scholarly journals The Morphology of Heart Development in Xenopus laevis

2000 ◽  
Vol 218 (1) ◽  
pp. 74-88 ◽  
Author(s):  
Timothy J. Mohun ◽  
Li Ming Leong ◽  
Wolfgang J. Weninger ◽  
Duncan B. Sparrow
2007 ◽  
Vol 31 (2) ◽  
pp. 81-89
Author(s):  
Won Seok Koh ◽  
Li Guang Li ◽  
In-Shik Kim ◽  
Young-Hoon Lee ◽  
Byung Seok Ko ◽  
...  

2000 ◽  
Vol 218 (1) ◽  
pp. 64-73 ◽  
Author(s):  
Sandra J Kolker ◽  
Urszula Tajchman ◽  
Daniel L Weeks

2018 ◽  
Author(s):  
Madison C. Sestak ◽  
Julia A. Pinette ◽  
Caithlin M. Lamoureux ◽  
Susan L. Whittemore

AbstractPolycyclic aromatic hydrocarbons (PAHs) are ubiquitous, persistent environmental contaminants, of which 16 are EPA-designated priority pollutants. Cardiotoxicity is observed in fish with developmental exposures to certain PAHs; however, the mechanism of toxicity can differ. Phenanthrene (PHE) and benzo(a)pyrene (BaP) are both cardiotoxic to fish, but PHE acts independently of aryl hydrocarbon receptor (AHR) activation while BaP-associated cardiotoxicity is AHR-dependent. To further understanding of mechanisms of toxicity, we compared the effects of early exposure to the priority PAHs pyrene (PYR), fluoranthene (FLA), PHE and BaP on cardiac function and cytochrome P450 type 1A (cyp1a) mRNA expression, an indicator of AHR activation, in a model system with lower AHR sensitivity than that of fish, the embryos and larvae of Xenopus laevis. Exposure to PYR, PHE, and FLA (0.25 – 25 μM) caused ventricular tachycardia early in heart development, but bradycardia and atrioventricular (AV) block in later stages. Elevated cyp1a mRNA levels indicate that FLA and BaP, but not PHE or PYR, are AHR agonists. The finding of FLA-induced cardiotoxicity and cyp1a expression (35-fold) is particularly surprising as FLA inhibits CYP1A activity in fish and, as a single compound, is not cardiotoxic. Our results suggest that early exposure to PHE, PYR, and FLA, but not to BaP, compromises cardiac function by altering normal pacemaker activity and conduction in Xenopus, effects associated with increased mortality. Our findings also reveal a considerable degree of species specificity between fish and frog regarding cardiac sensitivity to developmental PAH exposures and have implications for the cardiovascular health of PAH-exposed humans and wild amphibians.


2007 ◽  
Vol 27 (18) ◽  
pp. 6420-6432 ◽  
Author(s):  
Yong Chen ◽  
Wai Hong Yuen ◽  
Jianlin Fu ◽  
Guochang Huang ◽  
Alirio J. Melendez ◽  
...  

ABSTRACT The mitochondrial respiratory chain (MRC) plays crucial roles in cellular energy production. However, its function in early embryonic development remains largely unknown. To address this issue, GRIM-19, a newly identified MRC complex I subunit, was knocked down in Xenopus laevis embryos. A severe deficiency in heart formation was observed, and the deficiency could be rescued by reintroducing human GRIM-19 mRNA. The mechanism involved was further investigated. We found that the activity of NFAT, a transcription factor family that contributes to early organ development, was downregulated in GRIM-19 knockdown embryos. Furthermore, the expression of a constitutively active form of mouse NFATc4 in these embryos rescued the heart developmental defects. NFAT activity is controlled by a calcium-dependent protein phosphatase, calcineurin, which suggests that calcium signaling may be disrupted by GRIM-19 knockdown. Indeed, both the calcium response and calcium-induced NFAT activity were impaired in the GRIM-19 or NDUFS3 (another complex I subunit) knockdown cell lines. We also showed that NFAT can rescue expression of Nkx2.5, which is one of the key genes for early heart development. Our data demonstrated the essential role of MRC in heart formation and revealed the signal transduction and gene expression cascade involved in this process.


1993 ◽  
Vol 187 (3) ◽  
Author(s):  
YvetteN. Frunchak ◽  
GaleN. Martha ◽  
KennethD. McFadden ◽  
NadineC. Milos

Author(s):  
Larry F. Lemanski ◽  
Eldridge M. Bertke ◽  
J. T. Justus

A recessive mutation has been recently described in the Mexican Axolotl, Ambystoma mexicanum; in which the heart forms structurally, but does not contract (Humphrey, 1968. Anat. Rec. 160:475). In this study, the fine structure of myocardial cells from normal (+/+; +/c) and cardiac lethal mutant (c/c) embryos at Harrison's stage 40 was compared. The hearts were fixed in a 0.1 M phosphate buffered formaldehyde-glutaraldehyde-picric acid-styphnic acid mixture and were post fixed in 0.1 M s-collidine buffered 1% osmium tetroxide. A detailed study of heart development in normal and mutant embryos from stages 25-46 will be described elsewhere.


Author(s):  
C. Uphoff ◽  
C. Nyquist-Battie

Fetal Alcohol Syndrone (FAS) is a syndrome with characteristic abnormalities resulting from prenatal exposure to ethanol. In many children with FAS syndrome gross pathological changes in the heart are seen with septal defects the most prevalent abnormality recorded. Few studies in animal models have been performed on the effects of ethanol on heart development. In our laboratory, it has been observed that prenatal ethanol exposure of Swiss albino mice results in abnormal cardiac muscle ultrastructure when mice were examined at birth and compared to pairfed and normal controls. Fig. 1 is an example of the changes that are seen in the ethanol-exposed animals. These changes include enlarged mitochondria with loss of inner mitochondrial membrane integrity and loss of myofibrils. Morphometric analysis substantiated the presence of these alterations from normal cardiac ultrastructure. The present work was undertaken to determine if the pathological changes seen in the newborn mice prenatally exposed to ethanol could be reversed with age and abstinence.


Author(s):  
Darcy B. Kelley ◽  
Martha L. Tobias ◽  
Mark Ellisman

Brain and muscle are sexually differentiated tissues in which masculinization is controlled by the secretion of androgens from the testes. Sensitivity to androgen is conferred by the expression of an intracellular protein, the androgen receptor. A central problem of sexual differentiation is thus to understand the cellular and molecular basis of androgen action. We do not understand how hormone occupancy of a receptor translates into an alteration in the developmental program of the target cell. Our studies on sexual differentiation of brain and muscle in Xenopus laevis are designed to explore the molecular basis of androgen induced sexual differentiation by examining how this hormone controls the masculinization of brain and muscle targets.Our approach to this problem has focused on a highly androgen sensitive, sexually dimorphic neuromuscular system: laryngeal muscles and motor neurons of the clawed frog, Xenopus laevis. We have been studying sex differences at a synapse, the laryngeal neuromuscular junction, which mediates sexually dimorphic vocal behavior in Xenopus laevis frogs.


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