PubMed Health⌕ Search

Biomedical subjects

J F Fallon

Publications and source records attributed to J F Fallon.

33 records · Page 2Linked to original sources
PubMed1986

Survival of motoneurons in the brachial lateral motor column of limbless mutant chick embryos depends on the periphery.

Motoneuron survival in the embryonic spinal cord is influenced by the presence or absence of the developing limb bud. We have recently begun a reexamination of the relationship between limb absence and motoneuron survival in a nonsurgical limb deletion model, the limbless mutant chick embryo. As in surgically limb-deleted normal embryos, only 10% of the motoneurons that are initially produced in the limbless mutant lateral motor column (LMC) survive the embryonic period (Lanser and Fallon, 1984). We now report that, when supplied with a normal periphery (i.e., a normal limb bud), more than 40% of the motoneurons initially produced in the limbless LMC survive the embryonic period. Motoneuron cell counts in one-winged limbless embryos reveal that over 3.5 times as many motoneurons survive the cell death period in the LMC on the side with the limb than on the opposite, limbless side. This demonstrates the dependence of embryonic LMC motoneurons on the developing limb for survival and indicates that the limbless mutant is an appropriate model for studying the death and survival of LMC motoneurons during development. Using the limbless mutant to study LMC motoneuron survival eliminates the complication of possible direct surgical effects on motoneuron death. In addition, we found that a substantial effect of the wing on rescuing LMC motoneurons was exerted prior to the 6th day of embryonic development. Normally, little cell loss occurs in the brachial LMC during this time. Accordingly, motoneuron death in the limb-deprived brachial LMC, whether in surgically limb-deleted normal embryos or in genetically limbless embryos, is accelerated with respect to cell death in the normal brachial LMC.

Animals↗
PubMed1985

The spatial pattern and temporal sequence in which feather germs arise in the white Leghorn chick embryo.

Feather germs arise in a specific sequence and spatio-temporal pattern within each of 10 feather areas on the White Leghorn chick embryo. The time of feather germ initiation was determined by histological and gross macroscopic analyses. Protruding feather germs are sequentially visualized in the dorsal, thigh, breast, head, humoral, ventral, wing, eye, and external auditory meatus feather areas, respectively, from stage 31- to stage 39+ [V. Hamburger and H.L. Hamilton (1951) J. Morphol. 88, 49-92]. The rate at which successive feather tracts appear was found to differ for different feather areas and was not simply due to the size of a feather area. Feather germ histogenesis was examined in the dorsal, thigh, breast, ventral, wing, and tail feather areas. The stages of feather germ histogenesis, examined on the wing feather area, are similar to those previously described for the dorsal surface. Gross and histological analyses gave different times and temporal sequences of feather germ visualization. Some feather areas were readily visualized at the time of feather germ initiation, while others showed a lag between the histological appearance of feather germs and their macroscopic visualization. Thus, macroscopic observations do not accurately reflect the pattern of histogenesis.

Animals↗
PubMed1978

Evidence of a role for cell death in the disappearance of the embryonic human tail.

The development and disappearance of the human tail between stages 14 and 22 were studied using scanning and transmission electron microscopy, supravital staining and light microscopy. The tail is a prominent feature of the human embryo during stage 14 and is composed of paired somites, mesenchyme and extensions of the neural tube, notochord and gut. The tail grows with the embryo through early stage 17 when it extends more than a millimeter from the trunk. Overgrowth by the trunk at the base of the tail may account for the loss of part of its length during late stage 17 and stage 18. However, during stage 17 cells begin to die in all structures throughout the tail. Cell death continues in the succeeding stages reaching massive numbers by stages 18 and 19, and the tail becomes less and less prominent with developmental time. Most of the dead cells are phagocytosed. The debris-laden macrophages appear to migrate from the tail to the body. By late stage 21 or early stage 22 there is no free tail. We conclude that cell death has a major role in the destruction of tail structures and the concurrent loss of the human tail.

Cell Survival↗
PubMed1978

Identification and distribution of gap junctions in the mesoderm of the developing chick limb bud.

Sub-ridge, core, anterior and posterior borders of mesoderm were dissected from stages 22-24 chick wing buds to investigate whether structures for intercellular coupling develop between mesenchymal cells. Fine structure was examined using techniques of transmission electron microscopy, freeze-fracture and scanning electron microscopy. Gap (communicating) junctions which were observed between mesenchymal cells of all limb bud regions were distributed between apposed cell bodies, points of contact between cell processes and other cell bodies, and between contacting tips of slender cell projections. In addition particularly in the the subridge region, filopodia were observed to extend through the intercellular matrix to contact other cells several micrometers distant. The observations reported in this paper show that mesodermal cells throughout the limb have the structural capability for electrotonic and metabolic coupling during a critical period of morphogenesis in the avian limb. Whether intercellular signals which are thought to be transmitted through gap junctions are active in normal limb development remains to be investigated.

Animals↗
PubMed1977

Interdigital cell death during limb development of the turtle and lizard with an interpretation of evolutionary significance.

Cell death accompanies the formation of free digits in birds and mammals. However, in species with webbing between the adult digits, little or no cell death occurs in the prospectively webbed region of the developing interdigit. Cell death does not occur during the formation of free digits in amphibians. In this paper we report that cell death accompanies the formation of the digits in snapping and painted turtles and in the skink (a lizard). We conclude that cell death accompanying the formation of free digits had its origin at the point of amniote emergence during evolution.

Animals↗
PubMed1975

Normal development of the chick wing following removal of the polarizing zone.

The negative results of assays for polarizing activity along the posterior border of the chick wing 24 and 48 hours after removal of the polarizing zone demonstrate that this zone is not regenerated following removal. These results, and the fact that normal wing development can occur after polarizing zone removal from stages 15 through 24 wing buds, indicate that during these stages the polarizing zone has no direct role in normal development of the limb bud. It is speculated that the polarizing zone is effective only during limb induction and that after this time it exists in latent or residual form.

Animals↗
PubMed1975

The role of beta-adrenergic activity in the production of cardiac and aortic arch anomalies in chick embryos.

The sympathomimetic amines isoproterenol, epinephrine, norepinephrine, and phenylephrine are structural derivatives of beta-phenylethylamine and have proportionately different effects on alpha- and beta-adrenergic receptors. Chick embryos in ovo were each administered a single dose of one of these compounds at concentrations ranging from 0.4 times 10(-9) to 20 times 10(-9) mol/5 mul saline during Hamburger and Hamilton stages 20-27. In other experiments embryos were pretreated with the beta-antagonist propranolol and subsequently administered isoproterenol. 743 cardiovascular anomalies were produced. The production of cardiovascular anomalies was proportional to the degree of beta-adrenergic activity of each drug. The frequency of anomalies was significantly reduced by pretreatment with propranolol. At all concentrations tested the anomaly rate was greater in chick embryos receiving an experimental compound than in controls. The general types of anomalies included aortic arch defects, ventricular septal defect, double outlet right ventricle, aortic hypoplasia, and truncus arteriosus. These results demonstrate that activation of the beta-adrenergic receptor mechanism is directly related to the cardiovascular anomalies produced in the chick embryos.

Abnormalities, Drug-Induced↗