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PubMed1999

Lymphangioblasts in the avian wing bud.

The development of the lymphatics has not yet been studied experimentally. Descriptive studies could not answer the question whether the lymphatics are exclusively derived by sprouts of the early embryonic lymph sacs, or whether lymphangioblasts in the mesenchyme contribute to the lymphatic system. We have studied the development of the lymphatics in quail-chick chimeras. In 6.5-day-old quail embryos, the endothelium of the jugulo-axillary lymph sac can be demonstrated with the QH1 antibody. In contrast to the jugular vein and the aorta, the lymph sac is irregularly shaped and does not possess a media of smooth muscle cells, and, the lymph sac endothelium starts to express the vascular endothelial growth factor receptor-3 (VEGFR-3). Cells of the quail paraxial mesoderm grafted into chick embryos integrate into the endothelium of the jugular lymph sac, strongly indicating the existence of lymphangioblasts. In the wing of 10-day-old quail embryos, VEGFR-3-positive lymphatics are accompanying all major blood vascular routes. On day 3.5 of development, that is about one day before the first occurrence of the jugulo-axillary lymph sac, we grafted distal wing buds of chick embryos homotopically into quail embryos. The chimeric wings were analyzed on day 10. The VEGFR-3 and QH1 double staining revealed that the lymphatics were formed by both chick and quail endothelial cells. This result shows that the lymphatics of the wing do not exclusively develop from sprouts of the lymph sacs, but also by recruitment of local lymphangioblasts.

Animals↗
PubMed2000

Extracellular matrix environment influences chondrogenic pattern formation in limb bud micromass culture: experimental verification of theoretical models.

Various theoretical models have been proposed to explain the periodicity in the pattern of limb chondrogenesis, but experimental comparison of these models have seldom been performed properly. In the present study, micromass culture of limb bud mesenchyme cells was undertaken to test the validity of three theoretical models: the reaction-diffusion model, the cell sorting model, and the mechanochemical model. Computer simulations were undertaken to predict the factors that can affect the coarseness of the chondrogenic pattern. According to the predictions, we performed micromass culture of limb mesenchyme in collagen and agarose gel. Then we carried out time-lapse observation to analyze the cell movement during pattern formation. From computer simulations it was theoretically predicted that changes in the surrounding extracellular matrix should alter the periodicity of the chondrogenic pattern in vitro, and we found that pattern changes actually occurred under different culture conditions. When compared with the culture in a liquid medium, the chondrogenic pattern became less coarse when the cells were cultured in collagen or agarose gel, and the pattern change appeared to be independent of the cell differentiation. Time-lapse observation revealed a decrease in cell motility when the cells were cultured in gel. It was found that both the reaction-diffusion and cell sorting models fit the pattern change produced and that the mechanochemical model is not primarily important in the chondrogenic pattern formation in vitro.

Agar↗
PubMed1997

Actions of the neurotrophins on calcium uptake.

The neurotrophins are important for their long-term effects on the survival and differentiation of many types of neurons during development. They also appear to protect mature neurons from injury caused by nutrient or oxygen deprivation. More recently, the neurotrophins have been implicated in such short-term processes as synaptic plasticity. A great deal of evidence suggests that intracellular calcium levels play a key role in neuronal survival during normal development, in neuronal injury following nutrient or oxygen deprivation, and in synaptic plasticity as well. Maintaining appropriate intracellular levels of calcium is important for proper biological function and it has been shown that one of the actions of the neurotrophins is to modulate intracellular calcium levels in a number of in vivo and in vitro systems. Some information about the mechanism(s) by which this is accomplished is now available. Understanding the mechanisms of neurotrophin action should provide insights into the processes by which the brain functions and, further, provide therapeutic tools for the treatment of neuronal injury and neurodegenerative diseases.

Animals↗
PubMed2000

Oligodendrocytes and the control of myelination in vivo: new insights from the rat anterior medullary velum.

The rat anterior medullary velum (AMV) is representative of the brain and spinal cord, overall, and provides an almost two-dimensional preparation for investigating axon-glial interactions in vivo. Here, we review some of our findings on axon-oligodendrocyte unit relations in our adult, development, and injury paradigms: (1) adult oligodendrocytes are phenotypically heterogeneous, conforming to Del Rio Hortega's types I-IV, whereby differences in oligodendrocyte morphology, metabolism, myelin sheath radial and longitudinal dimensions, and biochemistry correlate with the diameters of axons in the unit; (2) oligodendrocytes derive from a common premyelinating oligodendrocyte phenotype, and divergence of types I-IV is related to the age they emerge and the presumptive diameter of axons in the unit; (3) during myelination, axon-oligodendrocyte units progress through a sequence of maturation phases, related to axon contact, ensheathment, establishment of internodal myelin sheaths, and finally the radial growth and compaction of the myelin sheath; (4) we provide direct in vivo evidence that platelet-derived growth factor-AA (PDGF-AA), fibroblast growth factor (FGF-2), and insulin-like growth factor-I (IGF-I) differentially regulate these events, by injecting the growth factors into the cerebrospinal fluid of neonatal rat pups; (5) in lesioned adult AMV, transected central nervous system (CNS) axons regenerate through the putatively inhibitory environment of the glial scar, but remyelination by oligodendrocytes is incomplete, indicating that axon-oligodendrocyte interactions are defective; and (6) in the adult AMV, cells expressing the NG2 chondroitin sulphate have a presumptive adult oligodendrocyte progenitor antigenic phenotype, but are highly complex cells and send processes to contact axolemma at nodes of Ranvier, suggesting they subserve a specific perinodal function. Thus, axons and oligodendrocyte lineage cells form interdependent functional units, but oligodendrocyte numbers, differentiation, phenotype divergence, and myelinogenesis are governed by axons in the units, mediated by growth factors and contact-dependent signals.

Animals↗
PubMed1996

Regulation of avian precardiac mesoderm development by insulin and insulin-like growth factors.

Endoderm within the heart forming regions of vertebrate embryos has pronounced effects on myocardial cell development. Previous studies have suggested that these effects are mediated by soluble growth factors, in particular fibroblast growth factor 2 (FGF-2) and activin-A. Since both insulin and insulin-like growth factors (IGFs) are present in developing avian embryos at the time of heart formation, we have investigated the potential role of these molecules in promoting development of premyocardial cells in quail. Culture of precardiac mesoderm explants from stage 5 quail embryos in medium containing insulin, IGF-I, or IGF-II increased proliferation of premyocardial cells, with maximal stimulation observed at approximately 25 nM for each ligand. A direct comparison of the proliferative response of precardiac mesoderm to endoderm, fetal calf serum, insulin, IGF-I, IGF-II, activin-A, and FGF-2 showed that FGF-2 and activin-A increased proliferation of premyocardial cells approximately 2-fold, while insulin, IGF-I, and IGF-II stimulated proliferation approximately 3-fold. Insulin and IGF-I enhanced the rate of myocyte differentiation, similar to previously reported effects of endoderm. In contrast, exposure of precardiac mesoderm explants to transforming growth factor beta (TGF beta) reduced proliferation of premyocardial cells and moderated the proliferative effects of IGF-I. TGF beta did not block the differentiation of stage 5 premyocardial cells. Reverse transcription-polymerase chain reaction (RT-PCR) analyses showed that mRNAs encoding insulin, IGF-II, insulin receptor, and IGF-I receptor were present in both precardiac mesoderm and endoderm, as well as in the forming heart at stage 8. Since premyocardial cells can survive and differentiate in a defined medium lacking these factors, precardiac mesoderm may produce IGF-II and insulin at levels that are sufficient to stimulate myocyte development. Taken together, these results suggest that insulin and/or IGF-II may promote cardiac development in vivo by both autocrine and paracrine mechanisms. Cardiogenesis may therefore be promoted by the combined action of several classes of growth factors.

Animals↗
PubMed1998

Multiple calvarial defects in lmx1b mutant mice.

The vertebrate cranial vault, or calvaria, forms during embryonic development from cranial mesenchyme of multiple embryonic origins. Inductive interactions are thought to specify the number and location of the calvarial bones, including interactions between the neuroepithelium and cranial mesenchyme. An important feature of calvarial development is the local inhibition of osteogenic potential which occurs between specific bones and results in the formation of the cranial sutures. These sutures allow for postnatal growth of the skull to accommodate postnatal increase in brain size. The molecular genetic mechanisms responsible for the patterning of individual calvarial bones and for the specification of the number and location of sutures are poorly understood at the molecular genetic level. Here we report on the function and expression pattern of the LIM-homeodomain gene, lmx1b, during calvarial development. Lmx1b is expressed in the neuroepithelium underlying portions of the developing skull and in cranial mesenchyme which contributes to portions of the cranial vault. Lmx1b is essential for proper patterning and morphogenesis of the calvaria since the supraoccipital and interparietal bones of lmx1b mutant mice are either missing or severely reduced. Moreover, lmx1b mutant mice have severely abnormal sutures between the frontal, parietal, and interparietal bones. Our results indicate that lmx1b is required for multiple events in calvarial development and suggest possible genetic interaction with other genes known to regulate skull development and suture formation.

Animals↗
PubMed1997

The effect of pulsed and sinusoidal magnetic fields on the morphology of developing chick embryos.

Several investigators have reported robust, statistically significant results that indicate that weak (approximately 1 microT) magnetic fields (MFs) increase the rate of morphological abnormalities in chick embryos. However, other investigators have reported that weak MFs do not appear to affect embryo morphology at all. We present the results of experiments conducted over five years in five distinct campaigns spanning several months each. In four of the campaigns, exposure was to a pulsed magnetic field (PMF); and in the final campaign, exposure was to a 60 Hz sinusoidal magnetic field (MF). A total of over 2500 White Leghorn chick embryos were examined. When the results of the campaigns were analyzed separately, a range of responses was observed. Four campaigns (three PMF campaigns and one 60 Hz campaign) exhibited statistically significant increases (P > or = 0.01), ranging from 2-fold to 7-fold, in the abnormality rate in MF-exposed embryos. In the remaining PMF campaign, there was only a slight (roughly 50%), statistically insignificant (P = 0.2) increase in the abnormality rate due to MF exposure. When the morphological abnormality rate of all of the PMF-exposed embryos was compared to that of all of the corresponding control embryos, a statistically significant (P > or = .001) result was obtained, indicating that PMF exposure approximately doubled the abnormality rate. Like-wise, when the abnormality rate of the sinusoid-exposed embryos was compared to the corresponding control embryos, the abnormality rate was increased (approximately tripled). This robust result indicates that weak EMFs can induce morphological abnormalities in developing chick embryos. We have attempted to analyze some of the confounding factors that may have contributed to the lack of response in one of the campaigns. The genetic composition of the breeding stock was altered by the breeder before the start of the nonresponding campaign. We hypothesize that the genetic composition of the breeding stock determines the susceptibility of any given flock to EMF-induced abnormalities and therefore could represent a confounding factor in studies of EMF-induced bioeffects in chick embryos.

Abnormalities, Radiation-Induced↗
PubMed1998

The superposition of a temporally incoherent magnetic field inhibits 60 Hz-induced changes in the ODC activity of developing chick embryos.

Previously, we have shown that the application of a weak (4 microT) 60 Hz magnetic field (MF) can alter the magnitudes of the ornithine decarboxylase (ODC) activity peaks which occur during gastrulation and neurulation of chick embryos. We report here the ODC activity of chick embryos which were exposed to the superposition of a weak noise MF over a 60 Hz MF of equal (rms strength). In contrast to the results we obtain with a 60 Hz field alone, the activity of ODC in embryos exposed to the superposition of the incoherent and 60 Hz fields was indistinguishable from the control activity during both gastrulation and neurulation. This result adds to the body of experimental evidence which demonstrates that the superposition of an incoherent field inhibits the response of biological systems to a coherent MF. The observation that a noise field inhibits ODC activity changes is consistent with our speculation that MF-induced ODC activity changes during early development may be related to MF-induced neural tube defects at slightly later stages (which are also inhibited by the superposition of a noise field).

Animals↗
PubMed2001

The parathyroid hormone-related protein and Indian hedgehog feedback loop in the growth plate.

Normal development of the growth plate requires coordinated proliferation and differentiation of chondrocytes and osteoblasts. In previous work, we have shown that Indian hedgehog (IHH), produced by prehypertrophic and hypertrophic chondrocytes, stimulates production of parathyroid hormone-related protein (PTHrP) by perichondrial and early chondrocytic cells. PTHrP then maintains chondrocytes in a proliferative, less differentiated state. Because this less differentiated state delays the production of IHH, IHH and PTHrP may participate in a negative feedback loop that synchronizes and determines the pace of differentiation of chondrocytes in the growth plate. To establish the roles of physiological levels of PTHrP and IHH, we have now injected PTH/PTHrP receptor (-/-) embryonic stem (ES) cells into normal blastocysts to generate mice with chimeric growth plates. The PTH/PTHrP receptor cells leave the proliferative cycle and differentiate prematurely in the middle of the normal proliferative columns. The columns of wild-type cells are longer than normal and the adjacent bone collar is also longer than normal. Patterns of gene expression and the use of chimeras using PTH/PTHrP receptor (-/-); IHH (-/-) ES cells suggest that modified patterns of IHH and PTHrP synthesis explain these abnormalities. Thus, IHH is a master regulator of both chondrocyte and osteoblast differentiation.

Animals↗
PubMed2000

Fate diversity of primitive streak cells during heart field formation in ovo.

In amniote embryos, cells from a rostral portion of the primitive streak migrate anterolaterally and establish the heart field mesoderm, from which two cardiac cell lineages, cardiomyocytes and endocardial endothelial cells, differentiate. The endoderm underlying the heart field has been postulated as the source of several paracrine factors that may serve to induce each of these cell types. However, it has been unclear how these signal molecules, which are expressed broadly in the endoderm, instruct individual cells of the heart field mesoderm to enter either the cardiomyocyte lineage or the endocardial cell lineage. To clarify lineage relationships of these two cardiac cell types, the fate of chicken primitive streak cells was traced for the first time in ovo. By using replication-defective retroviral-mediated gene transfer, we demonstrate that cells in the rostral half of Hamburger and Hamilton (HH) stage 3 primitive streak generate a daughter population that proliferates and migrates into the heart field, differentiating into either endocardial or myocardial cells, but not both cell types. The results suggest that the rostral portion of the primitive streak at HH stage 3 consists of at least two distinct subpopulations, entering either the cardiomyocyte lineage or the endocardial cell lineage. Thus, in ovo these two cell lineages of the heart are already segregated within the primitive streak, significantly before their migration to the heart field. When the precardiomyocytes and pre-endocardial cells arrive at the heart field, each mesodermal cell subpopulation may be permissive to paracrine signal(s) from underlying endoderm to initiate their terminal differentiation into either muscle or endothelial cells.

Animals↗
PubMed2001

New insights into critical events of avian gastrulation.

The formation and progression of the primitive streak are key events of avian gastrulation. We examine these processes in detail, using various morphological approaches. We show that formation of the primitive streak occurs locally at the caudal midline of the area pellucida, as cells in the caudal midline undergo an epithelial-to-mesenchymal transformation, and that extensive migration of delaminated cells arising from more rostral or peripheral areas of the blastoderm is not involved in streak formation. Instead, such delamination occurs earlier and is restricted to the process of hypoblast formation. Moreover, we provide evidence that progression of the primitive streak involves two processes: convergent-extension movements within the streak per se, and progressive delamination of midline epiblast cells in a caudal-to-rostral sequence. We have identified a subpopulation of primitive-streak cells located at its dorsal midline surface that undergoes extensive rostral displacement concomitant with streak progression. The fact that these cells are located only dorsally and do not elongate ventrally as do adjacent ingressing cells, suggests that these cells retain their residency within the primitive streak, at least until regression of the primitive streak occurs. Finally, by following labeled cells over time we establish the timing of movement of epiblast cells toward and into the primitive streak, providing direct evidence that cell-cell intercalation occurs within the primitive streak during its progression. Collectively, our results provide new insight into complex and central events of avian gastrulation.

Animals↗
PubMed2001

An arrow for wingless to take-off.

The Wnt family of secreted glycoproteins is involved in the regulation of diverse developmental processes. The classical Wnt/beta-catenin pathway has been thoroughly investigated resulting in the identification of a plethora of components involved in the activation of beta-catenin target genes. Moreover, two additional Wnt-triggered pathways have been identified. These various signalling cascades require at least one component that confers signalling specificity. This function is fulfilled at least in part by the Wnt receptor Frizzled. The recent identification of a potential Frizzled co-receptor, an LDL-receptor-related-protein (LRP), sheds more light on Wnt-signal transduction specificity and promises more exciting revelations.

Animals↗
PubMed2001

Hensen's node.

With the 125th anniversary of the original description of Hensen's node in the rabbit coming up and with current research focused on the function of this pivotal embryonic structure, this article proposes a simplified use of terms for the gastrulation organizer in amniote embryos and reemphasizes the achievements of Victor Hensen (1835-1924) in embryology. A partial translation of Hensen's paper (originally published in German) is accompanied by a short historical introduction that concentrates on the framework of embryological research at Hensen's time and on the subsequent reception of his classic paper.

Amphibians↗
PubMed1984

Remodelling of the basement membrane: morphogenesis and maturation.

We have analysed the reciprocal interactions between mouse embryo submandibular epithelium and mesenchyme which result in branching morphogenesis of the epithelium. The interactions modify the composition and metabolism of the basal and reticular laminae which comprise the basement membrane lying between these tissues. The mesenchyme remodels the basement membrane by depositing a type I collagen-rich matrix on the basal lamina and by producing a neutral hyaluronidase, which degrades hyaluronate and chondroitin sulphate, components of this basal lamina. By analogy with mouse mammary epithelial cells, the submandibular epithelial cells have a heparan sulphate-rich proteoglycan on their cell surfaces which is anchored to the cells. The extracellular domain of this integral membrane proteoglycan binds to interstitial collagen. Interfering with the collagen-proteoglycan interaction appears to reduce the morphological stability of the cells. Together with other processes, including epithelial cell proliferation, this remodelling leads to branching epithelial morphogenesis. Basement membrane remodelling may be a general process for regulating cell behaviour during development and is one of the mechanisms of morphogenetic tissue interaction. Remodelling may also cause maturation of basement membranes from a dynamic state of high turnover in the embryo to their persistence and stability in the adult organism.

Animals↗
PubMed1983

Contributions of placodal and neural crest cells to avian cranial peripheral ganglia.

The method of embryonic tissue transplantation was used to confirm the dual origin of avian cranial sensory ganglia, to map precise locations of the anlagen of these sensory neurons, and to identify placodal and neural crest-derived neurons within ganglia. Segments of neural crest or strips of presumptive placodal ectoderm were excised from chick embryos and replaced with homologous tissues from quail embryos, whose cells contain a heterochromatin marker. Placode-derived neurons associated with cranial nerves V, VII, IX, and X are located distal to crest-derived neurons. The generally larger, embryonic placodal neurons are found in the distal portions of both lobes of the trigeminal ganglion, and in the geniculate, petrosal and nodose ganglia. Crest-derived neurons are found in the proximal trigeminal ganglion and in the combined proximal ganglion of cranial nerves IX and X. Neurons in the vestibular and acoustic ganglia of cranial nerve VIII derive from placodal ectoderm with the exception of a few neural crest-derived neurons localized to regions within the vestibular ganglion. Schwann sheath cells and satellite cells associated with all these ganglia originate from neural crest. The ganglionic anlagen are arranged in cranial to caudal sequence from the level of the mesencephalon through the third somite. Presumptive placodal ectoderm for the VIIIth, the Vth, and the VIIth, IXth, and Xth ganglia are located in a medial to lateral fashion during early stages of development reflecting, respectively, the dorsolateral, intermediate, and epibranchial positions of these neurogenic placodes.

Animals↗
PubMed1992

The talpid2 chick limb has weak polarizing activity and can respond to retinoic acid and polarizing zone signal.

The talpid2 (ta2) chick mutant has wide, polydactylous wings and legs. Talpid2 limb cartilages have abnormal morphology and a very subtle anteroposterior polarity. Specifically, posterior ta2 limb structures are identifiable, while more anterior cartilages are less distinctive. Here, we investigate the development of anteroposterior limb pattern in the ta2 embryo. We show that ta2 posterior limb bud mesoderm is capable of respecifying the anteroposterior axis of a normal wing. However, the average duplication obtained after grafting a ta2 polarizing region was significantly less than the average duplication formed after a graft of normal wing bud polarizing zone. Thus, polarizing activity appears to be weak in ta2. Grafts of normal polarizing zone to the posterior edge of ta2 wing buds had no effect on the ta2 phenotype. This result suggests that a weakly functioning polarizing signal does not account for the altered anteroposterior polarity in ta2 limbs, and that normal polarizing zone activity is not sufficient for formation of normal limb bud cartilages. We demonstrated that transmission of a polarizing signal through the ta2 limb mesoderm was normal. In addition, ta2 anterior border mesoderm had no polarizing activity. We also assessed the ability of ta2 limb bud mesoderm to respond to a polarizing signal. Either normal polarizing zone tissue or a bead containing retinoic acid was placed at the anterior edge of ta2 wing buds at stages 18-23. Both polarizing zone and retinoic acid caused respecification of the ta2 wing anteroposterior axis. The result was that a ta2 ulna replaced the radius, and the most posterior digit was duplicated anteriorly. Limb cartilages with normal morphology never formed. When a bead containing retinoic acid was placed at the posterior edge of ta2 wing buds, there was no effect on anteroposterior pattern. However, beads with retinoic acid always caused a reduction in the number of ta2 wing digits which formed, whether the beads were placed at the anterior or posterior edge of the developing ta2 limb.

Animals↗
PubMed1992

Expression patterns of engrailed-like proteins in the chick embryo.

The protein products of both of the identified chick engrailed-like (En) genes, chick En-1 and chick En-2, are localized in cells of the developing brain, mandibular arch, spinal cord, dermatome, and ventral limb bud ectoderm, as demonstrated by labeling with the polyclonal antiserum alpha Enhb-1 developed by Davis et al. (Development 111:281-298, 1991). A subpopulation of cephalic neural crest cells is also En-protein-positive. The monoclonal antibody 4D9 recognizes the chick En-2 gene product exclusively (Patel et al.: Cell 58:955-968, 1989; Davis et al., 1991) and colocalizes with chick En-2 mRNA in the developing head region of the chick embryo as shown by in situ hybridization (Gardner et al.: J. Neurosci. Res. 21:426-437, 1988). In the present study we examine the pattern of alpha Enhb-1 and 4D9 localization throughout the chick embryo from the first appearance of antibody (Ab)-positive cells at stage 8 (Hamburger and Hamilton: J. Morphol. 88:49-92, 1951) through stage 28 (1-5.5 days). We compare the localization patterns of the two Abs to each other, as well as to the localization of the monoclonal Ab, HNK-1, which recognizes many neural crest cells, using double- and triple-label fluorescence immunohistochemistry. Most En protein-positive cells in the path of neural crest cell migration are not HNK-1 positive. In detailed examination of alpha Enhb-1 and 4D9 localization, we find previously undetected patterns of En protein localization in the prechordal plate, hindbrain, myotome, ventral body-wall mesoderm, and extraembryonic membranes. Based upon these observations we propose: 1) that En expression in the mesoderm may be induced through interaction with En expressing cells in the neuroectoderm; 2) that En expression in the head mesenchyme is associated with somitomere 4; and 3) that En expression may be involved in epithelial-mesenchymal cell transformations.

Animals↗