situ hybridization, we found that these genes were expressed only in the odontoblastic lineage, but not in other dental papilla cells. Levels of c-jun and jun-B mRNAs increased along the gradient of differentiation of odontoblasts. These levels of c-jun mRNAs were maintained in both young and mature odontoblasts. However, unlike the c-jun gene, expression of the jun-B gene became sparse in mature odontoblasts compared with young odontoblasts. For further analysis, Northern hybridization of total RNA extracted from differentiated odontoblasts was performed for the examination of levels of jun-B mRNAs, indicating that levels of jun-B mRNAs of mature odontoblasts were clearly less than those of young odontoblasts. These results suggest that c-jun and jun-B genes may participate in the transcriptional regulation of odontoblasts of bovine tooth germs, and may control the odontoblast phenotype. Furthermore, our results suggest that these genes can be markers of odontoblasts during dentinogenesis; especially, high expression of jun-B gene can be a marker of young odontoblasts that start to form the new dentin matrix.

Animals↗

PubMed2000

Transcriptional repression of p21((Waf1/Cip1/Sdi1)) gene by c-jun through Sp1 site.

Previously, we found that c-jun represses the tumor suppressor p21((Waf1/Cip1/Sdi1)) (p21) gene expression. In this study, we further investigated the mechanism of the inhibitory effect of c-jun on p21. After analysis of a series of deletion and point mutants of p21 promoter, we found that Sp1-3 site (-77 and -83) relative to the transcription start site played an important role for c-jun-repressing-responsive element in the p21 promoter. Both Sp1 and Sp3 transcription factors were the key factors for this event. However, the data from electrophoretic mobility shift assay indicated that c-jun did not change the Sp1 DNA-binding affinity, suggesting that additional factors may be involved in the repression of p21 by c-jun. Furthermore, c-jun could inhibit butyrate-inducing p21 gene expression through Sp1, indicating at least one common pathway whereby p21 expression is affected by c-jun and butyrate in opposing actions. Moreover, the hyperphosphorylated retinoblastoma protein (Rb) increased in c-jun expressing cells, indicating that phosphorylated Rb may play a role in regulating Sp1 to repress p21 expression. This is the first demonstration of how housekeeping factors and oncogene product counteract the function of tumor suppressor genes to control cell cycle progression.

Binding Sites↗

PubMed2001

Repression of glucocorticoid receptor gene transcription by c-Jun.

The regulation of glucocorticoid receptor gene expression by members of the AP-1 family was examined in glucocorticoid-free NIH3T3 cells transfected with the human glucocorticoid receptor gene promoter driving expression of a CAT reporter gene. c-Jun inhibited the promoter activity by 80% and JunB by 30%, whereas c-Fos and JunD had no inhibitory effect. Electrophoretic mobility shift assays showed that c-Jun is unable to efficiently interact with the AP-1-like site present in the human glucocorticoid receptor promoter. Moreover, c-Jun was still able to repress promoter mutants in which the region containing the AP-1-like site was deleted. NIH3T3 cell clones overexpressing c-Jun exhibited lower glucocorticoid receptor mRNA levels, which suggests that the murine glucocorticoid receptor gene can also be regulated by AP-1. These results provide a new mechanism for cross-talk between the glucocorticoid receptor and the AP-1 family of transcription factors in the absence of glucocorticoid ligands.

3T3 Cells↗

PubMed1995

Effects of c-Jun and a negative dominant mutation of c-Jun on differentiation and gene expression in lens epithelial cells.

We have used a retroviral vector (RCAS) to overexpress wild-type chicken c-Jun or a deletion mutant of chicken c-Jun (Jun delta 7) lacking the DNA binding region to investigate the possible role of c-Jun in lens epithelial cell proliferation and differentiation. Both constructs were efficiently expressed in primary cultures of embryonic chicken lens epithelial cells. Overexpression of c-Jun increased the rate of cell proliferation and greatly delayed the appearance of "lentoid bodies," structures which contain differentiated cells expressing fiber cell markers. Excess c-Jun expression also significantly decreased the level of beta A3/A1-crystallin mRNA, without affecting alpha A-crystallin mRNA. In contrast, the mutated protein, Jun delta 7, had no effect on proliferation or differentiation but markedly increased the level of alpha A-crystallin mRNA in proliferating cell cultures. These results suggest that c-Jun or Jun-related proteins may be negative regulators of alpha A- and beta A3/A1-crystallin genes in proliferating lens cells.

Amino Acid Sequence↗