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PubMed1992

Expression of collagenase and IL-1 alpha in developing rat hearts.

During development, extracellular matrix (ECM) molecules are thought to play a major role in regulating the formation of the heart. The change in the heart from a simple tube to a complex, four-chambered organ requires the modification of both the cellular components as well as the surrounding ECM. Matrix metalloproteinases (MMP), which include collagenases, are enzymes present in the ECM that have the potential to modify the existing ECM during the development of the heart. Using both monoclonal and polyclonal antisera against collagenase, specific temporal and spatial patterns have been documented during critical periods of heart development. The cytokine interleukin 1 alpha (IL-1 alpha), a potent inducer of the MMP expression, was also shown to have a similar staining pattern in the developing heart. The monoclonal anti-rat collagenase (Mab) intensely stained the surfaces of the myocytes in the trabeculae and the ventricular and atrial walls of the 11.5 or 12.5 embryonic day (ED) rat hearts. In contrast, the polyclonal anti-human collagenase (Pab) stained not only the cardiomyocytes but also the hypertrophic endocardial cells. Pab appeared to stain the leading edge of the mesenchymal cells that migrate into the cardiac jelly of the 11.5 or 12.5 ED hearts. Immunohistochemical staining showed IL-1 alpha on the endocardial endothelium and the surface of cardiomyocytes near the cardiac jelly just before or coincident with the appearance of migrating cells. IL-1 alpha was detected on the endocardial endothelium, cardiomyocytes in the trabeculae, and the ventricular and atrial walls, as well as in the myocardial basement membrane of the truncal or atrioventricular region. However, no staining could be detected on the migrating cells in the cardiac cushions. These results indicate the presence of collagenase and IL-1 alpha on the surface of cardiomyocytes and mesenchymal cells at times when the heart is undergoing acute remodeling during septation and trabeculation. These data suggest a role for collagenase/cytokine interaction in tissue remodeling during critical stages of cardiac embryogenesis where modification of the ECM is essential to cardiac morphogenesis.

Animals↗
PubMed1991

Decreased 1,2-diacylglycerol levels in myopathic hamster hearts during the development of heart failure.

1,2-Diacylglycerol is believed to play an important role in cellular functions through protein kinase C activation, although its role in cardiac functions remains largely unexplored. We determined the level of 1,2-diacylglycerol and its fatty acid composition in heart tissues from Syrian hamsters with hereditary cardiomyopathy (BIO 14.6 strain) during the development of congestive heart failure from 90 days to 240 days of age. The myopathic hamsters had lower contents of triglyceride and of the major phospholipids, phosphatidylcholine, phosphatidylethanolamine and cardiolipin, in the myocardium when compared to normal hamsters, whereas there was no difference in the cholesterol content. No difference in the myocardial 1,2-diacylglycerol content was observed at 90 days of age. On the other hand, 1,2-diacylglycerol contents in myopathic hearts at 160 and 240 days of age were significantly lower by 21% and 52%, respectively, then in age-matched normal hamsters. The oldest hamsters (240-day-old) showed reduced 1,2-diacylglycerol levels in both groups despite an age-related increase in most lipids. The 1,2-diacylglycerol fatty acid composition profile was found to be different from that of other lipids, and there were several differences in the fatty acid composition of 1,2-diacylglycerol between the two groups at 240 days of age. These results indicate that decreased levels of 1,2-diacylglycerol occur concomitantly with congestive heart failure in the myopathic hamsters.

Animals↗
PubMed2005

Changes of chymase, angiotensin converting enzyme and angiotensin II type 1 receptor expressions in the hamster heart during the development of heart failure.

BACKGROUND: Little is known about the role of dual angiotensin II forming pathways during heart failure. In the present study, the changes of chymase and angiotensin converting enzyme (ACE) expressions in the failing hearts of hamsters were analysed. METHODS: Heart failure was induced by ligation of left anterior descending branch of the coronary artery. Chymase, ACE and angiotensin II type 1 receptor (AT1R) mRNA levels were analysed by reverse transcription polymerase chain reaction (RT-PCR). The activities of chymase and ACE were determined by radioimmunoassay (RIA). Myocardial collagen fibre analysis was performed under optical microscope. RESULTS: Left ventricular systolic pressure (LVSP) and maximum left ventricular developed pressure increase rate (dp/dtmax, mmHg/s) gradually moved lower at 2, 3, 4 and 8 weeks after operation. On the other hand, left ventricular end-diastolic pressure (LVEDP) increased gradually after operation. Compared with the control group (3.55 +/- 0.06, 4.79 +/- 0.70), the heart weight/body weight ratio in operation group had increased significantly at 4 weeks and 8 weeks (4.28 +/- 0.43, 6.17 +/- 0.73) (P < 0.01). Collagen staining showed that the quantity of myocardial collagen fibre increased significantly in the operation group. RT-PCR showed that the chymase mRNA level in the operation group was consistently greater than that in the control group. AT1R mRNA level was also increased significantly at 3 weeks and 4 weeks, both being 1.3 times that of the control group (P < 0.01), whereas ACE mRNA level was not changed. Higher activity of chymase was detected in operation group, being 4, 8, 13 and 19 times that of the control group at 2, 3, 4 and 8 weeks (P < 0.01), respectively. ACE activity was also significantly higher at the same time, being 7, 10, 10 and 3.5 times that of the control (P < 0.01). Angiotensin II (Ang II) level in operation group increased significantly, being 2.5, 2.7, 3.5 and 2 times that of the control group at 2, 3, 4 and 8 weeks, respectively (P < 0.01). CONCLUSIONS: A dual Ang II forming pathway from both ACE and chymase in the hamster hearts plays an important role during the development of heart failure. At the decompensatory stage, the reduction of AngII level may be associated with the decrease of ACE activity.

Angiotensin II↗
PubMed2006

Developmental regulation of cardiac MAP4 protein expression.

It has been shown that the level of expression of microtubule-associated protein 4 (MAP4) mRNAs changes throughout neonatal heart development [Chapin SJ, et al. 1995. Biochemistry 34:2289]. In the present study, both immunofluorescence and western blotting methods were used to monitor MAP4 protein expression levels in the developing heart. By both methods, it was shown that the levels of total MAP4 protein were maximal during the first postnatal week, and then declined progressively to adulthood. In addition, four major electrophoretic species that reacted with MAP4-specific antibodies (called bands 1-4) were observed in all heart tissue samples. Three of the four bands decreased in abundance throughout postnatal development, but at different rates. The fourth band remained relatively constant in abundance with increasing postnatal age. To determine if phosphorylation events might contribute to this heterogeneity, western blotting experiments using phospho-specific antibodies and phosphatase digestion of extract samples were performed. No phosphorylation-specific antibody staining was observed and no significant changes were demonstrated in the bands after phosphatase treatment, implying that the observed complexity was due mainly to alternative start site or differential isoform expression. Finally, it was discovered that cardiomyocyte MAP4 associated with drug- and cold-stable microtubules in early neonatal myocytes. Thus, the complex regulation of MAP4 protein expression may play a key role in the functional differentiation of myocyte microtubules during heart development.

Alkaline Phosphatase↗
PubMed1999

Expression of the Mf1 gene in developing mouse hearts: implication in the development of human congenital heart defects.

The transcription factor FKHL7 gene has recently been associated with the anterior segment dysgenesis disorder of the eye known as Axenfeld-Rieger anomaly (ARA). A growing body of evidence indicates that mutations in FKHL7 cause not only defects in the anterior segment of the eye but defects in the heart valves and septa as well. In order to evaluate its contribution to normal heart septation and valve formation, expression of the mouse homologue Mf1 in embryonic hearts was analyzed by in situ hybridization. A weak but significant level of Mf1 expression could be detected in the endocardium of mouse embryos as early as day 8.5 post-conception (p.c.). Mf1 expression was undetectable in the hearts of day 9.5 p.c. embryos, but by day 10.5-11 p.c., Mf1 transcripts could be found again in the endocardium of both the atrium and ventricle and a relatively strong signal was observed in the dorsal portion of the septum primum, in what appeared to be the spinal vestibule. At day 13 p.c. when aortic and pulmonary trunks are separated, relatively more Mf1 transcripts were detected in the leaflets of aortic, pulmonary, and venous valves, the ventral portion of the septum primum, as well as in the single layer of cells on the edges of the atrioventricular cushion tissues. Surprisingly, there was no signal detected in the developing interventricular septum. At day 15 p.c., overall Mf1 signals were greatly decreased. However, significant levels of expression could still be observed in the atrial septum, the tricuspid valve, the mitral valve, and in the venous valve but not in the interventricular septum. The temporal and spatial expression patterns of the Mf1 gene in developing mouse hearts suggest that Mf1 may play a critical role in the formation of valves and septa with the exception of the interventricular septum. This is further supported by our studies showing that mutations in the FKHL7 gene were associated with defects in the anterior segment of the eye as well as atrial septal defects or mitral valve defects. Dev Dyn 1999;216:16-27.

Animals↗
PubMed1990

Changes in myofibrillar activation and troponin C Ca2+ binding associated with troponin T isoform switching in developing rabbit heart.

Postnatal development of the mammalian heart is associated with changes in the population of isoforms of the thin filament proteins. We correlated the change in thin filament proteins, which occur in rabbit hearts between 5 days and 22 days of age, with changes in Ca2+ dependence of myofibrillar ATPase activity, force generation, and troponin C Ca2+ binding. The preparations derived from the 5-day-old animals exhibited a high molecular weight isoform of troponin T not found in the hearts of the 22-day-old animals. Other troponin T isoforms were also found to be present in different relative amounts. No other major differences in thin filament protein composition could be identified. Compared with the 5-day-old rabbit heart preparations, the ATPase activity of myofibrils from 22-day-old rabbit hearts exhibited a reduced Ca2+ sensitivity. The pCa50 (negative log of the half-maximal-activity free Ca2+) of the MgATPase activity was shifted by 0.15 pCa units with maturation. Maturation of the myofibrils was also associated with an increased effect of Mg2+ on pCa50. On increasing the Mg2+ from 2 to 10 mM at constant MgATP2-, the pCa50 of 5-day myofibrils was increased (shifted to the right) by 0.39 pCa units for 5-day-old rabbit hearts and 0.45 pCa units for 22-day-old rabbit hearts. Although similar changes in pCa50 of force developed by myofibrils were marginally significant, fibers from hearts of 5-day-old rabbits exhibited a greater Hill coefficient than hearts from 22-day-old rabbits (3.0 vs. 2.1). Despite the increased sensitivity of 5-day-old rabbit hearts to Ca2+, these hearts exhibited significantly less Ca2+ bound to myofibrillar troponin C than did the 22-day-old rabbit hearts. Moreover, the models that best described the Ca2+ binding data are different for the two age groups. Our data indicate that the Ca2+ activation and Ca2+ binding properties of myofibrillar troponin C are altered in developing cardiac myofibrils and that the changes in these properties may be influenced by changes in the troponin T isoforms present in the myofibril.

Animals↗
PubMed2002

Effects of different inotropic interventions on myocardial function in the developing rabbit heart.

The development of the mammalian heart is characterized by substantial changes in myocardial performance. We studied the ontogeny of myocardial function with and without various inotropic interventions in the developing isolated, antegrade-perfused rabbit heart (2d, 8d, 14d, 28d, n = 96). Myocardial function was related to the protein expression of the sarcolemmal Na(+)-Ca2+ exchanger and to the sarcoplasmic Ca(2+)-ATPase. In neonatal hearts an age-dependent increase in maximal developed pressure velocity (dP/dtmax) by 45% and peak negative pressure velocity (dP/ dtmin) by 75% within days 2 to 8 were observed. In response to inotropic intervention with isoproterenol, ouabain, calcium and the Na(+)-channel modulator BDF 9148, dP/dtmax and dP/dtmin increased in a concentration dependent manner. Significant differences between neonatal, juvenile and adult hearts could be demonstrated in a repeated measurement ANOVA model on the concentration-response curves for BDF 9148 (dP/dtmax and dP/dtmin), ouabain (dP/dtmin) and calcium (dP/dtmin), but not for isoproterenol. At the maximum isoproterenol concentration of 1 micromol/l, the increase in dP/dtmax and dP/dtmin was significantly higher in adult compared to neonatal hearts (t-test, p < 0.01). The significant decline of the Na(+)-Ca2+ exchanger protein expression from neonatal (1822 +/- 171) to adult hearts (411 +/- 96 S.E.M. [units per 20 microg protein], p < 0.01) was related to an increase in myocardial function (dP/dtmax r = 0.63, p < 0.01, dP/dtmin r = 0.62, p < 0.01). Contractility, relaxation and the observed positive inotropic effects were in general significantly lower in neonatal compared to adult hearts. In the individual heart an increase in contractility and relaxation was related to a decrease in Na(+)-Ca2+ exchanger expression.

Adrenergic beta-Agonists↗
PubMed2005

Form follows function: developmental and physiological view on ventricular myocardial architecture.

The arrangement of myocytes within the ventricle is critical for its contractile performance, as evidenced by significant functional impairment seen in cardiomyopathies associated with myofiber disarray or post-infarction remodeling. A review on this topic by Anderson and associates provides anatomical insight gained from a multitude of approaches, and concludes that the best concept is that of syncytial continuum with supporting collagenous matrix. The overall arrangement is in the form of several intertwined helices, and the authors find no support for a recently suggested ventricular myocardial band hypothesis. This commentary aims at providing a developmental and physiological perspective on this purely anatomical concept. Unlike some other organ systems, the developing heart has to function since very early stages to support the oxygen and nutrition demands of the growing embryo, thus putting some constraints on heart development. The ventricular myocardial architecture transforms from a single-layered tube through trabeculated stages into a mature form that relies on a multi-layered compact zone. The first evidence of helical patterns is found in trabeculated hearts during ventricular contraction, and layers with different helix pitch develop during later fetal stages as the compact zone thickens. The second major point determining ventricular contraction is the sequence of its electrical activation. The ventricular activation sequence changes concomitantly with its morphology, from slow peristaltoid through base-to-apex pattern found in looped trabeculated hearts, to mature apex-to-base direction. Thus, adult ventricular myocardial architecture is best understood when one also considers the way it developed together with its electrical activation sequence and contraction pattern.

Adult↗
PubMed2004

Heart and head defects in mice lacking pairs of connexins.

Gene ablation studies in mice have revealed roles for gap junction proteins (connexins) in heart development. Of the 20 connexins in vertebrates, four are expressed in developing heart: connexin37 (Cx37), connexin40 (Cx40), connexin43 (Cx43), and connexin45 (Cx45). Although each cardiac connexin has a different pattern of expression, some heart cells coexpress multiple connexins during cardiac morphogenesis. Since different connexins could have overlapping functions, some developmental phenotypes may only become evident when more than one connexin is ablated. In this study, we interbred Cx40(-/-) and Cx43(-/-) mice to generate mice lacking both Cx40 and Cx43. Cx40(-/-)Cx43(-/-) mice die around embryonic day 12.5 (E12.5), much earlier than either Cx40(-/-) or Cx43(-/-) mice, and they exhibit malformed hearts with ventricles that are abnormally rotated, suggesting a looping defect. Some Cx40(-/-)Cx43(-/-) animals also develop head defects characteristic of exencephaly. In addition, we examined mice lacking both Cx40 and Cx37 and found a high incidence of atrial and ventricular septal defects at birth. These results provide further evidence for the importance of gap junctions in embryonic development. Moreover, ablating different pairs of cardiac connexins results in distinct heart defects, suggesting both common and unique functions for Cx40, Cx43, and Cx37 during cardiac morphogenesis.

Animals↗
PubMed1997

Regulation of cardiac mesodermal and neural crest development by the bHLH transcription factor, dHAND.

dHAND and eHAND are related basic helix-loop-helix (bHLH) transcription factors that are expressed in mesodermal and neural crest-derived structures of the developing heart. In contrast to their homogeneous expression during avian cardiogenesis, during mouse heart development we show that dHAND and eHAND are expressed in a complementary fashion and are restricted to segments of the heart tube fated to form the right and left ventricles, respectively. dHAND and eHAND represent the earliest cardiac chamber-specific transcription factors yet identified. Targeted gene deletion of dHAND in mouse embryos resulted in embryonic lethality at embryonic day 10.5 from heart failure. Our description of the cardiac phenotype of dHAND mutant embryos is the first demonstration of a single gene controlling the formation of the mesodermally derived right ventricle and the neural crest-derived aortic arches and reveals a novel cardiogenic subprogramme for right ventricular development.

Animals↗
PubMed1998

Expression of type VI collagen in the developing mouse heart.

During development, the embryonic atrioventricular (AV) endocardial cushions undergo a morphogenic process to form mature valve leaflets and the membranous septa in the heart. Several extracellular matrix (ECM) proteins are expressed in the developing AV endocardial cushions, but it remains to be established if any specific ECM proteins are necessary for normal cushion morphogenesis. Abnormal development of the cardiac AV valves is a frequent cause of congenital heart defects, particularly in infants with trisomy 21 (Down syndrome). The genes encoding the alpha1 and alpha2 chains of type VI collagen are located on human chromosome 21 within the region thought to be critical for congenital heart defects in trisomy 21 infants. This suggests that the type VI collagen alpha1(VI) and alpha2(VI) chains may be important in normal AV valve morphogenesis. As a first step in understanding the role of type VI collagen in valve development, the authors examined the normal spatial and temporal expression patterns of mRNA and protein for type VI collagen in the embryonic mouse heart. Ribonuclease protection assay analysis demonstrates cardiac expression of the type VI collagen for alpha1(VI), alpha2(VI), and alpha3(VI) transcripts beginning at embryonic days 11-11.5 of mouse development. In situ hybridization studies demonstrate a coordinated pattern of cardiac expression within the AV valves for each type VI collagen chain from embryonic day 11.5 through the neonatal period. Immunohistochemical studies confirm a concentrated type VI collagen localization pattern in the endocardial cushions from the earliest stages of valve development through the neonatal period. These data indicate that type VI collagen is expressed in the developing AV canal in a pattern consistent with cushion tissue mesenchymal cell migration and proliferation, and suggest that type VI collagen plays a role in the morphogenesis of the developing cardiac AV endocardial cushions into the valve leaflets and membranous septa of the heart.

Animals↗
PubMed2006

Slit coordinates cardiac morphogenesis in Drosophila.

Slit is a secreted guidance cue that conveys repellent or attractive signals from target and guidepost cells. In Drosophila, responsive cells express one or more of three Robo receptors. The cardial cells of the developing heart express both Slit and Robo2. This is the first report of coincident expression of a Robo and its ligand. In slit mutants, cardial cell alignment, polarization and uniform migration are disrupted. The heart phenotype of robo2 mutants is similar, with fewer migration defects. In the guidance of neuronal growth cones in Drosophila, there is a phenotypic interaction between slit and robo heterozygotes, and also with genes required for Robo signaling. In contrast, in the heart, slit has little or no phenotypic interaction with Robo-related genes, including Robo2, Nck2, and Disabled. However, there is a strong phenotypic interaction with Integrin genes and their ligands, including Laminin and Collagen, and intracellular messengers, including Talin and ILK. This indicates that Slit participates in adhesion or adhesion signaling during heart development.

Animals↗
PubMed2003

Hopping to the beat. Hop regulation of cardiac gene expression.

Hop is a recently discovered homeodomain only protein with atypical characteristics. Unlike other homeodomain proteins, Hop lacks DNA binding activity, although it localizes predominantly to the nucleus. During embryogenesis, Hop is expressed in the myocardium of the developing heart and it functions downstream of Nkx2-5, an early cardiac-specific transcription factor. One role of Hop is to modify the expression of cardiac-specific genes and thereby finely regulate heart development. This article reviews the discovery, characteristics, roles, and future perspectives of Hop.

Amino Acid Sequence↗
PubMed2005

Comparison of the four mouse fasciclin-containing genes expression patterns during valvuloseptal morphogenesis.

All four mammalian fasciclin-containing genes are expressed in the adult valves and are localized in partially overlapping and reciprocal patterns during cardiovascular development. Spatiotemporal comparison of the fasciclin-containing secreted adhesion genes, TGFbeta induced clone H3 (betaigH3) and periostin, revealed that they are co-localized within the outflow tract endocardial cushions, but that betaigH3 expression is restricted to the septal cushions within the atrioventricular canal. Conversely, the fasciclin-containing transmembrane gene, stabilin-1, is predominately expressed in the endocardial layer overlaying the cushions and lining the developing heart. However, expression of the fasciclin-containing transmembrane gene, stabilin-2 is only present in the post-natal mature valve endothelial cells. These data illustrate for the first time that the primitive endocardial cushions dynamically express multiple fasciclin-containing adhesion molecules as they undergo the key steps of seeding, proliferation, differentiation, fusion, mesenchymal condensation and remodeling during mouse heart development.

Animals↗
PubMed2002

Modulation of cardiac growth and development by HOP, an unusual homeodomain protein.

We have discovered an unusual homeodomain protein, called HOP, which is comprised simply of a homeodomain. HOP is highly expressed in the developing heart where its expression is dependent on the cardiac-restricted homeodomain protein Nkx2.5. HOP does not bind DNA and acts as an antagonist of serum response factor (SRF), which regulates the opposing processes of proliferation and myogenesis. Mice homozygous for a HOP null allele segregate into two phenotypic classes characterized by an excess or deficiency of cardiac myocytes. We propose that HOP modulates SRF activity during heart development; its absence results in an imbalance between cardiomyocyte proliferation and differentiation with consequent abnormalities in cardiac morphogenesis.

Amino Acid Sequence↗
PubMed2004

The Hand1 and Hand2 transcription factors regulate expansion of the embryonic cardiac ventricles in a gene dosage-dependent manner.

The basic helix-loop-helix transcription factors Hand1 and Hand2 display dynamic and spatially restricted expression patterns in the developing heart. Mice that lack Hand2 die at embryonic day 10.5 from right ventricular hypoplasia and vascular defects, whereas mice that lack Hand1 die at embryonic day 8.5 from placental and extra-embryonic abnormalities that preclude analysis of its potential role in later stages of heart development. To determine the cardiac functions of Hand1, we generated mice harboring a conditional Hand1-null allele and excised the gene by cardiac-specific expression of Cre recombinase. Embryos homozygous for the cardiac Hand1 gene deletion displayed defects in the left ventricle and endocardial cushions, and exhibited dysregulated ventricular gene expression. However, these embryos survived until the perinatal period when they died from a spectrum of cardiac abnormalities. Creation of Hand1/2 double mutant mice revealed gene dose-sensitive functions of Hand transcription factors in the control of cardiac morphogenesis and ventricular gene expression. These findings demonstrate that Hand factors play pivotal and partially redundant roles in cardiac morphogenesis, cardiomyocyte differentiation and cardiac-specific transcription.

Alleles↗
PubMed2003

Epicardium is required for the full rate of myocyte proliferation and levels of expression of myocyte mitogenic factors FGF2 and its receptor, FGFR-1, but not for transmural myocardial patterning in the embryonic chick heart.

Proper heart development requires patterning across the myocardial wall. Early myocardial patterning is characterized by a transmural subdivision of the myocardium into an outer, highly mitotic, compact zone and an inner, trabecular zone with lower mitotic activity. We have shown previously that fibroblast growth factor receptor (FGFR) -mediated signaling is central to myocyte proliferation in the developing heart. Consistent with this, FGFR-1 and FGF2 are more highly expressed in myocytes of the compact zone. However, the mechanism that regulates the transmural pattern of myocyte proliferation and expression of these mitogenic factors is unknown. The present study examined whether this transmural patterning occurs in a myocardium-autonomous manner or by signals from the epicardium. Microsurgical inhibition of epicardium formation in the embryonic chick gives rise to a decrease in myocyte proliferation, accounting for a thinner compact myocardium. We show that the transmural pattern of myocyte mitotic activity is maintained in these hearts. Consistent with this, the expression patterns of FGF1, FGF2, and FGFR-1 across the myocardium persist in the absence of the epicardium. However, FGF2 and FGFR-1 mRNA levels are reduced in proportion to the depletion of epicardium. The results suggest that epicardium-derived signals are essential for maintenance of the correct amount of myocyte proliferation in the compact myocardium, by means of levels of mitogen expression in the myocardium. However, initiation and maintenance of transmural patterning of the myocardium occurs largely independently of the epicardium.

Animals↗
PubMed2005

Expression profile of the RNA-binding protein gene hermes during chicken embryonic development.

The hermes gene encodes an RNA-binding protein containing an RNA-recognition motif. Its expression has been described previously in Xenopus and in the developing heart of very young chicken embryos. We have analyzed the expression of cHermes in later heart development, where expression is maintained in the myocardium, and also in previously undescribed sites. cHermes expression first appears in the somites in the first terminally differentiated myocytes of both the epaxial and the hypaxial myotome. Expression is also seen in the primordium of the allantois and continues in the developing allantoic sac. cHermes expression in the pronephric and mesonephric kidneys coincides temporally and spatially with the appearance of the vascular components of the glomeruli. In addition, cHermes expression was seen in the mesoderm of the gut and in the notochord.

Allantois↗