David Ottoson (1918-2001)

View larger version (86K): [in this window] [in a new window]   David Ottoson. Photograph © IBRO.   A master in our field of sensory physiology has passed awayafter a short, but painful illness. He left his wife Inger anddaughter Gabrielle Ahlberg. David Ottoson was born and spent his childhood in Chalgan, China,where his parents were missionaries. David first studied odontology,then medicine, and started his scientific career in 1952 asa research assistant at the Department of Physiology at KarolinskaInstitutet, Stockholm. His thesis `Analysis of the electrical     

Jacques Le Magnen (1916-2002)

View larger version (162K): [in this window] [in a new window]   Jacques Le Magnen with his wife Régine on July 14, 1976, the eve of ISOT VI, which he organized at Gif-sur-Yvette.   One of the pioneers in research on olfaction and taste, andon the regulation of water and food intake left us on Thursday,May 23, 2002, at the age of 85. Jacques Le Magnen was a discipleof the famous French physiologist Henri Piéron at theCollège de France, and from 1949 till 1989 developedhis own laboratory of sensory     

Rhythmic and Light-Inducible Appearance of Clock-Associated Pseudo-Response Regulator Protein PRR9 through Programmed Degradation in the Dark in Arabidopsis thaliana

The above article was published in Plant and Cell Physiology48(11): 1644–1651. Figure 1 was shown incorrectly online. The figure legend inFigure 1C was missing. The correct figure is given below. View larger version (26K):   Fig. 1 Construction     

Editorial

The first 150 words of the full text of this article appear below. THE RICH DIVERSITY OF GENOMICS—A REPORT ON THE ‘COMPARATIVE AND FUNCTIONAL GENOMICS (BITS) WORKSHOP’, HINXTON, UK, 27–30 OCTOBER 2005 The Comparative and Functional Genomics (BITS) Workshop hasa history that in many ways reflects the changing face of moderngenomics. Started 15 years ago under the banner of ‘Identificationof the Transcribed Sequence’, the meeting was designedto bring together leading researchers from around the worldwho were pioneering new global approaches to gene discoveryin a small workshop setting. As more and more transcribed sequencesbecame known, the emphasis of the meeting, like the communityit served, focused on how to characterize the function of allthe newly acquired genes. A decision was therefore made to changeits name to ‘Beyond the Identification of the TranscribedSequence Workshop’, or BITS for short. As the years havepassed the meeting has continued to diversify and change (ashas its name), but it has continued to attract scientists tothe cutting edge of genomics research. At this year's meeting,hosted . . . [Full Text of this Article]     

Expression, localization, and functional evaluation of CFTR in bovine corneal endothelial cells

HCO-dependentfluid secretion by the corneal endothelium controls corneal hydrationand maintains corneal transparency. Recently, it has been shown thatmRNA for the cystic fibrosis transmembrane conductance regulator (CFTR) is expressed in the corneal endothelium; however, protein expression, functional localization, and a possible role in HCO transport have not been reported. Immunoblotting for CFTR showed asingle band at ~170 kDa for both freshly isolated and primary cultures of bovine corneal endothelial cells. Indirectimmunofluorescence confocal microscopy indicated that CFTR locates tothe apical membrane. Relative changes in apical and basolateralchloride permeability were estimated by measuring the rate offluorescence quenching of the halide-sensitive indicator6-methoxy-N-ethylquinolinium iodide during Clinflux in the absence and presence of forskolin (FSK). Apical andbasolateral Cl permeability increased 10- and 3-fold,respectively, in the presence of 50 µM FSK. FSK-activated apicalchloride permeability was unaffected by H₂DIDs (250 µM);however, 5-nitro-2-(3-phenylpropyl-amino)benzoic acid (NPPB; 50 µM) and glibenclamide (100 µM) inhibited activated Clfluxes by 45% and 30%, respectively. FSK-activated basolateral Cl permeability was insensitive to NPPB, glibenclamide,or furosemide but was inhibited 80% by H₂DIDS.HCO permeability was estimated by measuring changesin intracellular pH in response to quickly lowering bath[HCO]. FSK (50 µM) increased apicalHCO permeability by twofold, which was inhibited42% by NPPB and 65% by glibenclamide. BasolateralHCO permeability was unaffected by FSK. Genistein(50 µM) significantly increased apical HCO andCl permeability by 1.8- and 16-fold, respectively. When50 µM genistein was combined with 50 µM FSK, there was no furtherincrease in Cl permeability; however,HCO permeability was reduced to the control level.In summary, we conclude that CFTR is present in the apical membrane ofbovine corneal endothelium and could contribute to transendothelialCl and HCO transport. Furthermore,there is a cAMP-activated Cl pathway on the basolateralmembrane that is not CFTR.

     

Timolol may inhibit aqueous humor secretion by cAMP-independent action on ciliary epithelial cells

The -adrenergic antagonisttimolol reduces ciliary epithelial secretion in glaucomatous patients.Whether inhibition is mediated by reducing cAMP is unknown. Elementalcomposition of rabbit ciliary epithelium was studied by electron probeX-ray microanalysis. Volume of cultured bovine pigmented ciliaryepithelial (PE) cells was measured by electronic cell sizing;Ca²⁺ activity and pH were monitored with fura 2 and2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein, respectively. Timolol (10 µM) produced similar K and Cl losses fromciliary epithelia in HCO/CO₂ solutionbut had no effect in HCO/CO₂-free solution or in HCO/CO₂ solutioncontaining the carbonic anhydrase inhibitor acetazolamide. Inhibitionof Na⁺/H⁺ exchange by dimethylamiloride inHCO/CO₂ solution reduced Cl and Kcomparably to timolol. cAMP did not reverse timolol's effects. Timolol(100 nM, 10 µM) and levobunolol (10 µM) produced cAMP-independentinhibition of the regulatory volume increase (RVI) in PE cells andincreased intracellular Ca²⁺ and pH. IncreasingCa²⁺ with ionomycin also blocked the RVI. The resultsdocument a previously unrecognized cAMP-independent transport effect oftimolol. Inhibition of Cl/HCO exchangemay mediate timolol's inhibition of aqueous humor formation.

     

Flow-induced calcium oscillations in rat osteoblasts are age, loading frequency, and shear stress dependent

Bone adaptation tomechanical loading is dependent on age and the frequency and magnitudeof loading. It is believed that load-induced fluid flow in the porousspaces of bone is an important signal that influences bone cellmetabolism and bone adaptation. We used fluid flow-induced shear stressas a mechanical stimulus to study intracellular calcium(Ca) signaling in rat osteoblastic cells (ROB)isolated from young, mature, and old animals. Fluid flow producedhigher magnitude and more abundant [Ca²⁺]_ioscillations than spontaneous oscillations, suggesting that flow-induced Ca signaling encodes a differentcellular message than spontaneous oscillations. ROB from old ratsshowed less basal [Ca²⁺]_i activity and wereless responsive to fluid flow. Cells were more responsive to 0.2 Hzthan to 1 or 2 Hz and to 2 Pa than to 1 Pa. These data suggest that thefrequency and magnitude of mechanical loading may be encoded by thepercentage of cells displaying [Ca²⁺]_ioscillations but that the ability to transduce this information may bealtered with age.

     

Society for Molecular Biology and Evolution (SMBE) Council and Business Meetings, 2004 State College, Pennsylvania, USA

Council Meeting

1. Call to order.—President John Avise called the meetingto order at 9:00 AM, 17 June 2004. In attendance were PresidentJohn Avise, Treasurer Marta L. Wayne, Editorial Advisory Boardmember Stanley A. Sawyer, Editor William Martin, Past- PresidentNaoyuki Takahata, Secretary Sudhir Kumar, and Councillors G.Brian Golding, Laura A. Katz, and Jody Hey. President-ElectJeffrey R. Powell arrived later due to flight delays. The meetingbegan with Introductions.
2. Approval of minutes.—Councilapproved the minutes of the2003 Council and Business meetings,published in the December2003 issue of the journal MolecularBiology and Evolution (MBE).
3. Editor's report.—Most ofthe meeting addressed a discussionconcerning the Journal'sfuture and dealings with the OxfordUniversity Press (OUP) (seereport).
4. Treasurer's report.—Treasurer Marta L. Waynesummarizedthe financial state of the Society (see report).The fiscalyear has now changed to January–December (coincidentwith     

Lyn- and ERK-mediated vs. Ca2+-mediated neutrophil O2- responses with thermal injury

We evaluated thedependency of neutrophil O production on PTK-Lyn andMAPK-ERK1/2 in rats after thermal injury. Activation of PTK-Lyn wasassessed by immunoprecipitation. Phosphorylation of ERK1/2 was assessedby Western blot analysis. O production was measuredby isoluminol-enhanced luminometry. Imaging technique was employed tomeasure neutrophil [Ca²⁺]_i in individualcells. Thermal injury caused marked upregulation of Lyn and ERK1/2accompanying enhanced neutrophil O production.Treatment of rats with PTK blocker (AG556) or MAPK blocker (AG1478)before burn injury caused complete inhibition of the respective kinaseactivation. Both AG556 and AG1478 produced an ~66% inhibition inO production. Treatment with diltiazem (DZ) producedan ~37% inhibition of O production withoutaffecting Lyn or ERK1/2 activation with burn injury. Ca²⁺mobilization was upregulated with burn injury but not affected bytreatment of burn rats with AG556. Unlike the partial inhibition ofburn-induced O production by AG556, AG1478, or DZ,platelet-activating factor antagonist (PAFa) treatment of burn ratsproduced near complete inhibition of O production.PAFa treatment also blocked activation of Lyn. The findings suggestthat the near complete inhibition of O production byPAFa was a result of blockade of PTK as well as Ca²⁺signaling. Overall, our studies show that enhanced neutrophil O production after thermal injury is a result ofpotentiation of Ca²⁺-linked and -independent signalingtriggered by inflammatory agents such as PAF.

     

Meeting Announcements

Complex Carbohydrate Research Center Training Courses

Aug 4–8, 2008 Separation and Characterization of     

Meeting Announcements

Complex Carbohydrate Research Center Training Courses

Aug 4–8, 2008 Separation and Characterization of     

Airway surface liquid pH in well-differentiated airway epithelial cell cultures and mouse trachea

Airway surface liquid (ASL) pH hasbeen proposed to be important in the pathophysiology of cysticfibrosis, asthma, and cough. Ratio image analysis was used to measurepH in the ASL after staining with the fluorescent pH indicator2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF)-dextran. ASL pH in bovine airway cell cultures grown at anair-liquid interface was 6.98 ± 0.06 in the absence and 6.81 ± 0.04 in the presence of HCO/CO₂. Steady-state ASL pH changed in parallel to changes in bath pH and wasacidified by Na⁺ or Cl replacement but wasnot affected by the inhibitors amiloride, glibenclamide, or4,4'-dinitrostilbene-2,2'-disulfonic acid. In response to suddenacidification or alkalization of the ASL by ~0.4 pH units byHCl/NaOH, ASL pH recovered to its initial value at a rate of 0.035 pHunits/min (HCO) and 0.060 pH units/min(+HCO); the pH recovery rate was reduced byamiloride and H₂DIDS. In anesthetized mice in which thetrachea was surgically exposed for measurement of BCECF-dextranfluorescence through the translucent tracheal wall, ASL pH was7.14 ± 0.01. ASL pH was sensitive to changes in blood pH createdby metabolic (HCl or NaHCO₃ infusion) or respiratory (hyperventilation, hypoventilation) mechanisms. ASL pH is thus primarily determined by basolateral fluid pH, andH⁺/OH transport between the ASL andbasolateral fluid involves amiloride-sensitive Na⁺/H⁺ exchange and stilbene-sensitiveCl/HCO exchange. The rapid response ofASL pH to changes in systemic acid-base status may contribute to airwayhypersensitivity in asthma and other airway diseases.

     

Meeting Announcements

Complex Carbohydrate Research Center Training Courses

Aug 4–8, 2008 Separation and Characterization of GlycoconjugateOligosaccharides

     

Meeting Announcements

Complex Carbohydrate Research Center Training Courses

Aug 4–8, 2008 Separation and Characterization of GlycoconjugateOligosaccharides

     

Meeting Announcements

Complex Carbohydrate Research Center Training Courses

Aug 4–8, 2008 Separation and Characterization of GlycoconjugateOligosaccharides

     

Role of SGK in hormonal regulation of epithelial sodium channel in A6 cells

The purpose of this study was to examinethe role of the serum- and glucocorticoid-induced kinase (SGK) in theactivation of the epithelial sodium channel (ENaC) by aldosterone,arginine vasopressin (AVP), and insulin. We used atetracycline-inducible system to control the expression of wild-type(SGK), constitutively active (S425Dmutation; SGK), or inactive (K130Mmutation; SGK) SGK in A6 cellsindependently of hormonal stimulation. The effect of SGK expression onENaC activity was monitored by measuring transepithelialamiloride-sensitive short-circuit current (I_sc) of transfected A6 cell lines. Expression ofSGK orSGK and aldosterone stimulation haveadditive effects on I_sc. Although SGK could playsome role in the aldosterone response, our results suggest that othermechanisms take place. SGK abrogatesthe responses to AVP and insulin; hence, in the signaling pathways ofthese hormones there is a shared step that is stimulated by SGK.Because AVP and insulin induce fusion of vesicles to the apicalmembrane, our results support the notion that SGK promotes incorporation of channels in the apical membrane.

     

Ca(2+) regulation of gap junctional coupling in lens epithelial cells

The quantitative effects of Ca²⁺signaling on gap junctional coupling in lens epithelial cells have beendetermined using either the spread of Mn²⁺ that is imagedby its ability to quench the fluorescence of fura 2 or the spread ofthe fluorescent dye Alexa Fluor 594. Gap junctional coupling wasunaffected by a mechanically stimulated cell-to-cell Ca²⁺wave. Furthermore, when cytosolic Ca²⁺ concentration(Ca) increased after the addition of the agonistATP, coupling was unaffected during the period thatCa was maximal. However, coupling decreasedtransiently ~5-10 min after agonist addition whenCa returned to resting levels, indicating that thistransient decrease in coupling was unlikely due to a direct action ofCa on gap junctions. An increase inCa mediated by the ionophore ionomycin that wassustained for several minutes resulted in a more rapid and sustaineddecrease in coupling (IC₅₀ ~300 nM Ca²⁺, Hillcoefficient of 4), indicating that an increase in Ca alone could regulate gap junctions. Thus Ca increases that occurred during agonist stimulation and cell-to-cell Ca²⁺ waves were too transient to mediate a sustaineduncoupling of lens epithelial cells.

     

Meeting Announcements

3^rd International Meeting on the Congenital Disorders of Glycosylation ASIEM - 6 rue Albert de Lapparent - 75007 PARIS, France October18–19, 2007