Biomedical subjects

S Zhang

Publications and source records attributed to S Zhang.

At least 631 records · Page 35Linked to original sources

PubMed1998

Direct binding to nucleic acids by Vpr of human immunodeficiency virus type 1.

Human immunodeficiency virus type 1 (HIV-1) viral protein R (Vpr) is a 15kDa regulatory protein packaged in the HIV-1 virion. Although the molecular mechanism of Vpr function during viral replication remains elusive, Vpr has been found to possess interesting biological activities, including cell-cycle arrest at the G2/M check point, promotion of the HIV-1 pre-integration complex for nuclear transport, and a low but significant level of transcriptional activation of a variety of viral and cellular promoters. We now present data suggesting that HIV-1 Vpr is a nucleic-acid-binding protein. This activity of Vpr was demonstrated by DNA-cellulose chromatography, antibody co-immunoprecipitation, and gel electrophoretic mobility shift assays. By mutational analysis, the C-terminal region of Vpr, which is rich in basic amino-acid residues, was shown to be critical for Vpr binding to nucleic acids. The nucleic-acid-binding activity of Vpr is consistent with several biological activities of Vpr and may provide an important clue for understanding the molecular interactions between HIV-1 and the host cells.

Amino Acid Sequence↗

PubMed1998

cDNA cloning and developmental expression of the porcine homologue of WT1.

Wilms' tumors occur most frequently in swines as sporadic tumors. To clarify the role of WT1 gene in the genesis of Wilms' tumors and genitourinary development, we have isolated the porcine homologue of the human WT1 gene (pWT1) and analyzed its expression in various organs including the kidney. The open reading frame of pWT1 cDNA was extremely homologous to the human counterpart: 94% identical at the nucleotide level and 98% at the polypeptide level. In particular, the zinc finger region was more than 97% similar to human WT1 gene at the nucleotide level and 100% at the polypeptide level. pWT1 mRNA was found to be expressed in new-born kidney, spleen, testis, and embryonic kidneys, suggesting a possible association of pWT1 with the development of the genitourinary system. In conclusion, the nucleotide sequence and expression patterns in organs of pWT1 were similar to those of human WT1. Therefore, swines could provide good models for analyzing the contributions of WT1 gene to genitourinary development and genesis of Wilms' tumors.

Amino Acid Sequence↗

PubMed1998

The hyaluronan receptor RHAMM regulates extracellular-regulated kinase.

We have identified two RHAMM (receptor for hyaluronan-mediated motility) isoforms that encode an alternatively spliced exon 4 (Hall, C. L., Yang, B., Yang, X., Zhang, S., Turley, M., Samuel, S., Lange, L. A., Wang, C., Curpen, G. D., Savani, R. C., Greenberg, A. H., and Turley, E. A. (1995) Cell 82, 19-26 and Wang, C., Entwistle, J., Hou, G., Li, Q., and Turley, E. A. (1996) Gene 174, 299-306). One of these, RHAMM variant 4 (RHAMMv4), is transforming when overexpressed and regulates Ras signaling (Hall et al.). Here we note using flow cytometry and confocal analysis that RHAMM isoforms encoding exon 4 occur both on the cell surface and in the cytoplasm. Epitope-tagging experiments indicate that RHAMMv4 occurs only in the cytoplasm. Several observations suggest that both cell surface RHAMM isoforms and RHAMMv4 are involved in regulating extracellular-regulated kinase (ERK) activity. Affinity-purified anti-RHAMM exon 4 antibodies block the ability of platelet-derived growth factor to activate ERK, and these reagents modify the protein tyrosine phosphorylation profile of proteins resulting from treatment with platelet-derived growth factor. A dominant negative form of RHAMMv4 inhibits mutant active Ras activation of ERK and coimmunoprecipitates with both mitogen-activated protein kinase kinase and ERK, suggesting that the intracellular RHAMMv4 acts downstream of Ras, possibly at the level of mitogen-activated protein kinase kinase-ERK interactions. Consistent with this, overexpression of RHAMMv4 constitutively activates ERK. These results identify a novel mechanism for the regulation of the Ras-ERK signaling pathway and suggest that RHAMM plays multiple roles in this regulation.

Animals↗

PubMed1998

[Polymorphisms of four microsatellite markers closely linked with PKD1 in Chinese].

OBJECTIVE: To investigate the polymorphisms and evaluate the value in gene diagnosis of four microsatellites, which are the KG8 that locating in 3'untranslated region of PKD1 and SM6, CW4 and CW2, closely linked to PKD1. METHODS: The DNAs of some unrelated Chinese Han people were analyzed by using PCR, PAGE and silver staining and the findings were compared with those reported on Caucasian. RESULTS: In Chinese, KG8 included 6 alleles and PIC was 0.312; in Caucasian,8 alleles,PIC 0.545. The number of alleles and PIC of KG8 in Chinese were not so many as those in Caucasian. SM6 included 24 kinds of alleles and PIC was 0.80 in Chinese; in Caucasian,16 alleles, PIC 0. 653. CW4 is 9 alleles in Chinese and PIC of SM6 were more than those in Caucasian. In Chinese CW4, 9 alleles, PIC 0.850; in Caucasian, 9 alleles, PIC 0.782. Although the number of CW4 allele in the two nations was the same, PIC in Chinese was higher than that in Caucasian. In Chinese CW2,7 alleles, PIC 0.814; and in Caucasian, 13 alleles, PIC 0.809. The number of allele of CW2 in Chinese was not so many as that in Caucasian; however,the PIC was about the same. CONCLUSION: The results indicate that there are differences in the number of allele and distribution of the four microsatellite markers between Chinese and Caucasian. So there exists difference of dinucleotide repeat between two nations. In addition,SM6, CW4 and CW2 could be used as valuable markers in gene linkage diagnosis and personal and related identification in forensic medicine.

Alleles↗

PubMed1998

Identification of glucocorticoid receptor domains necessary for transcriptional activation of the mouse mammary tumor virus promoter integrated in the genome.

It has previously been determined that the mouse mammary tumor virus (MMTV) promoter when integrated in the genome assumes a defined chromatin structure which is disrupted upon addition of glucocorticoids. In contrast, a transiently introduced MMTV promoter has a random nucleoprotein structure. To reveal glucocorticoid receptor (GR) domains necessary for transcriptional activation of the MMTV promoter we compared the effects of mutations of the GR on transcriptional activation of the stably integrated versus transiently introduced MMTV promoter. For this purpose we generated a GR-negative cell line which has an MMTV promoter/reporter construct integrated in the genome and studied the transcriptional activation of this construct by different GR mutants introduced into the cells. Transcriptional activation of the integrated and transiently introduced promoter was achieved by the wild-type GR or a chimeric receptor in which the MR hormone-binding domain (HBD) replaced the GR HBD. In contrast, we found that deletion of the HBD of the GR or replacement of this region with the equivalent domain of the estrogen receptor produced receptors that were unable to activate the MMTV promoter integrated in the genome although these receptors efficiently activated the transiently introduced MMTV promoter. The HBD was not the sole determinant of MMTV transcriptional activation when integrated in the genome. Chimeric receptors which harbored the MR amino terminal domain or the wild-type MR were also unable to activate the integrated MMTV promoter. Taken together, these data indicate a rigid requirement for sequences in both the GR amino and the carboxy terminal domains for transcriptional activation of a hormone response element in the defined chromatin context of the MMTV promoter.

Aldosterone↗

PubMed1998

Chorismate mutase-prephenate dehydratase from Escherichia coli. Study of catalytic and regulatory domains using genetically engineered proteins.

The bifunctional P-protein, which plays a central role in Escherichia coli phenylalanine biosynthesis, contains two catalytic domains (chorismate mutase and prephenate dehydratase activities) as well as one R-domain (for feedback inhibition by phenylalanine). Six genes coding for P-protein domains or subdomains were constructed and successfully expressed. Proteins containing residues 1-285 and residues 1-300 retained full mutase and dehydratase activity, but exhibited no feedback inhibition. Proteins containing residues 101-386 and residues 101-300 retained full dehydratase activity, but lacked mutase activity. Fluorescence emission spectra and binding assays indicated that residues 286-386 were crucial for phenylalanine binding. The mutase (residues 1-109), dehydratase (residues 101-285), and regulatory (residues 286-386) activities were thus shown to reside in discrete domains of the P-protein. Both the mutase domain and the native P-protein formed dimers. Deletion of the mutase domain diminished phenylalanine binding to the regulatory site as well as prephenate binding to the dehydratase domain, both through cooperative effects. Besides eliminating feedback inhibition, removal of the R-domain decreased the affinity of chorismate mutase for chorismate.

Allosteric Regulation↗

PubMed1998

Cdkn2a, the cyclin-dependent kinase inhibitor encoding p16INK4a and p19ARF, is a candidate for the plasmacytoma susceptibility locus, Pctr1.

Plasma cell tumor induction in mice by pristane is under multigenic control. BALB/c mice are susceptible to tumor development; whereas DBA/2 mice are resistant. Restriction fragment length polymorphisms between BALB/c and DBA/2 for Cdkn2a(p16) and Cdkn2b(p15), and between BALB/c and Mus spretus for Cdkn2c(p18(INK4c)) were used to position these loci with respect to the Pctr1 locus. These cyclin-dependent kinase (CDK) inhibitors mapped to a 6 cM interval of chromosome 4 between Ifna and Tal1. C.D2-Chr 4 congenic strains harboring DBA/2 alleles associated with the Pctr1 locus contained DBA/2 "resistant" alleles of the CDK4/CDK6 inhibitors p16 and p15. On sequencing p16 and p18 cDNAs, two different allelic variants within ankyrin repeat regions of p16 were found between BALB/c and DBA/2 mice. By using an assay involving PCR amplification and restriction enzyme digestion, allelic variants were typed among several inbred strains of mice. One of the variants, G232A, was specific to two inbred strains, BALB/cAn and ABP/Le, of mice and occurred in a highly conserved amino acid in both human and rat p16. When tested with wild-type (DBA/2) p16, both A134C and G232A BALB/c-specific variants of p16 were inefficient in their ability to inhibit the activity of cyclin D2/CDK4 in kinase assays with retinoblastoma protein, suggesting this defective, inherited allele plays an important role in the genetic susceptibility of BALB/c mice for plasmacytoma induction and that p16(INK4a) is a strong candidate for the Pctr1 locus.

Amino Acid Sequence↗

PubMed1998

Type IB secretory phospholipase A2 is contained in insulin secretory granules of pancreatic islet beta-cells and is co-secreted with insulin from glucose-stimulated islets.

Stimulation of pancreatic islets with d-glucose induces insulin secretion from secretory granules contained within the islet beta-cells. Accumulating evidence suggests that secretory phospholipases A2 (sPLA2) may play a role in the distal events of secretory processes in many different cell types. Since intact pancreatic islets have been reported to contain sPLA2, it was of interest to determine the cellular and subcellular localization of the sPLA2 enzymes in pancreatic islets. Our findings indicate that rat pancreatic islets express mRNA for both types IB and IIA sPLA2 enzymes and mRNA for an sPLA2 membrane receptor. Immunoblotting analyses with antibodies directed against type IB sPLA2 or against type IIA sPLA2 indicate that the type IB isoform is much more abundant than the type IIA isoform in islets. Studies with purified populations of islet beta-cells prepared from dispersed islet cells by fluorescence-activated cell sorting indicate that both sPLA2 activity and type IB sPLA2 immunoreactive protein are substantially more abundant in beta-cells than in non-beta-cells. Subcellular fractionation studies indicate that sPLA2 activity and type IB sPLA2 immunoreactive protein are contained in insulin secretory granules. Stimulation of intact islets with insulin secretagogues results in the co-secretion of insulin and of sPLA2 activity and type IB sPLA2 immunoreactive protein into the incubation medium. These findings raise the possibility that type IB sPLA2 participates in the secretory process of pancreatic islet beta-cells.

Animals↗

PubMed1998

Evidence for in vivo ribosome recycling, the fourth step in protein biosynthesis.

Ribosome recycling factor (RRF) catalyzes the fourth step of protein synthesis in vitro: disassembly of the post-termination complex of ribosomes, mRNA and tRNA. We now report the first in vivo evidence of RRF function using 12 temperature-sensitive Escherichia coli mutants which we isolated in this study. At non-permissive temperatures, most of the ribosomes remain on mRNA, scan downstream from the termination codon, and re-initiate translation at various sites in all frames without the presence of an initiation codon. Re-initiation does not occur upstream from the termination codon nor beyond a downstream initiation signal. RRF inactivation was bacteriostatic in the growing phase and bactericidal during the transition between the stationary and growing phase, confirming the essential nature of the fourth step of protein synthesis in vivo.

Alleles↗

PubMed1998

[Shadow bands in PCR amplification of trinucleotide repeats and their elimination].

OBJECTIVE: To explore a method for eliminating the shadow bands in PCR amplification of trinucleotide repeats. METHODS: CTG trinucleotide repeat sequence in the 3'-untranslated region of the human myotonin protein kinase gene was used as templates DNA in PCR amplification, and the effects of Taq DNA polymerase alone and its mixture with Pwo DNA polymerase on occurrence of the shadow bands' were compared. The PCR products containing(CTG)5, both from Taq DNA polymerase and from Taq+Pwo polymerase amplification, were cloned into pBluecript KS and sequenced on ALF express TM DNA sequencer respectively. RESULTS: The PCR of DNA sequence containing CTG repeats frequently produced a main band (usually darker) and a shadow band (lighter) that differed from the main band by 3 base pairs when Taq DNA polymerase was used alone. However, when the mixture of Taq DNA polymerase and Pwo DNA polymerase was used, the shadow bands usually disappeared. In the 4 clones containing PCR products amplificated by Taq DNA polymerase, one clone contained only 4 CTG repeats. However, this kind of decrease of repeat copy was not observed in the 5 clones containing PCR products amplified by using mixture of Taq+Pwo DNA polymerase. CONCLUSION: The results of this experiment demonstrate that shadow bands occur during the PCR. Pwo DNA polymerase in known to possess not only DNA polymerase activity, but also 3'-5' exonuclease activity, or proofreading ability. The mixture of Taq DNA polymerase and Pwo DNA polymerase has higher processivity than Taq DNA polymerase itself. This explain the effect on eliminating or reducing the occurrence of shadow bands in polymerase chain reaction.

Adult↗

PubMed1998

Human mast cells express stem cell factor.

Stem cell factor (SCF) is a major cytokine regulator of mast cell growth and function. The present study demonstrates that human mast cells are able to produce SCF. Constitutive synthesis of SCF mRNA was seen in the mast cells isolated from human lung and skin by RT-PCR. This was confirmed by in situ hybridization in conjunctival mast cells of both tryptase-only (MCT) and tryptase/chymase (MCTC) subsets. SCF protein product was found in conjunctival MCT and MCTC mast cells by immunohistochemistry. Soluble SCF protein was detected in the culture supernatant of isolated lung mast cells by ELISA, and cross-linkage of IgE receptor (Fc epsilon-RI) on the lung mast cells in culture did not alter SCF mRNA expression, or the secreted soluble SCF protein. This was consistent with the finding that levels of SCF mRNA expression in conjunctival mast cells were similar between normal subjects and patients with seasonal allergic conjunctivitis (SAC). This study shows that human mast cells themselves are a cellular source of SCF, as well as being target cells for this growth factor. SCF may regulate mast cell growth and function via both paracrine and autocrine mechanisms. The production of SCF by mast cells may be regulated via mechanisms other than IgE receptor-mediated pathways.

Cell Culture Techniques↗

PubMed1998

Enhanced cyclooxygenase-1 expression within the superior mesenteric artery of portal hypertensive rats: role in the hyperdynamic circulation.

Portal hypertension (PHT) is characterized by splanchnic hyperemia due to enhanced production of vasodilator substances. Enhanced vasodilation and increased splanchnic blood flow contribute to the elevated portal pressure characteristic of PHT. The aim of this study was to determine whether cyclooxygenase (Cox) expression is altered in PHT vessels and whether chronic inhibition of this enzyme impacts on splanchnic blood flow in PHT. PHT was created in Sprague-Dawley rats by a partial portal vein ligation. Control animals were sham operated. Plasma 6-keto-PGF1alpha (prostaglandin F1alpha) levels were significantly elevated in PHT after 2 days as compared with sham and remained elevated up to day 15. Treatment with indomethacin (2 mg/kg i.p. daily for 15 days) resulted in a significant decrease in 6-keto-PGF1alpha levels, which was concomitant with a significant decrease in superior mesenteric artery blood flow (Qsma) after 15 days in PHT rats. Cox-I expression was differentially enhanced in the PHT superior mesenteric artery and thoracic aorta during the development and progression of PHT. In contrast, Cox-II messenger RNA (mRNA) and protein expression was not detected in either of these vessels throughout the development of PHT. These data suggest that PHT is associated with enhanced Cox-I expression within the splanchnic vasculature concomitant with elevated plasma prostacyclin levels and a significant pressor response to indomethacin in PHT animals. We conclude that enhanced Cox-I expression results in increased prostacyclin levels that partially contribute to the maintenance of the hyperemia typical of PHT.

Animals↗

PubMed1998

Increased expression of endothelin receptors in the vasculature of portal hypertensive rats: role in splanchnic hemodynamics.

Portal hypertension (PHT) is characterized by increased portal pressure caused in part by a reduction in mesenteric vascular resistance. The aim of this study was to evaluate the role of endothelin (ET) and specific ET receptors in maintaining the vasculopathy of PHT. PHT was created in Sprague-Dawley rats by a partial portal vein ligation. Control animals were sham-operated. ET receptor expression was determined in the superior mesenteric artery of sham and PHT rats by in situ autoradiography, radioligand binding analysis, and reverse-transcription polymerase chain reactions (RT-PCR). The pressor response to ET-1 was determined in vitro using isolated vascular rings and in vivo by measuring mean arterial pressure, splanchnic blood flow, and portal venous pressure following treatment with ET and selective ET receptor antagonists. The pressor response to ET in vitro was significantly enhanced in PHT concomitant with increased ET-A and ET-B receptor expression. There was a significant increase in the peak pressor response to ET (10 microg/kg intravenously) in portal hypertensive rats without any significant change in plasma ET-1 levels. There was no significant difference in the peak splanchnic blood flow or portal venous pressure response following ET-A receptor blockade with JKC-301 infusion (200 microg/kg intravenously). In contrast, ET-B receptor blockade with IRL-1038 (200 microg/kg intravenously) preferentially decreased splanchnic blood flow and portal venous pressure in portal hypertensive rats. These data suggest that enhanced ET-B receptor expression in portal hypertensive vessels contributes to the maintenance of elevated portal pressure in these animals.

Animals↗

PubMed1998

RGS3 and RGS4 are GTPase activating proteins in the heart.

RGS family members are regulatory molecules that act as GTPase activating proteins (GAPs) for G alpha subunits of heterotrimeric G proteins. RGS proteins are able to deactivate G protein subunits of the Gi alpha, Go alpha and Gq alpha subtypes when tested in vitro and in vivo. Although the function of RGS proteins in cardiac physiology is unknown, their ability to deactivate Galpha subunits suggests that they may inhibit the action of muscarinic, alpha-adrenergic, endothelin, and other agonists. To evaluate the role of RGS family members in the regulation of cardiac physiology, we investigated the expression pattern of two RGS genes in normal and diseased rat heart tissue. RGS3 and RGS4 mRNAs and proteins were detected in adult myocardium. RGS3 and RGS4 gene expression was markedly enhanced in two model systems of cardiac hypertrophy: growth factor-stimulated cultured neonatal rat cardiomyocytes and pulmonary artery-banded (PAB) mice. RGS3 and RGS4 mRNA levels were reduced in failing myocardium obtained from SHHF/Mcc-fa(cp) (SHHF) rats. These findings support the hypothesis that RGS gene expression is highly regulated in myocardium and imply that RGS family members play an important role in the regulation of cardiac function.

Amino Acid Sequence↗

PubMed1998

Effects of alpha1-adrenergic stimulation on L-type Ca2+ current in rat ventricular myocytes.

The effect of alpha1-adrenergic stimulation on L-type Ca2+ current (ICa,L) in adult rat ventricular myocytes was investigated using three different methods of current recording. During conventional whole-cell recordings with 5 mm-BAPTA included in the pipette solution, phenylephrine (20 microM) did not increase ICa,L after 10 min of application. With nystatin perforated-patch whole-cell recordings, phenylephrine potentiated ICa,L, although there were variations among myocytes. The most frequent response was a transient suppression of peak ICa,L at approximately 2 min of exposure followed by a sustained increase of current amplitude evident after 5-10 min exposure. The relative current amplitude 10 min after phenylephrine application was 1.08+/-0.05 compared to control (n=14 cells,P<0.05). During cell-attached single channel recordings, phenylephrine (1 microM) increased the L-type Ca2+ channel open probability (NPo) by 2.25+/-0.31-fold (n=21,P<0.01). It potentiated NPo by increasing the number of openings per sweep and also by promoting longer openings. These effects developed slowly in approximately 10 min. Phenylephrine had no on unitary current amplitude. The potentiation was also elicited by methoxamine (5 microM) and was blocked by prazosin (1 microM), indicating that it was mediated by alpha1-adrenergic receptor stimulation. The increase in NP(o) was suppressed by chelerythrine, a protein kinase C inhibitor. Our results demonstrate that ICa,L can be enhanced by alpha1-adrenergic stimulation, and stress the importance of not disturbing the intracellular environment during studies of the modulation of cardiac ICa,L by alpha1-adrenergic stimulation.

Adrenergic alpha-Agonists↗

PubMed1998

Bloch-Siegert shift compensated and cyclic irradiation sidebands eliminated, double-adiabatic homonuclear decoupling for 13C- and 15N-double-labeled proteins.

A Gaussian-shaped, offset-independent adiabatic decoupling is adopted to decouple 13CO from 13C alpha or vice versa for 13C- and 15N-double-labeled proteins, together with a compensating decoupling applied on the opposite side of the 13C alpha resonance frequency. In a quite broad range, the double-adiabatic decoupling eliminates efficiently the cyclic sidebands caused by direct irradiation of the adiabatic decoupling and reduces significantly the Bloch-Siegert shift. The remaining Bloch-Siegert shift, which is almost a linear function of offset, can be removed by a dilated evolution time. The decoupling sequence is also quite insensitive to the RF field intensity or inhomogeneity due to the reduced transverse components of RF field at 13C alpha, leading to an efficient decoupling even under unfavorable conditions.

Algorithms↗

PubMed1998

Experimental study on the treatment of diabetes by phloridzin in rats.

Male rats at six weeks of age were divided into 5 groups at random: in group I, the rats with diabetes received 70% pancreatectomy; group II had sham-operation serving as controls; diabetic rats in group III were treated with phloridzin; In group IV rats received sham-operation and phloridzin treatment and group V were phloridzin-treated diabetic rats to be studied after discontinuance of phloridzin. 70 days after surgery, the weights and insulin contents of operated remnant pancreas were markedly higher than the expected value of 30%, reaching 44% (48.2% +/- 15.2%), demonstrating that the remnant pancreas still had capacities of compensatory regeneration and proliferation capacities. Phloridzin-treated diabetic rats completely returned to normal in terms of oral glucose tolerance and insulin sensitivity. Discontinuation of phloridzin treatment in diabetic rats resulted in the recurrence of insulin resistance. These results suggested that normalization of hyperglycemia could ameliorate insulin resistance under diabetic conditions.

Animals↗

PubMed1998

Expression of CDC2Zm and KNOTTED1 during in-vitro axillary shoot meristem proliferation and adventitious shoot meristem formation in maize (Zea mays L.) and barley (Hordeum vulgare L.).

Expression of CDC2Zm and KNOTTED1 (KN1) in maize (Zea mays L.) and their cross-reacting proteins in barley (Hordeum vulgare L.) was studied using immunolocalization during in-vitro axillary shoot meristem proliferation and adventitious shoot meristem formation. Expression of CDC2Zm, a protein involved in cell division, roughly correlated with in-vitro cell proliferation and in the meristematic domes CDC2Zm expression was triggered during in-vitro proliferation. Analysis of the expression of KN1, a protein necessary for maintenance of the shoot meristem, showed that KN1 or KN1-homologue(s) expression was retained in meristematic cells during in-vitro proliferation of axillary shoot meristems. Multiple adventitious shoot meristems appeared to form directly from the KN1- or KN1 homologue(s)-expressing meristematic cells in the invitro proliferating meristematic domes. However, unlike Arabidopsis (Arabidopsis thaliana) and tobacco (Nicotiana tabacum) leaves ectopically expressing KN1 (G. Chuck et al., 1996 Plant Cell 8: 1277-1289; N. Sinha et al., 1993 Genes Dev. 7: 787-797), transgenic maize leaves over-expressing KN1 were unable to initiate adventitious shoot meristems on their surfaces either in planta or in vitro. Therefore, expression of KN1 is not the sole triggering factor responsible for inducing adventitious shoot meristem formation from in-vitro proliferating axillary shoot meristems in maize. Our results show that genes critical to cell division and plant development have utility in defining in-vitro plant morphogenesis at the molecular level and, in combination with transformation technologies, will be powerful tools in identifying the fundamental molecular and-or genetic triggering factor(s) responsible for reprogramming of plant cells during plant morphogenesis in-vitro.

Antibodies↗