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PubMed1983

The pattern of MAP-2 binding on microtubules: visual enhancement of MAP attachment sites by antibody labeling and electron microscopy.

We used affinity-purified rabbit antibody to hog brain microtubule-associated protein 2 (MAP-2) to examine the pattern of attachment of MAPs to microtubules purified by cycles of in vitro assembly and disassembly. Microtubules were fixed, deposited on EM grids, and labeled with antibody and protein A-gold colloid followed by negative staining. We observed that: The sites of MAP attachment were greatly enhanced by antibody binding in negatively stained preparations. The axial repeat revealed by antibody (100 +/- 5 nm) was greater than the previously reported value of 32 nm based on thin sectioning and negative staining procedures. The antibody was arranged in a broad band and revealed a helical pattern of binding. Microtubules with and without treatment with alpha-chymotrypsin to remove the projection portion of MAP-2 looked similar, suggesting that the antibody-enhanced pattern may reflect the sites of MAP attachment on microtubules. Microtubules with an increased MAP:tubulin ratio exhibited the same 100-nm periodicity.

Animals↗
PubMed1991

MAP-1 and MAP-2 binding sites at the C-terminus of beta-tubulin. Studies with synthetic tubulin peptides.

The interaction of microtubule-associated proteins MAP-1 and MAP-2 with different peptides containing sequences covering the C-terminal region of beta-tubulin isoforms has been analyzed. Our results indicate that MAP-1 and MAP-2 bind to a common sequence within the variable C-terminal region of the different beta-tubulin isoforms, while MAP-2 also interacts with the subdomain beta (422-434) of the constant region, in agreement with previous results (Maccioni, R.B., Rivas, C., & Vera, J.C. (1988) EMBO J. 7, 1957-1963). The productive interaction of MAP-2 with the latter domain appears to be involved in the assembly of microtubules.

Amino Acid Sequence↗
PubMed2006

Effect of spatial smoothing on t-maps: arguments for going back from t-maps to masked contrast images.

Voxelwise statistical analysis has become popular in explorative functional brain mapping with fMRI or PET. Usually, results are presented as voxelwise levels of significance (t-maps), and for clusters that survive correction for multiple testing the coordinates of the maximum t-value are reported. Before calculating a voxelwise statistical test, spatial smoothing is required to achieve a reasonable statistical power. Little attention is being given to the fact that smoothing has a nonlinear effect on the voxel variances and thus the local characteristics of a t-map, which becomes most evident after smoothing over different types of tissue. We investigated the related artifacts, for example, white matter peaks whose position depend on the relative variance (variance over contrast) of the surrounding regions, and suggest improving spatial precision with 'masked contrast images': color-codes are attributed to the voxelwise contrast, and significant clusters (e.g., detected with statistical parametric mapping, SPM) are enlarged by including contiguous pixels with a contrast above the mean contrast in the original cluster, provided they satisfy P < 0.05. The potential benefit is demonstrated with simulations and data from a [11C]Carfentanil PET study. We conclude that spatial smoothing may lead to critical, sometimes-counterintuitive artifacts in t-maps, especially in subcortical brain regions. If significant clusters are detected, for example, with SPM, the suggested method is one way to improve spatial precision and may give the investigator a more direct sense of the underlying data. Its simplicity and the fact that no further assumptions are needed make it a useful complement for standard methods of statistical mapping.

Algorithms↗
PubMed1993

A protein factor for ras p21-dependent activation of mitogen-activated protein (MAP) kinase through MAP kinase kinase.

To identify the direct target molecule of ras p21 in higher eukaryotes, we have recently developed the cell-free system in which ras p21 activates mitogen-activated protein (MAP) kinase/extracellular signal-regulated kinase (ERK). In this cell-free system, the guanosine 5'-[gamma-thio]triphosphate- bound form of Ki-ras p21, but not the GDP-bound form, activates endogenous Xenopus MAP kinase as well as recombinant ERK2 in the presence of the cytosol fraction of Xenopus oocytes. We separated two protein factors from the cytosol fraction of Xenopus oocytes by column chromatography: one was the inactive form of MAP kinase kinase and the other was a factor tentatively named ras p21-dependent ERK-kinase stimulator (REKS). The former and latter showed M(r) values of approximately 45,000 and 150,000-200,000, respectively, as estimated by gel filtration. Both factors were necessary for Ki-ras p21-dependent activation of MAP kinase/ERK2. These results indicate that an additional protein factor (REKS) is essential for Ki-ras p21 to activate MAP kinase through MAP kinase kinase.

Animals↗
PubMed1997

Mitogen-activated protein (MAP) kinase regulates production of tumor necrosis factor-alpha and release of arachidonic acid in mast cells. Indications of communication between p38 and p42 MAP kinases.

Aggregation of the high affinity IgE receptor (FcepsilonRI) in a mast cell line resulted in activation of the p42 and the stress-activated p38 mitogen-activated protein (MAP) kinases. Selective inhibition of these respective kinases with PD 098059 and SB 203580 indicated that p42 MAP kinase, but not p38 MAP kinase, contributed to the production of the cytokine, tumor necrosis factor-alpha, and the release of arachidonic acid in these cells. Neither kinase, however, was essential for FcepsilonRI-mediated degranulation or constitutive production of tumor growth factor-beta. Studies with SB 203580 and the p38 MAP kinase activator anisomycin also revealed that p38 MAP kinase negatively regulated activation of p42 MAP kinase and the responses mediated by this kinase.

Animals↗
PubMed1999

p42/44 MAP kinase-dependent and -independent signaling pathways regulate caveolin-1 gene expression. Activation of Ras-MAP kinase and protein kinase a signaling cascades transcriptionally down-regulates caveolin-1 promoter activity.

Caveolin-1 is a principal component of caveolae membranes in vivo. Caveolin-1 mRNA and protein expression are down-regulated in NIH 3T3 cells in response to transformation by activated oncogenes, such as H-Ras(G12V) and v-Abl. The mechanisms governing this down-regulation event remain unknown. Here, we show that caveolin-1 gene expression is directly regulated by activation of the Ras-p42/44 MAP kinase cascade. Down regulation of caveolin-1 protein expression by Ras is independent of (i) the type of activating mutation (G12V versus Q61L) and (ii) the form of activated Ras transfected (H-Ras versus K-Ras versus N-Ras). Treatment of Ras or Raf-transformed NIH 3T3 cells with a well characterized MEK inhibitor (PD 98059) restores caveolin-1 protein expression. In contrast, treatment of v-Src and v-Abl transformed NIH 3T3 cells with PD 98059 does not restore caveolin-1 expression. Thus, there must be at least two pathways for down-regulating caveolin-1 expression: one that is p42/44 MAP kinase-dependent and another that is p42/44 MAP kinase-independent. We focused our efforts on the p42/44 MAP kinase-dependent pathway. The activity of a panel of caveolin-1 promoter constructs was evaluated using transient expression in H-Ras(G12V) transformed NIH 3T3 cells. We show that caveolin-1 promoter activity is up-regulated approximately 5-fold by inhibition of the p42/44 MAP kinase cascade. Using electrophoretic mobility shift assays we provide evidence that the caveolin-1 promoter (from -156 to -561) is differentially bound by transcription factors in normal and H-Ras(G12V)-transformed cells. We also show that activation of protein kinase A (PKA) signaling is sufficient to down-regulate caveolin-1 protein expression and promoter activity. Thus, we have identified two signaling pathways (Ras-p42/44 MAP kinase and PKA) that transcriptionally down-regulate caveolin-1 gene expression.

3T3 Cells↗
PubMed2005

Participation of p38 MAP kinase, but not p44/42 MAP kinase, in stimulation of corneal epithelial migration by substance P and IGF-1.

PURPOSE: Substance P and insulin-like growth factor-1 (IGF-1) synergistically promote corneal epithelial migration both in vitro and in vivo. The mechanism of this action was investigated. METHODS: The effects of various inhibitors and activators of intracellular signaling pathways on corneal epithelial migration were examined by measuring the length of the migration path in rabbit corneal blocks in culture. RESULTS: Inhibitors of signaling by p38 or p44/42 isoforms of mitogen-activated protein (MAP) kinase or of phosphatidylinositol (PI) 3-kinase reduced the extent of spontaneous migration of the corneal epithelium, whereas modulators of signaling by cyclic AMP- or cyclic GMP-dependent protein kinases had no effect. The inhibitors of p38 MAP kinase and of PI 3-kinase also abolished the stimulatory effect of substance P and IGF-1 on epithelial migration, whereas inhibitors of signaling by p44/42 MAP kinase or modulators of cyclic nucleotide-dependent signaling did not. CONCLUSIONS: These results suggest that various signal transduction systems participate in spontaneous corneal epithelial migration as well as in the combined effect of substance P and IGF-1 on this process. In particular, although both p38 and p44/42 isoforms of MAP kinase appear to regulate spontaneous corneal epithelial migration, the stimulatory effect of substance P and IGF-1 appears to be mediated by p38 MAP kinase but not by p44/42 MAP kinase.

Animals↗
PubMed2003

Spatiotemporal characterization of paced cardiac activation with body surface potential mapping and self-organizing maps.

In this study self-organizing maps (SOM) were utilized for spatiotemporal analysis and classification of body surface potential mapping (BSPM) data. Altogether 86 cardiac depolarization (QRS) sequences paced by a catheter in 18 patients were included. Spatial BSPM distributions at every 5 ms over the QRS complex were first presented to an untrained SOM. The learning process of the SOM units organized the maps in such a way that similar BSPMs are represented in particular areas of the SOM network. Thereafter, time trajectories and distance maps were created on the trained SOM from sequential maps in a selected paced QRS. The trajectories and distance maps can be applied as such for the localization of abnormal ventricular activation, as well as quantitative input for statistical classification. The results indicate that the method has potential for locating endocardial sites of abnormal ventricular activation, despite the patient material being too limited to provide a reliable statistical evaluation of the source localization accuracy.

Algorithms↗
PubMed1997

Global electrophysiological mapping of the atrium: computerized three-dimensional mapping system.

The atria are anatomically complex three-dimensional (3-D) structures. Impulse propagation is dynamic and complex during both normal conduction and arrhythmia. Atria activation has traditionally been represented on two-dimensional surface maps, which have inherent inaccuracies and are difficult to interpret. Interactive computerized 3-D display facilitates interpretation of complex atrial activation sequence data obtained from form-fitting multipoint electrodes. Accordingly, the purpose of this article is to describe the application of 3-D form-fitting electrode molds to the 3-D mapping and display system developed in this laboratory for the study of complex cardiac arrhythmias. Computer generated 3-D surface models are created from a database of serial cross-sectional anatomical images. Points chosen on endocardial and epicardial surfaces in each cross-sectional image are processed to create polygons defining myocardial wall boundaries. The polygons from adjacent serial images are then combined, to create a 3-D surface model. The discrete anatomical locations of unit electrodes on multipoint electrode templates are then assigned in the proper position on the surface model. Computer analysis of simultaneous activation data from each unit electrode is performed based on parameters set by the user. Activation data from each unit electrode site are displayed on the computer surface model in a color spectrum correlating with a user-defined time scale. Activation sequence maps can be visualized as static isochrone maps, interval maps, or as dynamic maps at variable speeds, from any 3-D perspective. Thus, an interactive computerized 3-D display system is described, which allows anatomically superior analysis and interpretation of complex atrial arrhythmias.

Arrhythmias, Cardiac↗
PubMed2003

Molecular mapping in tropical maize (Zea mays L.) using microsatellite markers. 1. Map construction and localization of loci showing distorted segregation.

Microsatellites have become the most important class of markers for mapping procedures. Primarily based on restriction fragment length polymorphism (RFLP) markers, several molecular genetic maps of maize have been developed, mainly using temperate inbred maize lines. To characterize the level of polymorphism of microsatellite loci and construct a genetic map in tropical maize, two elite inbred lines, L-08-05F and L-14-4B, were crossed to produce 400 F(2) individuals that were used as a mapping population. A survey of 859 primer pair sequences of microsatellites was used. The polymorphism screens of each microsatellite and genotype assignment were performed using high-resolution agarose gels. About 54 % of the primer sets gave clearly scorable amplification products, 13 % did not amplify and 33 % could not be scored on agarose gels. A total of 213 polymorphic markers were identified and used to genotype the mapping population. Among the polymorphic markers, 40 showed loci deviating from expected Mendelian ratios and clusters of deviating markers were located in three chromosome regions. Non-Mendelian scoring was present in 19 markers. The final genetic map with 117 markers spanned 1634 cM in length with an average interval of 14 cM between adjacent markers.

Genetic Linkage↗
PubMed1993

Mos stimulates MAP kinase in Xenopus oocytes and activates a MAP kinase kinase in vitro.

Several protein kinases, including Mos, maturation-promoting factor (MPF), mitogen-activated protein (MAP) kinase, and MAP kinase kinase (MAPKK), are activated when Xenopus oocytes enter meiosis. De novo synthesis of the Mos protein is required for progesterone-induced meiotic maturation. Recently, bacterially synthesized maltose-binding protein (MBP)-Mos fusion protein was shown to be sufficient to initiate meiosis I and MPF activation in fully grown oocytes in the absence of protein synthesis. Here we show that MAP kinase is rapidly phosphorylated and activated following injection of wild-type, but not kinase-inactive mutant, MBP-Mos into fully grown oocytes. MAP kinase activation by MBP-Mos occurs within 20 min, much more rapidly than in progesterone-treated oocytes. The MBP-Mos fusion protein also activates MPF, but MPF activation does not occur until approximately 2 h after injection. Extracts from oocytes injected with wild-type but not kinase-inactive MBP-Mos contain an activity that can phosphorylate MAP kinase, suggesting that Mos directly or indirectly activates a MAPKK. Furthermore, activated MBP-Mos fusion protein is able to phosphorylate and activate a purified, phosphatase-treated, rabbit muscle MAPKK in vitro. Thus, in oocytes, Mos is an upstream activator of MAP kinase which may function through direct phosphorylation of MAPKK.

Animals↗
PubMed1994

Microtubule-stabilizing activity of microtubule-associated proteins (MAPs) is due to increase in frequency of rescue in dynamic instability: shortening length decreases with binding of MAPs onto microtubules.

The role of microtubule associated proteins (MAPs) on the dynamic instability of microtubules was examined under a dark-field microscope using bovine brain tubulin purified by DEAE-Sepharose column chromatography. In the absence of MAPs, the transition from the shortening phase to the growing phase (the rescue) occurred rarely both in self-assembled microtubules and seeded ones, especially at the plus end. Even under the conditions unfavorable to stabilize microtubule, the addition of a small amount of crude MAPs or purified microtubule associated protein 2 (MAPs) to the microtubules allowed them to undergo the rescue. At increased concentrations of MAPs or MAP2, both the length change required for a rescue during shortening phase ("shortening length") and for a catastrophe (transition from the growing to the shortening phase) ("growth length") decreased. Under these conditions, the rescue often occurred at the same site where previous rescues occurred. Distribution of immunofluorescent MAP2 antibodies along individual microtubules showed that MAP2 molecules bound onto microtubules by forming discrete clusters. The number of MAP2 molecules per cluster was estimated to be between 25 and 60. Because both the "shortening length" and the distance between MAP2 clusters in a microtubule decreased with increased MAPs concentration, we suggest that the MAP2 clusters may form the specific site at which the shortening of the microtubule readily stops. MAP2 possibly regulates the dynamic instability by stopping the shortening, which is a prerequisite for the rescue.

Animals↗
PubMed2000

Detailed comparative gene map of rat chromosome 1 with mouse and human genomes and physical mapping of an evolutionary chromosomal breakpoint.

We report the localization of 92 new gene-based markers assigned to rat chromosome 1 by linkage or radiation hybrid mapping. The markers were chosen to enrich gene mapping data in a region of the rat chromosome known to contain several of the principal quantitative trait loci in rodent models of human multifactorial disease. The composite map reported here provides map information on a total of 139 known genes, including 80 that have been localized in mouse and 109 that have been localized in human, and integrates the gene-based markers with anonymous microsatellites. The evolutionary breakpoints identifying 16 segments that are homologous regions in the human genome are defined. These data will facilitate genetic and comparative mapping studies and identification of novel candidate genes for the quantitative trait loci that have been localized to the region.

Animals↗
PubMed2001

A complete map of the human ribosomal protein genes: assignment of 80 genes to the cytogenetic map and implications for human disorders.

Mapping of the human ribosomal protein (RP) genes has been completed, and all 80 different genes were placed on a cytogenetic map of the human genome. Because of the existence of processed pseudogenes, the localization of the RP genes was complicated, and five genes had remained to be mapped. Here we developed a novel strategy to identify sequence-tagged sites (STSs) at introns of the RP genes, and we localized RPL14, RPL22, RPL35, RPL36, and RPL39 within the chromosomes by radiation hybrid mapping. Unlike the case of eubacteria or archaebacteria, human RP genes are widely scattered about the genome. Together with the previous results, both sex chromosomes and 20 autosomes (all but chromosomes 7 and 21) were found to carry one or more RP genes. To explore the possible involvement of RP genes in human disorders, all 80 genes were assigned to cytogenetic bands according to a published cytogenetic BAC-STS map of the human genome. We compared the assigned positions with candidate regions for Mendelian disorders and found certain genes that might be involved in particular human disorders.

Animals↗
PubMed2005

c-Jun controls the efficiency of MAP kinase signaling by transcriptional repression of MAP kinase phosphatases.

The mammalian JNK signaling pathway regulates the transcriptional response of cells to environmental stress, including UV irradiation. This signaling pathway is composed of a classical MAP kinase cascade; activation results in phosphorylation of the transcription factor substrates c-Jun and ATF2, and leads to changes in gene expression. The defining components of this pathway are conserved in the fission yeast S. pombe, where the genetic studies have shown that the ability of the JNK homolog Spc1 to be activated in response to UV irradiation is dependent on the presence of the transcription factor substrate Atf1. We have used genetic analysis to define the role of c-Jun in activation of the mammalian JNK signaling pathway. Our results show that optimal activation of JNK requires the presence of its transcription factor substrate c-Jun. Mutational analysis shows that the ability of c-Jun to support efficient activation of JNK requires the ability of Jun to bind DNA, suggesting a transcriptional mechanism. Consistent with this, we show that c-Jun represses the expression of several MAP kinase phosphatases. In the absence of c-Jun, the increased expression of MAP kinase phosphatases leads to impaired activation of the ERK, JNK, and p38 MAP kinases after pathway activation. The results show that one function of c-Jun is to regulate the efficiency of signaling by the ERK, p38, and JNK MAP kinases, a function that is likely to affect cellular responses to many different stimuli.

Animals↗
PubMed2005

Preheating accelerates mitogen-activated protein (MAP) kinase inactivation post-heat shock via a heat shock protein 70-mediated increase in phosphorylated MAP kinase phosphatase-1.

Heat shock (HS) activates mitogen-activated protein (MAP) kinases. Although prior exposure to nonlethal HS makes cells refractory to the lethal effect of a subsequent HS, it is unclear whether this also occurs in MAP kinase activation. This study was undertaken to evaluate the effect of a heat pretreatment on MAP kinase activation by a subsequent HS and to elucidate its possible mechanism. Preheating did not make BEAS-2B cells refractory to extracellular signal-regulated protein kinase (ERK) and c-Jun N-terminal kinase (JNK) activation by a second HS but accelerated their inactivation after HS. The rapid inactivation of ERK and JNK was dependent on de novo protein synthesis and associated with the up-regulation of heat shock protein 70 (HSP70). Moreover, the inhibition of phosphatase activity reversed this rapid inactivation. MAP kinase phosphatase-1 (MKP-1) expression was increased by HS, and the presence of its phosphorylated form (p-MKP-1) correlated with the observed rapid ERK and JNK inactivation. Blocking induction of p-MKP-1 with antisense MKP-1 oligonucleotides suppressed the rapid inactivation of ERK and JNK in preheated cells. HSP70 overexpression caused the early phosphorylation of MKP-1. Moreover, MKP-1 phosphorylation and the rapid inactivation of ERK were inhibited by blocking HSP70 induction in preheated cells. In addition, MKP-1 was insolubilized by HS, and HSP70 associated physically with MKP-1, suggesting that a chaperone effect of HSP70 might have caused the early phosphorylation of MKP-1. These results indicate that preheating accelerated MAP kinase inactivation after a second HS and that this is related to a HSP70-mediated increase in p-MKP-1.

Adenoviridae↗
PubMed1994

Mapping of DBR1 and YPK1 suggests a major revision of the genetic map of the left arm of Saccharomyces cerevisiae Chromosome XI.

The Saccharomyces cerevisiae dbr1 mutation has been mapped on the left arm of chromosome XI. XIL is a chromosome arm that was until now rather sparsely populated with accurately mapped markers. On the basis of physical data, the overall order of markers is inverted relative to the existing genetic map of XI. We present tetrad analyses using a variety of markers on XI that indicate that the existing genetic map of XIL should be inverted, at least for the strains in which our mapping was carried out, and probably for other S. cerevisiae strains.

Chromosome Mapping↗
PubMed2004

Integration of the rat recombination and EST maps in the rat genomic sequence and comparative mapping analysis with the mouse genome.

Inbred strains of the laboratory rat are widely used for identifying genetic regions involved in the control of complex quantitative phenotypes of biomedical importance. The draft genomic sequence of the rat now provides essential information for annotating rat quantitative trait locus (QTL) maps. Following the survey of unique rat microsatellite (11,585 including 1648 new markers) and EST (10,067) markers currently available, we have incorporated a selection of 7952 rat EST sequences in an improved version of the integrated linkage-radiation hybrid map of the rat containing 2058 microsatellite markers which provided over 10,000 potential anchor points between rat QTL and the genomic sequence of the rat. A total of 996 genetic positions were resolved (avg. spacing 1.77 cM) in a single large intercross and anchored in the rat genomic sequence (avg. spacing 1.62 Mb). Comparative genome maps between rat and mouse were constructed by successful computational alignment of 6108 mapped rat ESTs in the mouse genome. The integration of rat linkage maps in the draft genomic sequence of the rat and that of other species represents an essential step for translating rat QTL intervals into human chromosomal targets.

Animals↗