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  • 1
    Electronic Resource
    Electronic Resource
    Inactivation determined by a single site in K+ pores (1993)
    Springer
    Pflügers Archiv 422 (1993), S. 354-363 
    Details
    ISSN: 1432-2013
    Keywords: K+ channel inactivation ; N-type inactivation ; C-type inactivation ; Pore or P-type inactivation ; External TEA enhancement of current ; External K+ enhancement of current ; Conductance ; Pore mutations
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract An N-terminus peptide or a C-terminus mechanism involving a single residue in transmembrane segment 6 produces inactivation in voltage-dependent K+ channels. Here we show that a single position in the pore of K+ channels can produce inactivation having characteristics distinct from either N- or C-type inactivation. In a chimeric K+ channel (CHM), the point reversion CHM V 369I produced fast inactivation and CHM V 369S had the additional effect of halving K+ conductance consistent with a position in the pore. The result was not restricted to CHM; mutating position 369 in the naturally occurring channel Kv2.1 also produced fast inactivation. Like N- and C-types of inactivation, pore or P-type inactivation was characterized by short bursts terminated by rapid entry into the inactivated state. Unlike C-type inactivation, in which external tetraethylammonium (TEA) produced a simple blockade that slowed inactivation and reduced currents, in P-type inactivation external TEA increased currents. Unlike N-type inactivation, internal TEA produced a simple reduction in current and K+ occupancy of the pore had no effect. External TEA was not the only cation to increase current; external K+ enhanced channel availability and recovery from inactivation. Additional features of P-type inactivation were residue-specific effects on the extent of inactivation and removal of inactivation by a point reversion at position 374, which also regulates conductance. The demonstration of P-type inactivation indicates that pore residues in K+ channels may be part of the inactivation gating machinery.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374291
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  • 2
    Electronic Resource
    Electronic Resource
    Mapping the origin of the avian enteric nervous system with a retroviral marker (1994)
    New York, NY [u.a.] : Wiley-Blackwell
    Developmental Dynamics 201 (1994), S. 236-244 
    Details
    ISSN: 1058-8388
    Keywords: Spleen necrosis virus ; Enteric nervous system ; Beta-galactosidase ; Chick embryo ; Somite ; Neural crest ; lac Z gene ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: The enteric nervous system is largely formed from the vagal neural crest which arises from the neuroaxis between somites 1 - 7. In order to evaluate the contribution of different regions of the vagal crest to the enteric nervous system, we marked crest cells by injecting somites 1 - 10 with a replication-defective spleen necrosis virus vector which contains the marker gene lacZ. After incubation in X-gal, lacZ-positive blue cells were found in the wall of the gut in three locations. Most were found at the peripheral edge of the developing circular muscle and within the developing submucosa, sites characteristic of developing ganglia. LacZ-positive cells in these ganglionic sites were always surrounded by HNK-1 immunostained cells, confirming their neural crest origin. LacZ-positive cells were also seen in a third location, the circular muscle layer of the esophagus and crop, and were separated from the HNK-1 positive ganglionic elements. These cells in the circular muscle are probably muscle cells derived from labeled mesodermal cells of the somite. Injection of somites 3, 4, 5, and 6 resulted in the largest percentage of preparations with lacZ-positive crest-derived cells and in the largest number of positive cells in the gut. After injection of these somites, lacZ-positive crest-derived cells were found in all regions of the gut from the proventriculus to the rectum. Very few positive crest-derived cells were found in the esophagus. Injection of somites 1, 2, and 7 resulted in a smaller percentage of preparations with positive crest-derived cells and in a smaller number of positive crest-derived cells, which were confined to the fore and midgut. The gizzard was the gut region most frequently containing labeled cells and the rectum was the region least frequently containing such cells. This suggests that the number of crest cells available for colonization of the gut decreases as the distance from the gizzard increases. We conclude that the region of the neuroaxis between somites 3 - 6 is the major source of crest cells to the gut and that crest cells from different segments of the neuroaxis do not appear to be segregated to different regions of the gut. © 1994 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aja.1002010307
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  • 3
    Electronic Resource
    Electronic Resource
    Clonal analysis of cardiac morphogenesis in the chicken embryo using a replication-defective retrovirus: I. Formation of the ventricular myocardium (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    American Journal of Anatomy 193 (1992), S. 11-23 
    Details
    ISSN: 0002-9106
    Keywords: Heart ; Development ; Cell lineage ; Myocardium ; Cardiac myocyte ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Cells of the precardiac mesoderm (stages 4-6) and dividing myocytes of early hearts (stages 10-15) were tagged with a replication-incompetent retrovirus (CXL) (Mikawa et al., 1991 b) encoding bacterial β-galactosidase (β-gal). Two protocols were used to infect the cardiogenic cells. (1) Small blocks (∼50 μm2) of anterolateral mesoderm were dissected from gastrula-stage embryos (stages 4-6) and incubated in liquid medium containing the retrovirus. After removal of CXL, the tissues were dispersed into single-cell suspensions and pressure injected into the precardiac areas of recipient embryos (stages 4-6). Such embryos were then incubated in vitro at 37°C for 2 days (New, 1968), and those embryos with beating hearts were fixed for X-gal histochemistry and paraffin serial sectioning. (2) CXL was pressure injected in ovo (embryonic stages 4-15) into cardiogenic tissues and the eggs subsequently returned to an incubator. At selected stages of development embryos or whole hearts were fixed, stained with X-gal, and serially sectioned after paraffin embedding. The first method showed that (1) cells of the precardiac mesoderm could be infected with the retrovirus, (2) the transplanted cells would differentiate into beating myocytes, and (3) β-gal expression was sufficiently high to be detected histochemically. With the second procedure we could show that (1) β-gal-tagged cells formed colonies in the myocardium, (2) the labeled cells were exclusively myocytes, (3) the number of cells per colony increased with increasing age of embryonic development, (4) the size of colonies was larger in the left than the right ventricle, (5) many of the colonies were transmural, i.e., they extended from epicardial to endocardial layers of the myocardium and generally exhibited a cone or funnel-shape with the base of the cone nearest the epicardium, (6) the orientation of myocytes within each colony changed at different layers of the myocardium, and (7) the cones contained both β-gal+ and β-gal- myocytes. DNA labeling studies with [3H]thymidine indicated that cardiogenic cells divided every 16-18 hr during the first week of development and that the CXL-labeled cells divided indistinguishably from unlabeled myocytes. Based on these observations a model for the growth of the myocardium is presented.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aja.1001930104
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