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  • 1
    Electronic Resource
    Electronic Resource
    Induction of Myofibrillogenesis in Cardiac Mutant Axolotls by RNA from Normal Embryonic Endoderm (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 588 (1990), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1990.tb13247.x
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  • 2
    Electronic Resource
    Electronic Resource
    Ultrastructure of coelomic organization in annelids (1980)
    Springer
    Zoomorphology 95 (1980), S. 235-249 
    Details
    ISSN: 1432-234X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary A comparative ultrastructural study of trunk segments of a variety of small polychaetes (body diameter less than 250 μrn) was undertaken to determine whether small body size is correlated with deviations from the typical annelid pattern of coelomic organization. Peritoneum is never found covering oblique or parapodial muscles traversing the body cavity. Aside from this, two major patterns of body cavity organization are seen: 1. spacious body cavity with varying extent of peritoneal lining (complete, partial, absent) and 2. the body tending toward the acoelomate condition, as a result of the expansion of lining cells or the lack of initial cavity formation. The significance of these anatomical variations is discussed with respect to functional and phylogenetic considerations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00998124
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  • 3
    Electronic Resource
    Electronic Resource
    Activin A and transforming growth factor-β stimulate heart formation in axolotls but do not rescue cardiac lethal mutants (1995)
    Springer
    Cell & tissue research 282 (1995), S. 227-236 
    Details
    ISSN: 1432-0878
    Keywords: Key words: Growth factors ; Cardiogenesis ; Cardiac mutant ; Myocardium ; Axolotl ; Ambystoma mexicanum (Urodela)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. In the Mexican axolotl (salamander), Ambystoma mexicanum, a recessive cardiac lethal mutation causes an incomplete differentiation of the myocardium. Mutant hearts lack organized sarcomeric myofibrils and do not contract throughout their lengths. We have previously shown that RNA purified from normal anterior endoderm or from juvenile heart tissue is able to rescue mutant embryonic hearts in an in vitro organ culture system. Under these conditions as many as 55% of formerly quiescent mutant hearts initiate regular contractions within 48 hours. After earlier reports that transforming growth factor-β1 and, to a lesser extent, platelet-derived growth factor-BB could substitute for anterior endoderm as a promoter of cardiac mesodermal differentiation in normal axolotl embryos, we decided to examine the effect of growth factors in the cardiac mutant axolotl system. In one type of experiment, stage 35 mutant hearts were incubated in activin A, transforming growth factors-β1 or β2, platelet-derived growth factor, or epidermal growth factor, but no rescue of mutant hearts was achieved. Considering the possibility that growth factors would only be effective at earlier stages of development, we tested transforming growth factors-β1 and β5, and activin A on normal and mutant precardiac mesoderm explanted in the absence of endoderm at neurula stage 14. We found that, although these growth factors stimulated heart tube formation in both normal and mutant mesodermal explants, only normal explants contained contractile myocardial tissue. We hypothesize that transforming growth factor-β superfamily peptides initiate a cascade of responses in mesoderm that result in both changes in cell shape (the basis for heart morphogenesis) and terminal myocardial cytodifferentiation. The cardiac lethal mutation appears to be deficient only in the latter process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004410050475
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  • 4
    Electronic Resource
    Electronic Resource
    Activin A and transforming growth factor-β stimulate heart formation in axolotls but do not rescue cardiac lethal mutants (1995)
    Springer
    Cell & tissue research 282 (1995), S. 227-236 
    Details
    ISSN: 1432-0878
    Keywords: Growth factors ; Cardiogenesis ; Cardiac mutant ; Myocardium ; Axolotl, Ambystoma mexicanum (Urodela)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract In the Mexican axolotl (salamander), Ambystoma mexicanum, a recessive cardiac lethal mutation causes an incomplete differentiation of the myocardium. Mutant hearts lack organized sarcomeric myofibrils and do not contract throughout their lengths. We have previously shown that RNA purified from normal anterior endoderm or from juvenile heart tissue is able to rescue mutant embryonic hearts in an in vitro organ culture system. Under these conditions as many as 55% of formerly quiescent mutant hearts initiate regular contractions within 48 hours. After earlier reports that transforming growth factor-β1 and, to a lesser extent, platelet-derived growth factor-BB could substitute for anterior endoderm as a promoter of cardiac mesodermal differentiation in normal axolotl embryos, we decided to examine the effect of growth factors in the cardiac mutant axolotl system. In one type of experiment, stage 35 mutant hearts were incubated in activin A, transforming growth factors-β1 or β2, platelet-derived growth factor, or epidermal growth factor, but no rescue of mutant hearts was achieved. Considering the possibility that growth factors would only be effective at earlier stages of development, we tested transforming growth factors-β1 and β5, and activin A on normal and mutant precardiac mesoderm explanted in the absence of endoderm at neurula stage 14. We found that, although these growth factors stimulated heart tube formation in both normal and mutant mesodermal explants, only normal explants contained contractile myocardial tissue. We hypothesize that transforming growth factor-β superfamily peptides initiate a cascade of responses in mesoderm that result in both changes in cell shape (the basis for heart morphogenesis) and terminal myocardial cytodifferentiation. The cardiac lethal mutation appears to be deficient only in the latter process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00319114
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  • 5
    Electronic Resource
    Electronic Resource
    Immunohistochemical analysis of C-protein isoforms in cardiac and skeletal muscle of the axolotl, Ambystoma mexicanum (1995)
    Springer
    Cell & tissue research 282 (1995), S. 399-406 
    Details
    ISSN: 1432-0878
    Keywords: Key words: C-protein ; Isoforms ; Cardiac muscle ; Skeletal muscle ; Western blots ; Immunofluorescent microscopy ; Axolotl ; Ambystoma mexicanum (Urodela)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Of the several proteins located within sarco-meric A-bands, C-protein, a myosin binding protein (MyBP) is thought to regulate and stabilize thick filaments during assembly. This paper reports the characterization of C-protein isoforms in juvenile and adult axolotls, Ambystoma mexicanum, by means of immunofluorescent microscopy and Western blot analyses. C-protein and myosin are found specifically within the A-bands, whereas tropomyosin and α-actin are detected in the I-bands of axolotl myofibrils. The MF1 antibody prepared against the fast skeletal muscle isoform of chicken C-protein specifically recognizes a cardiac isoform (Axcard1) in juvenile and adult axolotls but does not label axolotl skeletal muscle. The ALD66 antibody, which reacts with the C-protein slow isoform in chicken, local- izes only in skeletal muscle of the axolotl. This slow axolotl isoform (Axslow) displays a heterogeneous distribution in fibers of dorsalis trunci skeletal muscle. The C315 antibody against the chicken C-protein cardiac isoform identifies a second axolotl cardiac isoform (Axcard2), which is present also in axolotl skeletal muscle. No C-protein was detected in smooth muscle of the juvenile and adult axolotl with these antibodies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004410050491
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  • 6
    Electronic Resource
    Electronic Resource
    Immunohistochemical analysis of C-protein isoforms in cardiac and skeletal muscle of the axolotl, Ambystoma mexicanum (1995)
    Springer
    Cell & tissue research 282 (1995), S. 399-406 
    Details
    ISSN: 1432-0878
    Keywords: C-protein ; Isoforms ; Cardiac muscle ; Skeletal muscle ; Western blots ; Immunofluorescent microscopy ; Axolotl, Ambystoma mexicanum (Urodela)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Of the several proteins located within sarcomeric A-bands, C-protein, a myosin binding protein (MyBP) is thought to regulate and stabilize thick filaments during assembly. This paper reports the characterization of C-protein isoforms in juvenile and adult axolotls, Ambystoma mexicanum, by means of immunofluorescent microscopy and Western blot analyses. C-protein and myosin are found specifically within the A-bands, whereas tropomyosin and α-actin are detected in the I-bands of axolotl myofibrils. The MF1 antibody prepared against the fast skeletal muscle isoform of chicken C-protein specifically recognizes a cardiac isoform (Axcard1) in juvenile and adult axolotls but does not label axolotl skeletal muscle. The ALD66 antibody, which reacts with the C-protein slow isoform in chicken, localizes only in skeletal muscle of the axolotl. This slow axolotl isoform (Axslow) displays a heterogeneous distribution in fibers of dorsalis trunci skeletal muscle. The C315 antibody against the chicken C-protein cardiac isoform identifies a second axolotl cardiac isoform (Axcard2), which is present also in axolotl skeletal muscle. No C-protein was detected in smooth muscle of the juvenile and adult axolotl with these antibodies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00318872
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  • 7
    Electronic Resource
    Electronic Resource
    Epicardial development in the axolotl, ambystoma mexicanum (1990)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 226 (1990), S. 228-236 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Recent studies on avian and mammalian embryos have established that the epicardium is derived, not from the early heart tube, but from mesothelial tissue overlying the sinus venosus. We tested the validity of this concept for Amphibia by examining normal and cardiac lethal (c/c) mutant axolotl embryos (stages 35-43) by electron microscopy.In axolotl embryos, the myocardial surface of the heart remains exposed to the pericardial fluid through stage 39. At this stage the transverse septum releases into the pericardial cavity mesothelial cells that subsequently flatten over the adjacent ventricular myocardium. However, mesothelial cells observed on the developing epicardium always appear rounded and may extend a filopodium up to 75 m̈m. This apparent “substrate-dependent” difference in mesothelial cell shape may promote the extension of the epicardium over the rest of the myocardium. The initial site of epicardial formation persists in the adult as the ventricular pericardial stalk that connects the epicardium to the peritoneal lining of the transverse septum.Cardiac lethal (c/c) mutant embryos, despite the non-contractility of their myocardia, form their epicardia in the same way. This suggests that the c/c mutation does not impair those properties of the myocardium that render it a suitable substrate for epicardial spreading. The abnormal pattern of epicardial coverage of the edematous stage 41 c/c mutant heart could be the result of its abnormally large myocardial surface area, the abnormal proximity of the atrium to the transverse septum, and/or the absence of heart contractions which could aid the dispersion of mesothelial cells within the pericardial cavity.Despite species differences, epicardial development in the axolotl is similar to the general pattern described for higher vertebrate embryos.
    Additional Material: 14 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092260212
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  • 8
    Electronic Resource
    Electronic Resource
    Extracellular matrix of the developing heart in normal and cardiac lethal mutant axolotls, Ambystoma mexicanum (1991)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 230 (1991), S. 387-405 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: As part of an ongoing study of heart development in normal and cardiac lethal mutant axolotls ( Mexican salamanders) we examined the extracellular matrix (ECM) by microscopical methods. With scanning electron microscopy we are unable to detect ECM on the apical surface of cells of the early cardiogenic mesoderm. During the period of lateral plate migration, which coincides with the period of cardiogenic induction of mesoderm by anterior endoderm, there is little ECM, aside from some microfibrils, on the basal surface of the endoderm or mesoderm of the pharyngeal region. Later, a basal lamina (BL) is found on the endoderm and along portions of the developing endocardial and myocardial tubes. By the time of heartbeat initiation the BLs are complete and invested with striated collagen-like fibrils that are sparsely distributed in the “cardiac jelly” of normal and mutant hearts. Striated fibril deposition, which increases with time, is generally random in orientation, with the exception of some regions where there is a preferred directionality. During the post-hatching period striated fibrils appear in the subepicardial space. In addition, branching fibers that are probably elastin appear in the bulbus arteriosus. In these later stages the density of fibrils in the cardiac lethal mutant heart is much less than normal. Indirect immunofluorescent microscopy reveals laminin and fibronectin in the basal; aminae of the endocardial and myocardial tubes of both normal and cardiac llethal mutant hearts. In addition, punctate and fibrillar staining for fibronectin, and punctate staining for laminin are found in the cardiac jelly. These matrix proteins are not abundant at the apical (exterior) surface of the myocardium until the epicardium appears. These results are similar to reports on ECM in other developing vertebrate hearts.
    Additional Material: 41 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092300312
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  • 9
    Electronic Resource
    Electronic Resource
    Myocardial cell relationships during morphogenesis in normal and cardiac lethal mutant axolotls, Ambystoma mexicanum (1988)
    New York, NY [u.a.] : Wiley-Blackwell
    American Journal of Anatomy 183 (1988), S. 245-257 
    Details
    ISSN: 0002-9106
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Sarcomere formation has been shown to be deficient in the myocardium of axolotl embryos homozygous for the recessive cardiac lethal gene c. We examined the developing hearts of normal and cardiac mutant embryos from tailbud stage 33 to posthatching stage 43 by scanning electron microscopy in order to determine whether that deficiency has any effect on heart morphogenesis. Specifically, we investigated the relationships of myocardial cells during the formation of the heart tube (stage 33), the initiation of dextral looping (stages 34-36), and the subsequent flexure of the elongating heart (stages 38-43). In addition, we compared the morphogenetic events in the axolotl to the published accounts of comparable stages in the chick embryo.In the axolotl (stage 33), changes in cell shape and orientation accompany the closure of the myocardial trough to form the tubular heart. The ventral mesocardium persists longer in the axolotl embryo than in the chick and appears to contribute to the asymmetry of dextral looping (stages 34-36) in two ways. First, as a persisting structure it places constraints on the simple elongation of the heart tube and the ability of the heart to bend. Second, after it is resorbed, the ventral myocardial cells that contributed to it are identifiable by their orientation, which is orthogonal to adjacent cells: a potential source of shearing effects. Cardiac lethal mutant embryos behave identically during these events, indicating that functional sarcomeres are not necessary to these processes. The absence of dynamic apical myocardial membrane changes, characteristic of the chick embryo (Hamburger and Hamilton stages 9-11), suggests that sudden hydration of the cardiac jelly is less likely to be a major factor in axolotl cardiac morphogenesis.Subsequent flexure (stages 38-43) of the axolotl heart is the same in normal and cardiac lethal mutant embryos as the myocardial tube lengthens within the confines of a pericardial cavity of fixed length. However, the cardiac mutant begins to exhibit abnormalities at this time. The lack of trabeculation (normally beginning at stage 37) in the mutant ventricle is evident at the same time as an increase in myocardial surface area, manifest in extra bends of the heart tube at stage 39. Nonbeating mutant hearts (stage 41) have an abnormally large diameter in the atrioventricular region, possibly the result of the accumulation of ascites fluid. In addition, mutant myocardial cells have a larger apical surface area compared to normals.
    Additional Material: 29 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aja.1001830307
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