Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Maps”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,099 records · Page 61Linked to original sources
PubMed1995

Analysis of MAP 4 function in living cells using green fluorescent protein (GFP) chimeras.

MAP 4 is a ubiquitous microtubule-associated protein thought to play a role in the polymerization and stability of microtubules in interphase and mitotic cells. We have analyzed the behavior of protein domains of MAP 4 in vivo using chimeras constructed from these polypeptides and the green fluorescent protein (GFP). GFP-MAP 4 localizes to microtubules; this is confirmed by colocalization of GFP-MAP 4 with microtubules that have incorporated microinjected rhodamine-tubulin, and by loss of localized fluorescence after treatment of cells with anti-microtubule agents. Different subdomains of MAP 4 have distinct effects on microtubule organization and dynamics. The entire basic domain of MAP 4 reorganizes microtubules into bundles and stabilizes these arrays against depolymerization with nocodazole. Within the basic domain, the PGGG repeats, which are conserved with MAP 2 and tau, have a weak affinity for microtubules and are dispensable for microtubule binding, whereas the MAP 4-unique PSP region can function independently in binding. The projection domain shows no microtubule localization, but does modulate the association of various binding subdomains with microtubules. The acidic carboxy terminus of MAP 4 strongly affects the microtubule binding characteristics of the other domains, despite constituting less than 6% of the protein. These data show that MAP 4 association with microtubules is modulated by sequences both within and outside the basic domain. Further, our work demonstrates that GFP chimeras will allow an in vivo analysis of the effects of MAPs and their variants on microtubule dynamics in real time.

Animals↗
PubMed1995

Comparison of elevation, curvature, and power descriptors for corneal topographic mapping.

Corneal topography systems sample thousands of surface points and from these data different descriptors are derived to create maps of the cornea. Without visualizing and comparing the maps, it is difficult to appreciate the implications of each descriptor for mapping. We created and compared several maps of an ellipsotoric cornea based on the following surface descriptors: relative elevation, dioptric curvature, and refractive power. Each map presented a different picture of the same cornea. Only elevation maps show true topography but must be calculated relative to an appropriate reference surface to reveal important features. Axial and to a greater degree instantaneous curvature maps bring out optically significant shape asymmetries but misrepresent refractive power away from the apex. Ray tracing maps display optical properties that are not apparent from the elevation or curvature maps, including spherical aberration. Oblique astigmatism can be described using a pair of maps for the sagittal and tangential powers at each surface point. A knowledge of these principles is necessary to interpret color maps of the corneal surface correctly.

Cornea↗
PubMed2003

The properties of (2Fo - Fc) and (Fo - Fc) electron-density maps at medium-to-high resolutions.

This paper reports on the efficacy of (F(o) - F(c)) versus (2F(o) - F(c)) electron-density maps at 3.2 A resolution. Firstly, a study is reported of a simple truncation at 2.3 and 3.2 A of the 1.6 A resolution crystal structure of concanavalin A at room temperature [Emmerich et al. (1994), Acta Cryst. D50, 749-756] with 149 known bound water molecules. Secondly, the concanavalin A 1.6 A resolution model was re-refined but with the data truncated to 3.2 A. In a similar evaluation, these procedures were repeated for the apocrustacyanin A1 cryotemperature 1.4 A resolution model [Cianci et al. (2001), Acta Cryst. D57, 1219-1229]. Maps at 1.4, 2.3 and 3.2 A resolutions were first generated and the structure was then re-refined at 3.2 A and additionally at 2.3 A resolution. The results on concanavalin A show that the number of bound water molecules that are resolved decreases by two thirds from 1.6 to 3.2 A, but that key structural waters, for example at the transition metal and the calcium ion, are still resolved in the (F(o) - F(c)) map but not in the (2F(o) - F(c)) map. For apocrustacyanin A1, the results with these two difference maps were less clear-cut. Two key structural bound waters (w93 and w105) were selected that had been previously identified in beta-crustacyanin [Cianci et al. (2002), Proc. Natl Acad. Sci. USA, 99, 9795-9800] in protein-carotenoid interactions. The behaviour of w93 is similar to that of concanavalin A key waters, but that of w105 is not. These behaviours were therefore explored in finer resolution increments, namely 2.9, 2.7 and 2.5 A. Finally, further tests on "real" data sets for peanut lectin and concanavalin A at medium resolution confirm these map properties, namely that an (F(o) - F(c)) difference electron-density map is more effective than a (2F(o) - F(c)) map in showing bound water structure at lower resolutions ( approximately 3.2 A). This result is important since a growing number of protein crystal structure studies are concerned with multi-macromolecular complexes and are at such resolutions. Details of the bound solvent can still be revealed at 3.2 A via the (F(o) - F(c)) map calculation. The physical basis of the limitation of the (2F(o) - F(c)) map presumably lies in the series-termination error effect on such a map involving the first negative ripple from the protein atom to which a bound water oxygen is hydrogen bonded, sufficiently cancelling its peak. In addition, re-refinements at 3.2 A show distances that can agree with known values but B values that do not agree with known values.

Arachis↗
PubMed1993

Ammonium injection induces an N-methyl-D-aspartate receptor-mediated proteolysis of the microtubule-associated protein MAP-2.

We have shown previously that chronic hyperammonemia increases, in brain, the polymerization of microtubules that is regulated mainly by the level and state of phosphorylation of microtubule-associated protein 2 (MAP-2). Activation of the N-methyl-D-aspartate (NMDA) receptor dephosphorylates MAP-2. Because we have found that acute ammonia toxicity is mediated by the NMDA receptor, we have tested the effect of high ammonia levels on MAP-2 in brain. Microtubules isolated from rats injected intraperitoneally with 6 mmol/kg ammonium acetate showed a marked decrease of MAP-2. Also, the amount of MAP-2 in brain homogenates, determined by immunoblotting, was markedly reduced, presumably by proteolysis. The content of MAP-2 was decreased by approximately 75% 1-2 h after ammonium injection and returned to normal values after 4 h. Proteolysis of MAP-2 was prevented completely by injection of 2 mg/kg MK-801, a specific antagonist of the NMDA receptor, suggesting that proteolysis is mediated by activation of this receptor. L-Carnitine, which protects rats against ammonia toxicity, also prevented MAP-2 degradation. Because activation of the NMDA receptor increases [Ca2+]i, we determined whether rat brain contains a Ca(2+)-dependent protease that selectively degrades MAP-2. We show that there is a cytosolic Ca(2+)-dependent protease that degrades MAP-2, but not other brain proteins. The protease has been identified tentatively as calpain I, for it is inhibited by a specific inhibitor of this protease. Our results suggest that ammonium injection activates the NMDA receptor, leading to an increase in [Ca2+]i, which activates calpain I. This, in turn, selectively degrades MAP-2.(ABSTRACT TRUNCATED AT 250 WORDS)

Ammonia↗
PubMed1986

The binding of MAP-2 and tau on brain microtubules in vitro: implications for microtubule structure.

We have presented data that indicate that MAP-2 associates with brain microtubules at nonrandomly distributed sites, whose distribution on the microtubule polymer can best be described by the 12-dimer MAP superlattice originally described by Amos; because of the additional spacings, however, between MAP-2 projections observed on MAP-2-saturated microtubules, we suggest that the 6-dimer MAP superlattice, or what we will call the double Amos superlattice, more completely specifies the total set of MAP-binding sites on cytoplasmic microtubules. Second, we have shown that brain microtubules reassembled in vitro contain a heterogeneous population of MAP-binding sites, which differ in their affinities for the two MAPs, MAP-2 and tau. Third, we have shown that microtubule populations that differ in their MAP content have subtle, but detectable differences in their tubulin isotype composition. Based on all the data presented here, we have presented the idea of a nonrandom distribution of tubulin isotypes within a microtubule as a means by which a cell could specify both the identity and the distribution of MAP-binding sites.

Animals↗
PubMed1994

Hormonal regulation of MAP kinase in cultured rat inner medullary collecting tubule cells.

Mitogen-activated protein (MAP) kinase is a widely expressed protein serine/threonine kinase that serves as a convergence point for many signaling pathways including receptor tyrosine kinases, G protein-coupled receptors, and protein kinase C (PKC). The hormonal regulation of MAP kinase was studied in cultured established rat inner medullary collecting tubule (RIMCT) cells. Neither vasopressin nor beta-adrenergic agonists stimulated MAP kinase, despite clear stimulation of adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase. In contrast, carbachol, ATP, and epidermal growth factor (EGF), which are known to antagonize vasopressin action in the RIMCT, stimulated the MAP kinase pathway. This stimulation was mimicked by the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate, which directly activates PKC. The potency with which EGF and carbachol activated MAP kinase was similar to the potency with which they inhibited vasopressin-stimulated cAMP accumulation. To assess the role of Gi proteins in these stimulatory events, RIMCT cells were pretreated with pertussis toxin to inhibit Gi-mediated signaling. Pertussis toxin did not influence ATP- or EGF-stimulated MAP kinase, but completely inhibited carbachol stimulation, suggesting that Gi proteins mediate muscarinic stimulation. Prolonged exposure of RIMCT cells to high phorbol ester concentrations to downregulate PKC ablated carbachol- and ATP-stimulated MAP kinase, but not EGF-stimulated MAP kinase, suggesting that PKC is a component of the network involved in MAP kinase activation by purinergic and muscarinic agonists. Investigation of the sidedness of the hormonal stimulations indicated that EGF-stimulated MAP kinase was highly polarized, occurring exclusively from the basolateral surface, whereas carbachol stimulated MAP kinase similarly from either cell surfaces.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Identification of the ventricular tachycardia isthmus after infarction by pace mapping.

BACKGROUND: Ventricular tachycardia (VT) isthmuses can be defined by fixed or functional block. During sinus rhythm, pace mapping near the exit of an isthmus should produce a QRS similar to that of VT. Pace mapping at sites proximal to the exit may produce a similar QRS with a longer stimulus-to-QRS interval (S-QRS). The aim of the study was to determine whether a VT isthmus could be identified and followed by pace mapping. METHODS AND RESULTS: Left ventricular pace mapping during sinus rhythm was performed at 819 sites in 11 patients with VT late after infarction, and corresponding CARTO maps were reconstructed. An isthmus site was defined by entrainment and/or VT termination by ablation. Pace-mapping data were analyzed from the identified isthmus site and from sites at progressively increasing distances from this initial isthmus site. Sites where pace mapping produced the same QRS with different S-QRS delays were identified to attempt to trace the course of the isthmus. In 11 patients, 13 confluent low-voltage infarct regions were present. In all these regions, parts of VT isthmuses were identified by pace mapping. In 11 of 13 of the identified isthmus parts, the QRS morphology of the pace map matched a VT QRS. In 10 of 11 patients, radiofrequency ablation rendered clinical VTs noninducible. Successful ablation sites were localized within an isthmus identified by pace mapping in all of these 10 patients. CONCLUSIONS: VT isthmuses can be identified and part of their course delineated by pace mapping during sinus rhythm. This method could help target isthmus sites for ablation during stable sinus rhythm.

Aged↗
PubMed1975

Precordial ST-segment mapping 1. Clinical studies in the coronary care unit.

Precordial ST-segment mapping Was applied serially in the coronary care unit for the study of 46 patients with myocardial infarction (MI), using a 49-lead system. Data from the maps were compared with clinical status of patients, conventional ECGs obtained simultaneously, and serum enzyme levels. Stability of the maps over a one hour period was noted in the early phase of admission. However, a drop of 32% of the sum of ST-segment elevations (+sigma ST) was detected in eight patients with uncomplicated anterior MI over the first 24 hours after admission. Extension of infarction was associated with abrupt rise of + sigma ST, and was diagnosed in two cases from maps in the presence of unchanged standard ECGs. The course of ST elevations was followed more accurately by the map than the standard ECG in eight patients. Pericarditis invalidated the technique completely, due to persistent + sigma ST. The standard ECG was superior to the map in following patients with inferior MI. A case of true posterior MI was more accurately delineated by maps of the posterior thorax than by the standard ECG. Intraventricular conduction defects and pacemaking interfered with maps. Early repolarization produced stable maps; however, mapping showed no advantages over the standard ECG. Preinfarction angina can probably be followed by serial mapping of ST-segment depression.

Adult↗
PubMed1989

Diagnostic value of QRST isointegral maps in detecting myocardial infarction complicated by bundle branch block.

The clinical usefulness of QRST isointegral maps (IQRST map) for detecting myocardial infarction that was complicated by intraventricular conduction disturbances was evaluated in patients with right bundle branch block (group RBBB, 64 patients) and left bundle branch block (group LBBB, 40 patients) by comparison with the normal mean IQRST map derived from 50 normal subjects. Myocardial infarction complicated the conduction disturbances in 24 of the 64 RBBB and in 18 of the 40 LBBB patients. A correlation coefficient was used for assessing the similarity of each map pattern with the normal mean IQRST map. The difference map was made by subtracting the average normal IQRST map from each abnormal IQRST map, and those differences that were less than 2 SD from the mean were retained as a significant area. The number of leads and their sum of differences were used to represent the size of the difference map. Correlation coefficients were significantly (p less than 0.001) smaller in patients with bundle branch block complicated by myocardial infarction than in patients with conduction disturbances not complicated by myocardial infarction. A significant area emerged in the difference map in all patients with myocardial infarction complicated by conduction disturbances. The emergence of a significant area revealed high diagnostic accuracy for detecting myocardial infarction in group RBBB (89.1%). The size of a significant area in a difference map was significantly larger in cases with complicated myocardial infarction than in cases with uncomplicated myocardial infarction in either group RBBB or group LBBB (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1998

MAP kinase activity increases during mitosis in early sea urchin embryos.

A MBP kinase activity increases at mitosis during the first two embryonic cell cycles of the sea urchin embryo. The activity profile of the MBP kinase is the same both in whole cell extracts and after immunoprecipitation with an anti-MAP kinase antibody (2199). An in-gel assay of MBP activity also shows the same activity profile. The activity is associated with the 44 kDa protein that cross-reacts with anti-MAP kinase antibodies. The 44 kDa protein shows cross-reactivity to anti-phosphotyrosine and MAP kinase-directed anti-phosphotyrosine/phosphothreonine antibodies at the times that MBP kinase activity is high. The 2199 antibody co-precipitates some histone H1 kinase activity, but the MBP kinase activity cannot be accounted for by histone H1 kinase-dependent phosphorylation of MBP. The MAP kinase 2199 antibody was used to purify the MBP kinase activity. Peptide sequencing after partial digestion shows the protein to be homologous to MAP kinases from other species. These data demonstrate that MAP kinase activation during nuclear division is not confined to meiosis, but also occurs during mitotic cell cycles. MAP kinase activity in immunoprecipitates also increases immediately after fertilization, which in the sea urchin egg occurs at interphase of the cell cycle. Treating unfertilized eggs with the calcium ionophore A23187 stimulates the increase in MAP kinase activity, demonstrating that a calcium signal can activate MAP kinase and suggesting that the activation of MAP kinase at fertilization is due to the fertilization-induced increase in cytoplasmic free calcium concentration. This signalling pathway must differ from the pathway responsible for calcium-induced inactivation of MAP kinase activity that is found in eggs that are fertilized in meiotic metaphase.

Amino Acid Sequence↗
PubMed2001

Intracellular glutathione regulates tumour necrosis factor-alpha-induced p38 MAP kinase activation and RANTES production by human bronchial epithelial cells.

BACKGROUND: RANTES plays an important role in the production of allergic inflammation of the airway through its chemotactic activity for eosinophils. The cellular reduction and oxidation (redox) changes are involved in the activation of p38 mitogen-activated protein (MAP) kinase and the induction of cytokine expression. It has previously been shown that tumour necrosis factor (TNF)-MA activates p38 mitogen-activated protein (MAP) kinase to produce cytokine, including RANTES, that N-acetylcysteine (NAC) attenuates cytokine production by human bronchial epithelial cells (BECs), and that sensitivity to TNFalpha is inversely correlated with cellular redox state. However, a role of cellular redox regulated by intracellular glutathione (GSH) in TNFalpha-induced p38 MAP kinase activation and p38 MAP kinase-mediated RANTES production by human BECs has not been determined. OBJECTIVE: Human BECs were exposed to NAC or buthionine sulfoximine (BSO). TNFalpha-induced p38 MAP kinase activation and p38 MAP kinase-mediated RANTES production by human BECs were then examined in order to clarify these issues. RESULTS: The results showed that: NAC attenuated TNFalpha-induced p38 MAP kinase activation and RANTES production; SB 203580 as the specific inhibitor of p38 MAP kinase activity attenuated TNF-alpha-induced RANTES production; BSO facilitated TNF-alpha-induced p38 MAP kinase activation and RANTES production; SB 203580 attenuated BSO-mediated facilitation of TNF-alpha-induced RANTES production; and the intracellular GSH increased in NAC-treated cells, whereas the intracellular GSH was reduced in BSO-treated cells. CONCLUSIONS: These results indicate that cellular redox regulated by GSH is critical for TNF-alpha-induced p38 MAP kinase activation and p38 MAP kinase-mediated RANTES production by human BECs.

Acetylcysteine↗
PubMed2003

[Research progress in forest tree genetic linkage map construction and its future prospects].

The research progress in genetic linkage map construction of forest tree species both at home and abroad were reviewed in the paper. Two main problems involved in the field were discussed. One was the limitation of the number of individuals of mapping populations and the other was the random markers mostly employed by the majority of studies. These problems have resulted in crossing combination specificity in the constructed maps and the QTLs located on the basis of the maps. As a result,the QTLs discovered up to now have low credibility and poor practicability in marker-assisted selection. Therefore considering the biological characteristics of forest tree species,the selection of the most suitable genetic markers is crucial to obtain a high quality genetic linkage map, and it is both important and necessary to carry out comparative genetic mapping. Progress in the ongoing expressed sequence tag (EST) sequencing projects were summarized and EST polymorphism (ESTP), the most informative and highly conservative marker with known function,as well as the main ESTP detection techniques were elaborated. It was pointed out that ESTP markers should be integrated into the present studies of genetic linkage map construction, QTL mapping and genome comparative mapping. Finally the future prospects in the fields of genetic linkage map and QTL mapping were discussed. In China, such studies around Populus, especially in the local Populus species should make a breakthrough in the related fields.

English Abstract↗
PubMed1985

[Ventricular activation sequence estimated by body surface isochrone map].

This study was performed to evaluate the usefulness of the body surface isochrone map (VAT map) for identifying the ventricular activation sequence, and it was correlated with the isopotential map. Subjects consisted of 42 normal healthy adults, 18 patients with artificial ventricular pacemakers, and 100 patients with ventricular premature beats (VPB). The sites of pacemaker implantations were the right ventricular endocardial apex (nine cases), right ventricular epicardial apex (five cases), right ventricular inflow tract (one case), left ventricular epicardial apex (one case), and posterior base of the left ventricle via the coronary sinus (two cases). An isopotential map was recorded by the mapper HPM-6500 (Chunichi-Denshi Co.) on the basis of an 87 unipolar lead ECG, and a VAT isochrone map was drawn by a minicomputer. The normal VAT map was classified by type according to alignment of isochrone lines, and their frequency was 57.1% for type A, 16.7% for type B, and 26.2% for type C. In the VAT map of ventricular pacing, the body surface area of initial isochrone lines represented well the sites of pacemaker stimuli. In the VAT map of VPB, the sites of origin of VPB agreed well with those as determined by the previous study using an isopotential map. The density of the isochrone lines suggested the mode of conduction via the specialized conduction system or ventricular muscle. The VAT map is a very useful diagnostic method to predict the ventricular activation sequence more directly in a single sheet of the map.

Bundle-Branch Block↗
PubMed1994

[Computer technology of the genogeographic study of the gene pool. I. Statistical information from the genogeographic map].

General statistical information that can be derived from an electronic map and listed in its legend is reviewed. Certain map information (extrema, mean and variance of mapped values, the number of initial and mapped values, their statistical distributions) can be used in analysis not only of gene pool, but also of phene pool maps. Another portion of map information, on total gene diversity, heterozygosity, and interpopulation differentiation, is important for consequent detailed analysis of a gene pool. Statistical information that is derived from a genogeographic map aids understanding of the content of a map and is used in comparative quantitative analysis of different regions and various mapped parameters. The possibilities for interpretation of statistical information of genogeographic maps are shown using the human gene pool as an example. Maps of frequencies of ABO-O and Rh-d blood group genes in three hierarchically subordinate gene pools of native inhabitants of Belarus, the Black Sea-Baltic region, and northeast Eurasia are presented for this purpose.

Computer Simulation↗
PubMed1994

elk-1 proteins interact with MAP kinases.

Mitogen activated protein kinases (MAP) or extracellular signal regulated protein kinases (ERK) are a family of protein serine/threonine kinases that are activated very rapidly in response to many extracellular stimuli. elk-1, an ets related gene codes for two transcriptional factors elk-1, which regulates c-fos transcription and delta elk-1, both of which are substrates for MAP kinases. A part of the C-terminal transcriptional activation domain (ETA-2) which is common to both the proteins was previously shown to function as an activator of MAP kinases. In this report, in an attempt to investigate the mechanism of activation of MAP kinases, purified preparations of recombinant elk-1 and P44mpk/ERK-1/ERK-2 proteins were used to show the association of elk-1 proteins with MAP kinases. The specific interactions of elk-1 proteins with MAP kinases were confirmed by co-immunoprecipitation studies. Thus elk-1 proteins appear to regulate the activity of MAP kinases by interacting with them ensuring a conformational change and stimulating their autophosphorylation and activation property. The activation was dependent on the presence of ATP and Mg2+. In vitro phosphorylation of elk-1 protein was not regulatory for autonomous DNA binding activity of elk-1 protein. Cells which were exposed to EGF showed a rapid stimulation of an elk-1 specific kinase activity, probably MAP kinase which phosphorylated MBP and was found to be associated with immobilized GST-elk-1. Furthermore, dephosphorylation studies indicate that elk-1 proteins can activate only tyrosine phosphorylated MAP kinase. These results demonstrate the presence of an alternative pathway/mechanism (other than MAP kinase kinase, MAPKK/Mek) for the activation of MAP kinases with tyrosine phosphorylation occurring before serine/threonine autophosphorylation and activation by elk-1 proteins.

3T3 Cells↗
PubMed1993

[Quantitative assessment of improvement in perfusion after coronary bypass grafting: assessed by thallium-201 bull's eye subtraction polar map method].

To assess redistribution (RD) and improvement in regional perfusion after coronary bypass grafting (CABG) on thallium-201 SPECT images quantitatively, the Bull's eye subtraction polar (BS) map was created. BS map was created after subtraction of a normalized bull's eye polar map from another normalized polar map. The quantitative assessment on this map was compared to the visual qualitative analysis in 23 patients (115 segments) who received CABG. All of the improved segments after CABG showed > or = 15% on the BS map. On the other hand, 60% of the non improved segments showed < 10% on the BS map. Furthermore, 67% of the RD segments showing > or = 15% on the BS map before CABG improved in perfusion by > or = 15% on the BS map after CABG. On the BS map, an excellent correlation was observed between the extent of redistribution before CABG and the extent of improvement after CABG. Thus, BS map permits quantitative assessment of improvement in perfusion on T1 SPECT imaging, and this technique seems to be valuable for predicting improvement in perfusion after CABG.

Adult↗
PubMed1997

Protein phosphatases control MAP kinase activation and microtubule organization during rat oocyte maturation.

Mitogen-activated protein kinase (MAP) is involved in many signal transduction pathways and is activated during meiotic maturation in various species. In this study, we used the rat oocyte to identify some of the control mechanisms involved in MAP kinase activation which is triggered at resumption of meiosis. We examined the respective contribution of this kinase and maturation promoting factor (MPF), or cdc2 kinase, in the regulation of microtubule behavior and in the reorganization of chromatin during meiotic maturation. We found that the resumption of meiotic division in rat oocytes coincided with the activation of MPF and was followed 3 h later by the activation of MAP kinase. The activation of the two kinases also occurred in oocytes undergoing maturation in the presence of the protein phosphatase inhibitor okadaic acid (OA). However, the activation of cdc2 kinase was only partial, whereas activation of MAP kinase was accelerated and began 1 h after the resumption of meiosis, i.e. 2 h earlier than in control oocytes. We also showed that protein synthesis was required to activate MAP kinase, but not cdc2 kinase. However, once MAP kinase was activated, ongoing protein synthesis was not necessary to maintain its activity. These results suggest that a negative regulation of MAP kinase slows down its activation at the resumption of meiosis, mediated through the level of phosphatase activity. Moreover, MAP kinase activation requires protein synthesis, even upon phosphatase inactivation by OA, suggesting also the existence of a positive control pathway. We observed that during the first meiotic M-phase, the spindle did not form immediately after cdc2 kinase activation, but that its formation coincided with the appearance of MAP kinase activity. However, earlier activation of MAP kinase by treatment with OA did not lead to premature spindle formation, but instead a large aster formed consisting of long microtubules radiating from the condensed chromatin. In OA-treated oocytes, spindles did not form and an interphase network of microtubule developed with time. Thus, MAP kinase is unable to substitute for MPF under these conditions, its activity alone being insufficient to maintain the progression through meiotic maturation.

Animals↗
PubMed2000

Cross-referencing radiation hybrid data to the recombination map: lessons from mouse chromosome 18.

We are building a framework map of known-order anchor markers between the mouse T31 radiation hybrid (RH) panel and the recombination map based on The Jackson Laboratory (TJL) interspecific backcross panels using the established genetic order to evaluate and strengthen the RH results. In making this map comparison, we have elucidated several problems inherent in RH mapping and minimized these by careful attention to data gathering and interpretation methods. We describe lessons and pitfalls of developing radiation hybrid maps, using the example of mouse Chromosome 18, for which we have built a framework map of microsatellite anchor loci spanning the entire chromosome at significant LOD with no gaps. Sixty-five D18Mit- simple sequence length polymorphism (SSLP) markers form a continuous linkage along the T31 RH Chromosome 18 (RH map length 1598 cR, genetic length 41 cM) with all LODs greater than 6. These markers are also placed on TJL interspecific backcrosses, and the order of the markers in the two systems is in complete agreement. We are continuing to cross-reference the RH data to TJL backcross data for the other mouse chromosomes to improve further the power of RH mapping and to integrate more precisely the extensive existing recombination mapping data for the mouse with the incoming radiation hybrid map data.

Alleles↗