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M Yuan

Publications and source records attributed to M Yuan.

At least 19 recordsLinked to original sources
PubMed1999

Proteolytic release and nuclear translocation of Notch-1 are induced by presenilin-1 and impaired by pathogenic presenilin-1 mutations.

The Notch family of proteins consists of transmembrane receptors that play a critical role in the determination of cell fate. Genetic studies in Caenorhabditis elegans suggest that the presenilin proteins, which are associated with familial Alzheimer's disease, regulate Notch signaling. Here we show that proteolytic release of the Notch-1 intracellular domain (NICD), an essential step in the activation of Notch signaling, is markedly reduced in presenilin-1 (PS1)-deficient cells and is restored by PS1 expression. Nuclear translocation of the NICD is also markedly reduced in PS1-deficient cells, resulting in reduced transcriptional activation. Mutations in PS1 that are associated with familial Alzheimer's disease impair the ability of PS1 to induce proteolytic release of the NICD and nuclear translocation of the cleaved protein. These results suggest that PS1 plays a central role in the proteolytic activation of the Notch-1-signaling pathway and that this function is impaired by pathogenic PS1 mutations. Thus, dysregulation of proteolytic function may underlie the mechanism by which presenilin mutations cause Alzheimer's disease.

Alzheimer Disease↗
PubMed1999

Investigation on process parameters involved in preparation of poly-DL-lactide-poly(ethylene glycol) microspheres containing Leptospira Interrogans antigens.

Block copolymer, poly-DL-lactide-poly(ethylene glycol) (PELA) with 11.5% of poly(ethylene glycol) (PEG) content was prepared by bulk ring-opening polymerization using stannous chloride as initiator. PELA microspheres with entrapped Leptospira Interrogans antigens, outer membrane protein (OMP) were elaborated by solvent extraction method based on the formation of multiple w/o/w emulsion, and the resulting microspheres were characterized with respect to particle size, OMP entrapment and morphology characteristics. The purpose of the present study is to perform the optimization of preparative parameters for OMP-loaded PELA micropsheres to control particle size and improve the OMP encapsulation efficiency. Of all the parameters investigated, the polymer concentration of organic phase and the external aqueous phase volume play major roles on particle size, while the organic phase volume, internal aqueous phase volume and the addition of surfactant into the internal aqueous phase display considerable effects on OMP loading efficiency. A small volume of internal aqueous phase and intermediate volumes of organic phase and external aqueous phase were favorable to achieve micropsheres with a size of 1-2 microns and high antigen encapsulation efficiency (70-80%). In vitro OMP release profiles from PELA microspheres consist of a small burst release followed by a gradual release phase. The OMP release rate shows some relations with the porous and water-swollen inner structure of the microspheres matrix. The presence of surfactant in microspheres accelerates OMP release, but the OMP entrapment within microspheres shows limited effects on the release profile.

Antigens, Bacterial↗
PubMed1999

Low-energy collisionally activated decomposition and structural characterization of cyclic heptapeptide microcystins by electrospray ionization mass spectrometry.

Characteristics of electrospray ionization mass spectrometry/collision-induced dissociation (ESIMS/CID) mass spectra of microcystins, cyanobacterial cyclic heptapeptide hepatoxins, were examined. The collision conditions showed remarkable effects on the quality of the CID mass spectra, which were divided into three patterns according to the number of Arg residues. A characteristic cleavage reaction and neutral losses of MeOH, NH3 and guanidine group(s) from the (2S,3S,8S,9S)-3-amino-9-methoxy-2,6,8-trimethyl-10-phenyldeca-4 E,6E-dienoic acid (Adda) and Arg residues were observed in the ESI and ESIMS/CID mass spectra, suggesting the most probable protonation sites in [M + H]+ and [M + 2H]2+ ions of microcystins. Microcystins with no Arg residue showed only [M + H]+ ions with a proton reacting at the methoxyl group in the Adda residue, and the ESIMS/CID/MS data revealed their structures unambiguously. The protonation site in [M + H]+ ions of microcystins with Arg residue(s) was the guanidine group. The [M + 2H]2+ ions of microcystins possessing one Arg residue had one proton on the Arg residue and probably another proton on the Adda residue, while the [M + 2H]2+ ions of microcystins having two Arg residues showed protonation at both Arg residues and the ESIMS/CID/MS data assigned their sequences. Structures of microcystins possessing one Arg residue can be assigned by ESIMS/CID/MS of [M + H]+ ions combined with those of [M + 2H]2+ ions.

Anabaena↗
PubMed1999

Electrospray ionization mass spectrometric analysis of microcystins, cyclic heptapeptide hepatotoxins: modulation of charge states and [M + H]+ to [M + Na]+ ratio.

Electrospray ionization mass spectrometry was used to develop a rapid, sensitive, and accurate method for determination and identification of hepatotoxic microcystins, cyanobacterial cyclic heptapeptides. To optimize the electrospray ionization conditions, factors affecting charge state distribution, such as amino acid components of sample, proton affinity of the additives, and additive concentration, were investigated in detail and a method for controlling charge states was developed to provide molecular-related ions for assignment of molecular weight and reasonably abundant precursor ions for MS/MS analysis. A procedure for identification of microcystins consisting of known amino acids was proposed: for microcystins giving abundant [M + 2H]2+ ions, the addition of nitrogen-containing bases to the aqueous sample solution is effective to obtain an increased intensity of [M + H]+ ions, whereas the addition of Lewis acids containing nitrogen can produce increased abundances of [M + 2H]2+ ions for microcystins giving weak [M + 2H]2+ ions. Microcystins possessing no arginine residue always give sodium adduct ions [M + Na]+ as the base peak, and these are difficult to fragment via low energy collision-induced dissociation to yield structurally informative products; the addition of oxalic acid increases [M + H]+ ion abundances, and these fragment readily.

Acetates↗
PubMed1999

Apoptosis induced by infection of primary brain cultures with diverse human immunodeficiency virus type 1 isolates: evidence for a role of the envelope.

Apoptosis of neurons and astrocytes is induced by human immunodeficiency type 1 (HIV-1) infection in vitro and has been demonstrated in brain tissue from patients with AIDS. We analyzed a panel of diverse HIV-1 primary isolates for the ability to replicate and induce neuronal and astrocyte apoptosis in primary human brain cultures. Apoptosis was induced three- to eightfold by infection with the blood-derived HIV-1 isolates 89.6, SG3, and ADA. In contrast, the brain-derived HIV-1 isolates YU2, JRFL, DS-br, RC-br, and KJ-br did not induce significant levels of apoptosis. The ability of HIV-1 isolates to induce apoptosis was independent of their replication capacity. Studies of recombinant chimeras between the SG3 and YU2 viruses showed that replacement of the YU2 Env with the SG3 Env was sufficient to confer the ability to induce apoptosis to the YU2 virus. Replacement of the Env V3 regions alone largely conferred the phenotypes of the parental clones. The SG3 Env used CXCR4 and CCR3 as coreceptors for virus entry, whereas YU2 used CCR5 and CCR3. The V3 regions of SG3 and YU2 conferred the ability to use CXCR4 and CCR5, respectively. In contrast, the 3' region of Env, particularly the C3V4 region, was required in conjunction with the V3 region for efficient use of CCR3. These results provide evidence that Env is a major determinant of neurodegenerative mechanisms associated with HIV-1 infection in vitro and raise the possibility that blood-derived viruses which emerge during the late stages of disease may affect disease progression in the central nervous system.

Animals↗
PubMed1998

Characterization of mutations in the cystathionine beta-synthase gene in Irish patients with homocystinuria.

We used single-strand conformational polymorphism and nucleotide sequencing to characterize defective cystathionine beta-synthase gene alleles in 18 independent Irish patients with homocystinuria. Six mutations were detected, three of which have been reported previously and three of which were novel. The novel mutations include T302C (L101P), C684G (N228K), and G1063C (A354P). Of the three, only T302C (L101P) was somewhat prevalent, being found in 3 of 37 independent alleles.

Cystathionine beta-Synthase↗
PubMed1998

Seven new microcystins possessing two L-glutamic acid units, isolated from Anabaena sp. strain 186.

Electrospray ionization mass spectrometry has been applied to the structure assignment of seven new microcystins (1-7), obtained from cultured Anabaena sp. strain 186. The seven new microcystins contain the dehydroalanine (Dha) or L-Ser unit instead of the N-methyldehydroalanine unit and the L-Glu and/or its delta-methyl ester [E(OMe)] units at the two variable L-amino acid units, and the structures were assigned as [Dha7]microcystin-E(OMe)E(OMe) (1), [D-Asp3,Dha7]microcystin-E(OMe)E(OMe) (2), [L-Ser7]microcystin-E(OMe)E(OMe) (3), [D-Asp3,L-Ser7]microcystin-E(OMe)E(OMe) (4), [Dha7]microcystin-EE(OMe) (5), [D-Asp3,Dha7]microcystin-EE(OMe) (6), and [L-Ser7]microcystin-EE(OMe) (7). These microcystins are the first examples containing dicarboxylic amino acids at the two variable L-amino acid units in microcystins.

Anabaena↗
PubMed1998

Aging renders the brain vulnerable to amyloid beta-protein neurotoxicity.

The formation of fibrillar deposits of amyloid beta protein (Abeta) in the brain is a pathological hallmark of Alzheimer's disease (AD). A central question is whether Abeta plays a direct role in the neurodegenerative process in AD. The involvement of Abeta in the neurodegenerative process is suggested by the neurotoxicity of the fibrillar form of Abeta in vitro. However, mice transgenic for the Abeta precursor protein that develop amyloid deposits in the brain do not show the degree of neuronal loss or tau phosphorylation found in AD. Here we show that microinjection of plaque-equivalent concentrations of fibrillar, but not soluble, Abeta in the aged rhesus monkey cerebral cortex results in profound neuronal loss, tau phosphorylation and microglial proliferation. Fibrillar Abeta at plaque-equivalent concentrations is not toxic in the young adult rhesus brain. Abeta toxicity in vivo is also highly species-specific; toxicity is greater in aged rhesus monkeys than in aged marmoset monkeys, and is not significant in aged rats. These results suggest that Abeta neurotoxicity in vivo is a pathological response of the aging brain, which is most pronounced in higher order primates. Thus, longevity may contribute to the unique susceptibility of humans to Alzheimer's disease by rendering the brain vulnerable to Abeta neurotoxicity.

Aging↗
PubMed1998

Epidemiological typing of klebsiellae with extended-spectrum beta-lactamases from European intensive care units.

Extended-spectrum beta-lactamases (ESBLs) are an increasing cause of resistance to oxyimino-aminothiazolyl cephalosporins, especially in klebsiellae. In a recent survey we detected ESBLs in 220 (23%) of 966 consecutive klebsiellae from 35 intensive care units (ICUs) in southern and western Europe. The present study examined the extent to which this distribution reflected epidemic strain spread, as against the distribution of ESBL genes into unrelated strains. All 220 ESBL producers were subjected to capsular serotyping and pulsed-field gel DNA electrophoresis (PFGE). Beta-Lactamases were typed for strains isolated on three or more occasions, with the emphasis on SHV enzymes, as these were commoner than TEM variants. Serotyping and PFGE typing defined 85 distinct strains, from 23 of the 35 participating centres. Of 14 centres that contributed five or more ESBL producers, all sent representatives of more than one strain, and two centres sent members of ten or more different strains in contributions of 17-21 ESBL-producing isolates. Nevertheless, epidemic strains-defined as those represented by three or more isolates-accounted for a majority (61%) of the collection. Fifty-two isolates of the same serotype K25 (occasionally acapsular) strain with SHV-4 beta-lactamase were recovered at two French hospitals and one in Belgium. This strain has been found by others in France, and has become particularly widespread. Another single strain was found in two separate Portuguese centres, and many individual hospitals had one or more epidemic strain(s), as well as a scatter of diverse ESBL producers. Major variation in antibiogram and plasmid profile was apparent within strains, with some intra-strain variation in beta-lactamase type. These data imply a fluid situation, with resistance determinants being gained, modified or lost. The endemicity of ESBL producers is disturbing since it limits the potential for control by blocking strain spread, while the diversity within strains is disturbing because it complicates the design of antibiotic policies even during 'single strain' outbreaks.

Anti-Bacterial Agents↗
PubMed1998

Interactions of beta-lactamases with sanfetrinem (GV 104326) compared to those with imipenem and with oral beta-lactams.

Sanfetrinem is a trinem beta-lactam which can be administered orally as a hexatil ester. We examined whether its beta-lactamase interactions resembled those of the available carbapenems, i.e., stable to AmpC and extended-spectrum beta-lactamases but labile to class B and functional group 2f enzymes. The comparator drugs were imipenem, oral cephalosporins, and amoxicillin. MICs were determined for beta-lactamase expression variants, and hydrolysis was examined directly with representative enzymes. Sanfetrinem was a weak inducer of AmpC beta-lactamases below the MIC and had slight lability, with a kcat of 0.00033 s(-1) for the Enterobacter cloacae enzyme. Its MICs for AmpC-derepressed E. cloacae and Citrobacter freundii were 4 to 8 microg/ml, compared with MICs of 0.12 to 2 microg/ml for AmpC-inducible and -basal strains; MICs for AmpC-derepressed Serratia marcescens and Morganella morganii were not raised. Cefixime and cefpodoxime were more labile than sanfetrinem to the E. cloacae AmpC enzyme, and AmpC-derepressed mutants showed much greater resistance; imipenem was more stable and retained full activity against derepressed mutants. Like imipenem, sanfetrinem was stable to TEM-1 and TEM-10 enzymes and retained full activity against isolates and transconjugants with various extended-spectrum TEM and SHV enzymes, whereas these organisms were resistant to cefixime and cefpodoxime. Sanfetrinem, like imipenem and cefixime but unlike cefpodoxime, also retained activity against Proteus vulgaris and Klebsiella oxytoca strains that hyperproduced potent chromosomal class A beta-lactamases. Functional group 2f enzymes, including Sme-1, NMC-A, and an unnamed enzyme from Acinetobacter spp., increased the sanfetrinem MICs by up to 64-fold. These enzymes also compromised the activities of imipenem and amoxicillin but not those of the cephalosporins. The hydrolysis of sanfetrinem was examined with a purified Sme-1 enzyme, and biphasic kinetics were found. Finally, zinc beta-lactamases, including IMP-1 and the L1 enzyme of Stenotrophomonas maltophilia, conferred resistance to sanfetrinem and all other beta-lactams tested, and hydrolysis was confirmed with the IMP-1 enzyme. We conclude that sanfetrinem has beta-lactamase interactions similar to those of the available carbapenems except that it is a weaker inducer of AmpC types, with some tendency to select derepressed mutants, unlike imipenem and meropenem.

Anti-Bacterial Agents↗
PubMed1997

Bases of variation in resistance to beta-lactams in Klebsiella oxytoca isolates hyperproducing K1 beta-lactamase.

Nineteen isolates of Klebsiella oxytoca were examined, representing 18 distinct strains. All were from a 1994 survey of resistance amongst klebsiellae in intensive care units in Europe, and all had reduced susceptibility, or were resistant, to cefuroxime, ceftriaxone and aztreonam, suggesting hyperproduction of the chromosomal K1 beta-lactamase. We sought to confirm this mechanism and to identify why the levels of resistance varied between isolates. Possible reasons for variation were differences in the quantity or subtype of the K1 enzyme or differences in this enzyme's interplay with permeability. Spectrophotometric assays showed that all 19 isolates had K1-like beta-lactamases and that these were present at > or = 15-fold higher levels than in beta-lactam-sensitive K. oxytoca isolates. Fourteen of the 19 isolates had the OXY-2 form of K1 enzyme, while the remaining five had the OXY-1 form, as determined by isoelectric focusing and PCR amplification. Most isolates with the OXY-2 enzyme were more resistant than those with the OXY-1 subtype, but this difference partly reflected enzyme quantity rather than subtype. More generally, and irrespective of enzyme subtype, levels of resistance were broadly related to beta-lactamase specific activity, and the degree of hyperproduction was a major determinant of the level of resistance. Nevertheless, other factors had a role too: several isolates had reduced susceptibility or were resistant to cefoxitin, which is not a substrate for K1 enzyme, and examination of outer membrane protein profiles revealed considerable strain-to-strain diversity in the molecular weight range typical of the major enterobacterial porins (40-48 kDa).

Anti-Bacterial Agents↗
PubMed1997

[Hypoglycemic effects of peroxovanadate complexes on glucose transportor of diabetic rats].

OBJECTIVE: To demonstrate the hypoglycemic effects and translocation of glucose transport (Glut 1 and Glut 4) promoted by peroxovanadate and nicotinic acid complexes (POR) in streptozotozin-induced diabetic rats. METHODS: Peroxovanadate complexes nicotinic acid (POR) was prepared in laboratory. POR and vanadate were administered in drink water. The muscles from diabetic rats were subjected to sucrose density gradient centrifugation to prepare plasma membrane and microsome membrane. Antibodies to COOH-terminal of glucose transportor were used in Western Blot to evaluate the translocation. RESULTS: Peroxovanadate complexes of nicotinic acid (POR) showed marked hypoglycemic effects on STZ-induced diabetic rats. 1mg/kg oral pathway POR could significantly reduce the plasma glucose levels (from 18.95 +/- 2.61mmol/L to 6.36 +/- 2.23mmol/L, t = 12.233, P < 0.01) over four week's treatment, whereas, same dose of single sodium vanadate or nicotinic acid did not have hypoglycemic effects. The net vanadium intake was about 1/90 of single effectively vanadate treatment. When Western blot was used POR increased the translocation of Glut 4 and Glut 1 from intracellular site of plasma membrane. CONCLUSION: Peroxovanadate-nicotinic acid complexes (POR) are the novel vanadyl that markedly reduce plasma glucose in a lower dose comparing to vanadate in STZ-DM rats by oral administration. Translocation of glucose transportor may play a part in hypoglycemic mechanism.

Animals↗
PubMed1997

Effects of peroxovanadate complexes on reducing glycemia in diabetic rats and translocation of glucose transporter.

OBJECTIVE: To demonstrate the hypoglycemic effects and translocation of glucose transporter (Glut 1 and Glut 4) promoted by peroxovanadate and nicotinic acid complexes (nicotinic chelated bitriperoxovanadate, POR; N-O nicotinic chelated peroxovanadate, POV) in streptozotozin-induced diabetic rats. METHODS: Peroxovanadate complexes of nicotinic acid (POR and POV) were prepared and characterized in laboratory. POR, POV and vanadate were administrated in drink water. The muscles from diabetic rats were subjected to prepare plasma membrane and microsome membrane. Antibodies to COOH-terminal of glucose transporter were used in Western Blot to evaluate the translocation. RESULTS: POR and POV showed markedly hypoglycemic effects in streptozotocin (STZ)-induced diabetic rats. POV, which may be a N-oxide compound of peroxovanadate, have high potency of acute effects comparing to carboxylate-complexes of peroxovanadate (POR). In chronic tests, 1 mg/kg oral pathway POR could significantly reduce the plasma glucose levels over four week's treatment, whereas the same dose of single sodium vanadate or nicotinic acid did not have hypoglycemic effects. The net vanadium intake is about 1/90 of single effectively vanadate treatment. The Western Blot showed that POR increased the translocation of Glut 4 and Glut 1 from intracellular site of membrane. CONCLUSIONS: Peroxovanadate-nicotinic acid complexes (POR and POV) are the novel vanadyl that acutely and markedly reduce plasma glucose in a lower dose comparing to vanadate in STZ-DM rats by oral administration. Translocation of glucose transportor may take a part in their hypoglycemic effects.

Animals↗
PubMed1996

Antibiotic resistance and production of extended-spectrum beta-lactamases amongst Klebsiella spp. from intensive care units in Europe.

Consecutive klebsiellae were collected from ICU patients at 35 centres in Western and Southern Europe. Of 966 isolates obtained, 716 were Klebsiella pneumoniae, 248 were Klebsiella oxytoca and two were Klebsiella ozaenae. Most were from Belgium, France, Germany, Holland, Italy, Portugal, Spain, Turkey and a few from Greece and the UK. Production of extended-spectrum beta-lactamases (ESBLs) was inferred in 220 isolates on the basis of synergy between ceftazidime and clavulanate. Putative ESBL producers were received from 23 centres, including 20 of the 27 that contributed more than 10 klebsiellae. Over 88% of putative ESBL producers were resistant to ceftazidime 2 mg/L, ceftriaxone 1 mg/L and aztreonam 1 mg/L, whereas, amongst ESBL-negative isolates, more than 98% of K. pneumoniae and 87% of K. oxytoca were susceptible to these concentrations. Putative ESBL producers wre also more resistant to cefuroxime and cefoxitin than non-producers, but not to biapenem. MIC distributions of ciprofloxacin, piperacillin/tazobactam and aminoglycosides were bimodal for ESBL producers, with some isolates highly sensitive and others very resistant. For example, 70% of putative ESBL producers were susceptible to piperacillin/tazobactam 16 + 4 mg/L, but 30% were resistant, some highly so. Resistance to this combination, and to ciprofloxacin, was clustered in certain centres. Two other groups of cephalosporin-resistant isolates were identified besides ESBL producers, viz. (i) nine isolates, from three centres, with AmpC beta-lactamases and (ii) 20 K. oxytoca, from 15 centres, that hyperproduced K1 enzyme. Examination of the hospitals' own susceptibility data indicated that up to 33% of putative ESBL producers had been reported susceptible to third-generation cephalosporins or monobactams. This is disturbing, since ESBLs have been associated with clinical failure even when only low-level resistance was apparent in vitro.

Ampicillin↗
PubMed1996

[Anti-tumor activity and immune responses induced by human cancer-associated mucin core peptide].

Mucin molecules are displayed on most human cancer cell surface, and are different from that expressed on normal epithelial cells. The molecular structure of mucin core peptide (apomucin) was identified recently. However, the function of apomucin is only poorly understood. To further elucidate the role of apomucin in the modulation of cancers, this study was to investigate the immune responses induced by mucin core peptide in mice. The mucin core peptide was isolated from pancreatic cancer cell line SW1990. When mice immunized with this apomucin (10 micrograms/time x 6) plus DETOX, all mice developed delayed-type hypersensitivity (DTH) after challanged with apomucin or synthetic mucin core peptide MUC-2 or MUC-3, while the mice immunized with only apomucin did not develop DTH. No antibodies were detected by ELISA after immunization. When the splenic cells of vaccinated mice were cocultured with this apomucin (10-50 micrograms/ml) and rhIL-2 (50 U/ml) in vitro, the proliferated lymphocytes showed cytotoxicity against human cancer cells, including colon cancer, gastric cancer, pancreatic cancer and leukemia as measured by Cr-51 release assay. The cytotoxicity could be blocked by antibodies against MUC-2 and MUC-3. These results provide a rational basis for the use of apomucin as a vaccine to stimulate anti-tumor immunity.

Animals↗
PubMed1995

Oxidatively modified very low density lipoprotein enhances monocyte adhesion to endothelial cells.

Very los density lipoprotein (VLDL) was incubated with CuCl2(10 mumol/L) at room temperature for 24 hours. The thiobarbituric acid reactive substance (TBARS) was much higher and the electrophoretic mobility was much faster in VLDL after incubation with CuCl2 than that in VLDL without incubation with CuCl2. It demonstrated that VLDL was oxidatively modified by Cu2+. Endothelial cells were pretreated with normal VLDL (N-VLDL) and oxidatively modified VLDL (O-VLDL) and then the adhesion of monocyte to endothelial cells was assayed. We observed that O-VLDL at all the concentrations used enhanced monocyte adhesion to endothelial cells significantly. The results suggest that oxidative modification of VLDL may play a role in the early stage of atherogenesis by increasing monocyte adhesion to endothelial cells.

Cell Adhesion↗
PubMed1995

Dynamic microtubules under the radial and outer tangential walls of microinjected pea epidermal cells observed by computer reconstruction.

By microinjecting rhodamine-conjugated pig brain tubulin into living pea stem epidermal cells it has been possible to follow cortical microtubules beneath the outer tangential wall (OTW) as they re-orientate from a transverse to a longitudinal alignment. Earlier immunofluorescence studies on fixed material have shown that parallel cortical microtubules circumnavigate the cell forming apparently continuous arrays which are transverse, oblique or longitudinal to the cell's long axis. If the array re-orientates as a whole then microtubules along the radial walls would be expected to share the alignment of those on the tangential walls. There are, however, reports that microtubules beneath the outer tangential wall have a different orientation from microtubules at the radial cell walls, raising important questions about the construction and behaviour of the array. Using computer-rotated stacks of optical sections collected by confocal scanning laser microscopy it has been possible to display the microtubules along radial as well as tangential walls of the same microinjected cells. These observations demonstrate for living epidermal cells that when microtubules are aligned longitudinally at the outer epidermal wall they remain oblique or transverse at the radial walls. The array may not therefore re-orientate as a whole but seems to undergo re-organization on only one cell face. However, despite the differing angles between the OTW and radial walls microtubules still form patterns which at the level of the confocal microscope are continuous from one cell face to another, around the cell.(ABSTRACT TRUNCATED AT 250 WORDS)

Computer Simulation↗