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PubMed2000

Srf(-/-) ES cells display non-cell-autonomous impairment in mesodermal differentiation.

The serum response factor (SRF) transcription factor is essential for murine embryogenesis. SRF+(-/-) embryos stop developing at the onset of gastrulation, lacking detectable mesoderm. This developmental defect may reflect cell-autonomous impairment of SRF(-/-) embryonic cells in mesoderm formation. Alternatively, it may be caused by a non-cell-autonomous defect superimposed upon inappropriate provision of mesoderm-inducing signals to primitive ectodermal cells. We demonstrate that the ability of SRF(-/-) embryonic stem (ES) cells to differentiate in vitro into mesodermal cells is indeed impaired. However, this impairment can be modulated by external, cell-independent factors. Retinoic acid, but not dimethylsulfoxide, permitted activation of the mesodermal marker gene T(Bra), which was also activated when SRF was expressed in SRF(-/-) ES cells. Embryoid bodies from SRF(-/-) ES cell aggregates also activated mesodermal marker genes, but displayed unusual morphologies and impairment in cavitation. Finally, in nude mice, Srf(-/-) ES cells readily differentiated into mesodermal cells of SRF(-/-) genotype, including cartilage, bone or muscle cells. We demonstrate that SRF contributes to mesodermal gene expression of ES cells and that SRF(-/-) ES cells display a non-cell-autonomous defect in differentiation towards mesoderm.

Animals↗
PubMed1994

fgfr-1 is required for embryonic growth and mesodermal patterning during mouse gastrulation.

Experiments in amphibians have implicated fibroblast growth factors (FGFs) in the generation and patterning of mesoderm during embryogenesis. We have mutated the gene for fibroblast growth factor receptor 1 (fgfr-1) in the mouse to genetically dissect the role of FGF signaling during development. In the absence of fgfr-1 signaling, embryos displayed early growth defects; however, they remained capable of gastrulating and generating mesoderm. The nascent mesoderm of fgfr-1 homozygous mutant embryos differentiated into diverse mesodermal subtypes, but mesodermal patterning was aberrant. Somites were never generated and axial mesoderm was greatly expanded at the expense of paraxial mesoderm. These results suggest that FGFR-1 transduces signals that specify mesodermal cell fates and regional patterning of the mesoderm during gastrulation.

Animals↗
PubMed2001

biniou (FoxF), a central component in a regulatory network controlling visceral mesoderm development and midgut morphogenesis in Drosophila.

The subdivision of the lateral mesoderm into a visceral (splanchnic) and a somatic layer is a crucial event during early mesoderm development in both arthropod and vertebrate embryos. In Drosophila, this subdivision leads to the differential development of gut musculature versus body wall musculature. Here we report that biniou, the sole Drosophila representative of the FoxF subfamily of forkhead domain genes, has a key role in the development of the visceral mesoderm and the derived gut musculature. biniou expression is activated in the trunk visceral mesoderm primordia downstream of dpp, tinman, and bagpipe and is maintained in all types of developing gut muscles. We show that biniou activity is essential for maintaining the distinction between splanchnic and somatic mesoderm and for differentiation of the splanchnic mesoderm into midgut musculature. biniou is required not only for the activation of differentiation genes that are expressed ubiquitously in the trunk visceral mesoderm but also for the expression of dpp in parasegment 7, which governs proper midgut morphogenesis. Activation of dpp is mediated by specific Biniou binding sites in a dpp enhancer element, which suggests that Biniou serves as a tissue-specific cofactor of homeotic gene products in visceral mesoderm patterning. Based upon these and other data, we propose that the splanchnic mesoderm layers in Drosophila and vertebrate embryos are homologous structures whose development into gut musculature and other visceral organs is critically dependent on FoxF genes.

Alleles↗
PubMed1982

Differentiation of the metameric pattern in the embryonic axis of the mouse. II. Somitomeric organization of the presomitic mesoderm.

The formation of the embryonic axis is brought about by the continuous recruitment of cells from the primitive streak, and at later stages from the tail bud. Presumptive somitic cells are first incorporated into presomitic mesoderm before they emerge as metamerically arranged somites. When the presomitic mesoderm was examined in stereo with the scanning electron microscope (SEM), mesenchymal cells were found to be already organized into segmental units. These segmental units are called somitomeres because of their striking similarity to structures in the embryonic axis of the chick embryo described by Meier [16]. Cells within the somitomere are arranged in concentric whorls about a core center, bisected by a medio-lateral seam which subdivides the cell population into anterior and posterior halves. The concentric configuration of the cells is most easily observed along the medial face of the presomitic mesoderm when it is generally wedge-shaped. Even tough the units are tandemly contiguous, somitomeric interfaces are distinguished by abrupt change in cellular orientation. Despite a nearly two-fold fluctuation in the overall size of the presomitic mesoderm during embryonic development, a relatively constant number of somitomeres (six) is found in tandem sequence. Somitomeric maturation culminating in somite formation involves compaction of the cell population, more orderly alignment of cells, reduction in extracellular space, and changes in the shape of the somitomere concomitant with neurulation. Though the more mature somitomere is about 70% the size of the most recently formed somitomere at the caudal end of the presomitic mesoderm, the average size of each somitomere is adjusted proportionally to the overall length of the presomitic mesoderm. In vitro culture of the presomitic mesoderm shows a direct developmental lineage between the somitomere and the somite, suggesting that somite formation is a morphologic manifestation of a somitomeric pattern laid down at an earlier stage in development. The somitomeric pattern in the paraxial mesoderm is the earliest recognizable morphologic evidence of metamerism in the embryonic axis. This pattern is later emulated by other tissues that are topographically associated with the paraxial mesoderm.

Animals↗
PubMed1995

Comparison of mesoderm-inducing activity with monomeric and dimeric inhibin alpha and beta-A subunits on Xenopus ectoderm.

Activin possesses mesoderm-inducing activity, erythroid-differentiating activity, and follicle-stimulating hormone-releasing activity. The chemical structures of the activin molecule are formed by a combination of two beta-subunit peptides of inhibin. Inhibin is a dimer consisting of an alpha and beta subunit. To examine the mesoderm-inducing activity of these substances, we tested several configurations including: (1) two types of alpha-subunit peptide; (2) two types of inhibin A and B dimer; (3) beta A-subunit peptide monomer; (4) three types of activins A, AB and B, and (5) follistatin (activin-binding protein) by the animal cap assay using Xenopus laevis ectoderm, and by the erythroid-differentiating factor (EDF) test. Activins, which are composed of dimeric inhibin beta A- or beta B-subunit peptides, had the highest mesoderm-inducing and EDF activities. The monomeric beta A-subunit peptide exhibited mesoderm-inducing and EDF activities that were much lower than activin A. The inhibitory effect of follistatin on mesodermal induction by the beta A-subunit peptide was also lower than that of activin. Both inhibins A and B had very weak mesoderm-inducing activity and no EDF activity. The two types of inhibin alpha-subunit monomer had little mesoderm-inducing activity and no EDF activity. The mesoderm induction caused by activin A was not suppressed by the addition of the alpha-subunit monomer and inhibin. The mesoderm-inducing activity in relation to the chemical structures of the monomeric and/or dimeric inhibin alpha and beta A subunits is discussed.

Activins↗
PubMed2004

Notch signaling patterns Drosophila mesodermal segments by regulating the bHLH transcription factor twist.

One of the first steps in embryonic mesodermal differentiation is allocation of cells to particular tissue fates. In Drosophila, this process of mesodermal subdivision requires regulation of the bHLH transcription factor Twist. During subdivision, Twist expression is modulated into stripes of low and high levels within each mesodermal segment. High Twist levels direct cells to the body wall muscle fate, whereas low levels are permissive for gut muscle and fat body fate. We show that Su(H)-mediated Notch signaling represses Twist expression during subdivision and thus plays a critical role in patterning mesodermal segments. Our work demonstrates that Notch acts as a transcriptional switch on mesodermal target genes, and it suggests that Notch/Su(H) directly regulates twist, as well as indirectly regulating twist by activating proteins that repress Twist. We propose that Notch signaling targets two distinct 'Repressors of twist' - the proteins encoded by the Enhancer of split complex [E(spl)C] and the HLH gene extra machrochaetae (emc). Hence, the patterning of Drosophila mesodermal segments relies on Notch signaling changing the activities of a network of bHLH transcriptional regulators, which, in turn, control mesodermal cell fate. Since this same cassette of Notch, Su(H) and bHLH regulators is active during vertebrate mesodermal segmentation and/or subdivision, our work suggests a conserved mechanism for Notch in early mesodermal patterning.

Animals↗
PubMed2005

FGF signalling and the mechanism of mesoderm spreading in Drosophila embryos.

FGF signalling is needed for the proper establishment of the mesodermal cell layer in Drosophila embryos. The activation of the FGF receptor Heartless triggers the di-phosphorylation of MAPK in the mesoderm, which accumulates in a graded fashion with the highest levels seen at the dorsal edge of the mesoderm. We have examined the specific requirement for FGF signalling in the spreading process. We show that only the initial step of spreading, specifically the establishment of contact between the ectoderm and the mesoderm, depends upon FGF signalling, and that unlike the role of FGF signalling in the differentiation of heart precursors this function cannot be replaced by other receptor tyrosine kinases. The initiation of mesoderm spreading requires the FGF receptor to possess a functional kinase domain, but does not depend upon the activation of MAPK. Thus, the dispersal of the mesoderm at early stages is regulated by pathways downstream of the FGF receptor that are independent of the MAPK cascade. Furthermore, we demonstrate that the activation of MAPK by Heartless needs additional cues from the ectoderm. We propose that FGF signalling is required during the initial stages of mesoderm spreading to promote the efficient interaction of the mesoderm with the ectoderm rather than having a long range chemotactic function, and we discuss this in relation to the cellular mechanism of mesoderm spreading.

Animals↗
PubMed2006

Mesoderm progenitor cells of common origin contribute to the head musculature and the cardiac outflow tract.

During early embryogenesis, heart and skeletal muscle progenitor cells are thought to derive from distinct regions of the mesoderm (i.e. the lateral plate mesoderm and paraxial mesoderm, respectively). In the present study, we have employed both in vitro and in vivo experimental systems in the avian embryo to explore how mesoderm progenitors in the head differentiate into both heart and skeletal muscles. Using fate-mapping studies, gene expression analyses, and manipulation of signaling pathways in the chick embryo, we demonstrate that cells from the cranial paraxial mesoderm contribute to both myocardial and endocardial cell populations within the cardiac outflow tract. We further show that Bmp signaling affects the specification of mesoderm cells in the head: application of Bmp4, both in vitro and in vivo, induces cardiac differentiation in the cranial paraxial mesoderm and blocks the differentiation of skeletal muscle precursors in these cells. Our results demonstrate that cells within the cranial paraxial mesoderm play a vital role in cardiogenesis, as a new source of cardiac progenitors that populate the cardiac outflow tract in vivo. A deeper understanding of mesodermal lineage specification in the vertebrate head is expected to provide insights into the normal, as well as pathological, aspects of heart and craniofacial development.

Animals↗
PubMed1987

An ECM substratum allows mouse mesodermal cells isolated from the primitive streak to exhibit motility similar to that inside the embryo and reveals a deficiency in the T/T mutant cells.

The mesodermal cell layer is created by ingression and migration of the cells from the primitive streak region in mouse embryos on day 7 of pregnancy. In order to study the mechanisms of mesodermal cell migration during development, the mesodermal cells isolated from the primitive streak were cultured on various substrata, and cell behaviour and motility were analysed with a time-lapse video system. The mesodermal cells on the surface of extracellular matrix (ECM)-coated dishes (ECM produced by bovine corneal endothelial cells) showed extensive migration at a mean rate of approx. 50 micron h-1. They also showed frequent cell division and exhibited contact paralysis of lamellipodia and contact inhibition of movement. On plastic or glass surfaces, however, the mesodermal cells became more flattened and less motile (approx. 20-30 micron h-1). Cell shape and mean rate of movement on the ECM were very similar to those in situ, as investigated in a previous study (Nakatsuji, Snow & Wylie, 1986). Therefore, this culture condition could provide a useful experimental system for analysing the cellular basis of normal and abnormal morphogenetic movements in mouse embryos. Employing such a culture system, we studied motility of the mesodermal cells from embryos homozygous for Brachyury (T) mutation, which are lethal at the midgestation stage in utero. Histological observations have suggested that anomalous morphogenesis of the T/T embryos may be brought about by defects in migration of the mesodermal cells derived from the primitive streak. When mesodermal cells from the primitive streak of the T/T mutant embryos on days 8-9 were cultured on the ECM substratum, mean rate of cell migration was significantly reduced compared to cells from normal embryos. Results support the idea of retarded migration by the mutant mesodermal cells as an important factor causing abnormalities in morphogenesis.

Animals↗
PubMed1990

A new homeobox-containing gene, msh-2, is transiently expressed early during mesoderm formation of Drosophila.

Many homeobox-containing genes of Drosophila regulate pathways of differentiation. These proteins probably function as promoter- or enhancer-selective transcription factors. We have isolated a new homeobox-containing gene, msh-2, by means of the polymerase chain reactions (PCR) using redundant primers. msh-2 is specifically expressed in mesodermal primordia during a short time period early in development. It first appears at blastoderm stage just before the ventral invagination of the mesoderm and shortly after twist, a gene required for mesoderm formation, is expressed. During germband elongation all the mesodermal cells in the segmented part of the embryo express msh-2, but soon afterwards msh-2 becomes restricted to the dorsal mesoderm, which includes the primordia for the visceral musculature and the heart. Prior to muscle differentiation, msh-2 expression ceases, except for two rows of cells that will be included in the dorsal vessel. Embryos that are deficient for the chromosomal region, 93C-F, which includes the msh-2 gene, show normal mesoderm invagination and dorsal spreading. However, later in development no visceral muscle and dorsal vessel differentiation can be detected, but some skeletal muscles do form, albeit abnormally. msh-2 expression, except for a patch in the head, is dependent on twist function. On the other hand, snail, another mesoderm determinant, does not appear to be required for msh-2 initiation, but is necessary for the maintenance of msh-2 expression after germband elongation. H2.0, a homeo-box-containing gene specifically expressed in visceral mesoderm, is not transcribed in the mesoderm in 93C-F deficiency embryos.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1999

Differential patterning of ventral midline cells by axial mesoderm is regulated by BMP7 and chordin.

Ventral midline cells in the neural tube have distinct properties at different rostrocaudal levels, apparently in response to differential signalling by axial mesoderm. Floor plate cells are induced by sonic hedgehog (SHH) secreted from the notochord whereas ventral midline cells of the rostral diencephalon (RDVM cells) appear to be induced by the dual actions of SHH and bone morphogenetic protein 7 (BMP7) from prechordal mesoderm. We have examined the cellular and molecular events that govern the program of differentiation of RDVM cells under the influence of the axial mesoderm. By fate mapping, we show that prospective RDVM cells migrate rostrally within the neural plate, passing over rostral notochord before establishing register with prechordal mesoderm at stage 7. Despite the co-expression of SHH and BMP7 by rostral notochord, prospective RDVM cells appear to be specified initially as caudal ventral midline neurectodermal cells and to acquire RDVM properties only at stage 7. We provide evidence that the signalling properties of axial mesoderm over this period are regulated by the BMP antagonist, chordin. Chordin is expressed throughout the axial mesoderm as it extends, but is downregulated in prechordal mesoderm coincident with the onset of RDVM cell differentiation. Addition of chordin to conjugate explant cultures of prechordal mesoderm and neural tissue prevents the rostralization of ventral midline cells by prechordal mesoderm. Chordin may thus act to refine the patterning of the ventral midline along the rostrocaudal axis.

Animals↗
PubMed1987

The formation of mesodermal tissues in the mouse embryo during gastrulation and early organogenesis.

Orthotopic grafts of [3H]thymidine-labelled cells have been used to demonstrate differences in the normal fate of tissue located adjacent to and in different regions of the primitive streak of 8th day mouse embryos developing in vitro. The posterior streak produces predominantly extraembryonic mesoderm, while the middle portion gives rise to lateral mesoderm and the anterior region generates mostly paraxial mesoderm, gut and notochord. Embryonic ectoderm adjacent to the anterior part of the streak contributes mainly to paraxial mesoderm and neurectoderm. This pattern of colonization is similar to the fate map constructed in primitive-streak-stage chick embryos. Similar grafts between early-somite-stage (9th day) embryos have established that the older primitive streak continues to generate embryonic mesoderm and endoderm, but ceases to make a substantial contribution to extraembryonic mesoderm. Orthotopic grafts and specific labelling of ectodermal cells with wheat germ agglutinin conjugated to colloidal gold (WGA-Au) have been used to analyse the recruitment of cells into the paraxial mesoderm of 8th and 9th day embryos. The continuous addition of primitive-streak-derived cells to the paraxial mesoderm is confirmed and the distribution of labelled cells along the craniocaudal sequence of somites is consistent with some cell mixing occurring within the presomitic mesoderm.

Animals↗
PubMed1975

The function of the ectodermal apical ridge and distinctive characteristics of adjacent distal mesoderm in the avian wing-bud.

Blocks of mesoderm about 0-1 mm in diameter were isolated from various regions of chick wing-buds of stages 17 through 22 and cultured individually, or sometimes in pairs, in microtest plate wells. Cell deaths had occurred after 10 h of culture in those explants that had come from the region associated with the thickest part of the ectodermal ridge, and after 11-12 h in all other mesoderm. When the adjacent ectodermal ridge was left attached to the mesodermal block there were almost no cell deaths for up to 24 h of culture. When the dorsal ectoderm immediately proximal to the apical ridge was left attached, but no ridge was present, cell deaths occurred just as they did in mesoderm with no ectoderm. When a number (usually six) of complete ridges were suspended in a wire basket at the top of a well, cell deaths did not occur in a test mesodermal block at the bottom of the well (six of eight cases). These experiments support previous evivence for a special function of the ectodermal apical ridge in limb morphogenesis, and indicate that there is a chemical messenger. The cells that migrated from distal mesodermal explants (the band up to 0-15 mm from the apical ridge) differed sharply in morphology and behavior from those coming from explants from any more proximal region. Within the proximal mesoderm there was a less striking variation alons the antero-posterior axis. These observations reveal that there is present even at early stages a detailed pattern within the mesoderm of the limb-bud. The particularly striking and distinctive characteristics of that mesoderm closest to the apical ectodermal ridge provide new possibilities for the understanding of the function of the ridge in limb morphogenesis.

Animals↗
PubMed1985

Mesoderm induction in Xenopus laevis: a quantitative study using a cell lineage label and tissue-specific antibodies.

We have compared the development of the animal pole (AP) region of early Xenopus embryos in normal development, in isolation, and in combination with explants of tissue from the vegetal pole (VP) region. For the grafts and the combinations the animal pole tissue was lineage labelled with FLDx in order to ascertain the provenance of the structures formed. The normal fate of the AP region was determined by orthotopic grafts at stages 7 1/2 (early blastula), 8 (mid blastula) and 10 (early gastrula). At later stages most of the labelled cells were found in ectodermal tissues such as epidermis, head mesenchyme and neural tube (the last from stages 7 1/2 and 8 only). However, in stage-7 1/2 and stage-8 grafts some of the labelled cells were also found in the myotomes and lateral mesoderm. In isolated explants the AP region of all three stages differentiated only as epidermis assessed both histologically and by immunofluorescence using an antibody to epidermal keratin. The fate of labelled cells in AP-VP combinations was quite different and confirms the reality of mesoderm induction. In combinations made at stages 7 1/2 and 8 the proportion of AP-derived mesoderm is substantially greater than the proportion of labelled mesoderm in the equivalent fate mapping experiments. This shows that the formation of mesoderm in such combinations is the result of an instructive rather than a permissive interaction. The formation of mesodermal tissues in stage-7 1/2 combinations was confirmed by using a panel of antibodies which react with particular tissues in normal tailbud-stage embryos: anti-keratan sulphate for the notochord, anti-myosin for the muscle and anti-keratin for epidermis and notochord. Combinations made at stage 10 gave no positive cases and reciprocal heterochronic combinations between stages 7 1/2 and 10 showed that this is the result of a loss of competence by the stage-10 AP tissue. Whereas stage-7 1/2 AP tissue combined with stage-10 VP tissue gave many positive cases, the reciprocal experiment gave only a few. We have also tested the regional specificity of the induction. Stage-7 1/2 vegetal pole explants were divided into dorsal and ventral regions and then combined, separately, with stage-7 1/2 animal poles. The dorsovegetal tissue induces 'dorsal-type' mesoderm (notochord and large muscle masses) while ventrovegetal tissue induces 'ventral-type' mesoderm (blood, mesothelium and a little muscle). We conclude that mesoderm formation in combinations is an instructive event and propose a double gradient model to explain the complex character of the response.

Animals↗
PubMed1981

Hepatic induction in the avian embryo: specificity of reactive endoderm and inductive mesoderm.

Mesoderm of precardiac and cardiac region ('cardiac' mesoderm) of chick, quail and mouse embryos could induce hepatic epithelium in the endoderm of the anterior half of young quail or chick embryos (anterior endoderm) in vitro as well as in vivo. No species specificity in the induction of hepatic epithelium by the 'cardiac' mesoderm could be observed. The hepatic induction, was controlled strictly by tissue specificity of both endoderm and mesoderm. Replacement of the 'cardiac' mesoderm or the anterior endoderm by non-cardiac mesoderms or endoderms other than the anterior endoderm resulted in failure of hepatic induction. Only the anterior endoderm was found to have competence for hepatic induction, indicating that it was committed, in unknown ways, to react with 'cardiac' mesoderm, and can properly be called pre-hepatic endoderm. Comparison between the development of hepatic endoderm and the hepatic induction potency of 'cardiac' mesoderm, which was most intense during 1- to 1.5- incubation days and decreased gradually with the increase of the stage, suggests that in normal development the 'cardiac' mesoderm actually induces hepatic epithelium in the competent endoderm. Hepatic-induction potency remained up to 6 days, and was found in truncus arteriosus, ventricle and auricle areas and in endocardial and myocardial layers of the heart.

Animals↗
PubMed2000

Can gastric endoderm change the regionally specific inducing ability of presumptive small intestinal mesoderm?

This study was designed to establish the source of gut mesoderm's ability to induce regional pattern in the endoderm. The most obvious possibility is induction by the endoderm through epithelial-mesenchymal interaction. To test this experimentally, reciprocal quail/chick combinations were prepared of early proventricular endoderm (that is already known to be regionally determined) and presumptive small intestinal mesoderm. The combinations were cultured for 7 days to allow for 'programming' of the mesoderm by the endoderm. After removal of the proventricular endoderm the mesoderm was combined with young gizzard endoderm. It is known that gizzard endoderm can be provoked to develop in either a proventricular or a small intestinal direction by association with the appropriate mesoderm. Thus, by combining intestinal mesoderm 'programmed' by association with proventricular endoderm with gizzard endoderm, the subsequent differentiation of the gizzard endoderm would indicate whether or not the inducing ability of the intestinal mesenchyme had been altered. In addition to such experimental grafts, three types of control graft were prepared. The results of the experiment, based on the morphology of the grafts and the immunocytochemical analysis of selected endocrine cell types, showed that in the majority of cases the gizzard endoderm developed the features of small intestine, not those of proventriculus. This indicates that at the stages studied, endoderm does not act to program mesoderm with which it is associated. If this does occur, it must take place at an earlier stage, i.e., before the time of explantation of the presumptive small intestinal mesoderm (1.25 days of incubation).

Animals↗
PubMed1992

Cell interaction and its role in mesoderm cell migration during Xenopus gastrulation.

In the Xenopus gastrula, the mesoderm moves as a coherent cell aggregate across the blastocoel roof toward the animal pole. We show that the cohesion of the mesoderm is not only mechanically necessary, but that aggregate formation has profound effects on the migratory behavior of mesoderm cells. Whereas isolated mesoderm cells are bi- or multipolar, move stepwise and change their direction of movement frequently, aggregated mesoderm cells migrating on their in vivo substrate appear unipolar and move continuously and persistently. Moreover, only mesoderm cell aggregates, but not single cells, can follow guidance cues present in the extracellular matrix of the blastocoel roof substrate. Thus, the cohesion of the mesodermal cell mass is an essential feature of mesoderm migration during Xenopus gastrulation. We show that the Ca(2+)-dependent cell adhesion molecule U-cadherin is involved in mediating this cohesion.

Animals↗
PubMed1994

Precardiac mesoderm is specified during gastrulation in quail.

The establishment of precardiac mesoderm and the role of anterolateral endoderm and ectoderm in regulating heart muscle cell development have been studied in quail using explant cultures. Mesoderm from precardiac regions of stage 4(+)-6 embryos was explanted alone or in combination with adjacent endoderm or ectoderm, cultured for 12 to 72 hr in several types of culture media, and then assayed by morphological and immunocytochemical criteria for the presence of differentiated cardiac myocytes. Results show that mesoderm from heart forming regions is capable of differentiating into beating cardiac myocytes in a defined medium lacking potential signaling molecules by stage 4+, the earliest time at which we could isolate mesoderm from adjacent cell layers. Although an interaction with anterolateral endoderm from stage 4+ onward is therefore not required for the specification of precardiac mesoderm in quail, explants consisting of mesoderm plus endoderm show an enhanced rate of myocyte differentiation and a shortened delay between expression of myosin heavy chain and the onset of beating. Endoderm also plays a central role in early heart morphogenesis since beating heart tubes form only in explants that contain both mesoderm and endoderm. In contrast, ectoderm from stage 4(+)-5+ embryos does not support development of precardiac mesoderm. These results suggest that early heart muscle cell development involves an initial specification step that occurs prior to or during gastrulation and which leads to the appearance of myocardial precursor cells, and a subsequent differentiation step during which endoderm plays a central role in enhancing the rate of myocyte differentiation and the degree of heart tube morphogenesis.

Animals↗