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PubMed2003

The B-cell maturation factor Blimp-1 specifies vertebrate slow-twitch muscle fiber identity in response to Hedgehog signaling.

Vertebrate skeletal muscles comprise distinct fiber types that differ in their morphology, contractile function, mitochondrial content and metabolic properties. Recent studies identified the transcriptional coactivator PGC-1alpha as a key mediator of the physiological stimuli that modulate fiber-type plasticity in postembryonic development. Although myoblasts become fated to differentiate into distinct kinds of fibers early in development, the identities of regulatory proteins that determine embryonic fiber-type specification are still obscure. Here we show that the gene u-boot (ubo), a mutation in which disrupts the induction of embryonic slow-twitch fibers, encodes the zebrafish homolog of Blimp-1, a SET domain-containing transcription factor that promotes the terminal differentiation of B lymphocytes in mammals. Expression of ubo is induced by Hedgehog (Hh) signaling in prospective slow muscle precursors, and its activity alone is sufficient to direct slow-twitch fiber-specific development by naive myoblasts. Our data provide the first molecular insight into the mechanism by which a specific group of muscle precursors is driven along a distinct pathway of fiber-type differentiation in response to positional cues in the vertebrate embryo.

Animals↗
PubMed2002

Post-nodal mesoblast caudalizes the host axis and inhibits cell population growth, and induces new primitive streaks in chick embryos.

One to eight post-nodal fragments (PN) or Hensen's nodes (HN) from full primitive streak stage chick embryos were transplanted onto the area pellucida or area opaca of stage 4 embryos and cultured for 20 h. Thirteen morphological and numerical parameters were affected in the host embryos and analyzed by multiple logistic regression for parametric hierarchy. In the area pellucida, both PN and HN transplants inhibited cell population growth while only PN caudalized the host axis and induced supernumerary primitive streaks expressing the mesoderm-specific gene Brachyury. In the area opaca, neither grafts influenced host axis morphogenesis, but PN inhibited the cell population growth significantly. Tracking [(3)H]TdR labeled grafts showed that PN cells migrated towards the host axis and participated in the formation of supernumerary somites and hearts. When placed near the host axis, PN caudalized it and inhibited cell population growth.

Animals↗
PubMed2000

Role of neurotropins in rat embryonic testis morphogenesis (cord formation).

The process of seminiferous cord formation is the first morphological event that differentiates a testis from an ovary and indicates male sex determination. Cord formation occurs by embryonic Day 14 (Day 0 = plug date; E14) in the rat. A series of experiments were conducted to determine if neurotropins and their receptors are important for the process of rat embryonic cord formation. The expression of low affinity neurotropin receptor (p75/LNGFR) was determined by immunohistochemistry on sections of both testis and ovary from E13 through birth (Day 0, P0) with an antibody to p75/LNGFR. The staining for p75/LNGFR was present in the mesonephros of E13 gonads and in a sex-specific manner appeared around developing cords at E14 in the embryonic testis. At birth, staining for p75/LNGFR was localized to a single layer of cells (i.e., peritubular cells) that surrounded the seminiferous cords. The genes for both neurotropin 3 (NT3) and for corresponding high affinity neurotropin trkC receptor were found to be expressed in the E14 rat testis, as well as other neurotropins and receptors. Immunocytochemical analysis of E14 rat testis demonstrated that NT3 was localized to the Sertoli cells and trkC was present in individual cells of the interstitium at E16 and in selected preperitubular cells at E18. Previously, the peritubular cells adjacent to the cords were demonstrated to be derived from migrating mesonephros cells around the time of cord formation. To determine if neurotropins were involved in cord formation, the actions of neurotropins were inhibited. A high affinity neurotropin receptor (trk)-specific kinase inhibitor, K252a, was used to treat organ cultures of testes from E13 rats prior to cord formation. Treatment of E13 testis organ cultures with K252a completely inhibited cord formation. K252a-treated organ cultures of E14 testis that contained cords did not alter cord morphology. A second experiment to inhibit neurotropin actions utilized a specific antagonist trk-IgG chimeric fusion protein and E13 testis organ cultures. The trk-IgG molecules dimerize with endogenous trk receptors and inhibit receptor signaling and activation of ligand function. Forty percent of E13 testis organ cultures treated with trkC-IgG had significantly reduced cord formation. TrkA-IgG had no effect on initiation of cords; however, in fifty percent of the treated organs, a "swollen" appearance of the cord structures was observed. Experiments using trkB-IgG chimeric protein on E13 organ cultures had no effect on cord formation or cord morphology. The testes from trkC and NT3 knockout mice were examined to determine if there were any morphological differences in the testis. NT3 knockouts appeared to have normal cord morphology in E15 and E17 testis. TrkC knockout mice also had normal cord morphology in E14 and P0 testis. Both NT3 and trkC knockout-mice testis had less interstitial area than wild-type controls. In addition, the trkC knockout mice have an increased number of cells expressing p75LNGFR within the cords when compared to controls or NT3 knockout mice. Combined observations suggest compensation between the different neurotropin ligands, receptors, and/or possibly different growth factors for this critical biological process. In summary, results suggest a novel nonneuronal role for neurotropins in the process of cord formation during embryonic rat testis development. The hypothesis developed is that neurotropins are involved in the progression of male sex differentiation and are critical for the induction of embryonic testis cord formation.

Animals↗
PubMed1995

An analysis of the response to gut induction in the C. elegans embryo.

Establishment of the gut founder cell (E) in C. elegans involves an interaction between the P2 and the EMS cell at the four cell stage. Here I show that the fate of only one daughter of EMS, the E cell, is affected by this induction. In the absence of the P2-EMS interaction, both E and its sister cell, MS, produce pharyngeal muscle cells and body wall muscle cells, much as MS normally does. By cell manipulations and inhibitor studies, I show first that EMS loses the competence to respond before it divides even once, but P2 presents an inducing signal for at least three cell cycles. Second, induction on one side of the EMS cell usually blocks the other side from responding to a second P2-derived signal. Third, microfilaments and microtubules may be required near the time of the interaction for subsequent gut differentiation. Lastly, cell manipulations in pie-1 mutant embryos, in which the P2 cell is transformed to an EMS-like fate and produces a gut cell lineage, revealed that gut fate is segregated to one of P2's daughters cell-autonomously. The results contrast with previous results from similar experiments on the response to other inductions, and suggest that this induction may generate cell diversity by a different mechanism.

Actin Cytoskeleton↗
PubMed1998

Gene activation during early stages of lens induction in Xenopus.

Several stages in the lens determination process have been defined, though it is not known which gene products control these events. At mid-gastrula stages in Xenopus, ectoderm is transiently competent to respond to lens-inducing signals. Between late gastrula and neural tube stages, the presumptive lens ectoderm acquires a lens-forming bias, becomes specified to form lens and begins differentiation. Several genes have been identified, either by expression pattern, mutant phenotype or involvement in crystallin gene regulation, that may play a role in lens bias and specification, and we focus on these roles here. Fate mapping shows that the transcriptional regulators Otx-2, Pax-6 and Sox-3 are expressed in the presumptive lens ectoderm prior to lens differentiation. Otx-2 appears first, followed by Pax-6, during the stages of lens bias (late neural plate stages); expression of Sox-3 follows neural tube closure and lens specification. We also demonstrate the expression of these genes in competent ectoderm transplanted to the lens-forming region. Expression of these genes is maintained or activated preferentially in ectoderm in response to the anterior head environment. Finally, we examined activation of these genes in response to early and late lens-inducing signals. Activation of Otx-2, Pax-6 and Sox-3 in competent ectoderm occurs in response to the early inducing tissue, the anterior neural plate. Since Sox-3 is activated following neural tube closure, we tested its dependence on the later inducing tissue, the optic vesicle, which contacts lens ectoderm at this stage. Sox-3 is not expressed in lens ectoderm, nor does a lens form, when the optic vesicle anlage is removed at late neural plate stages. Expression of these genes demarcates patterning events preceding differentiation and is tightly coupled to particular phases of lens induction.

Animals↗
PubMed2004

QSulf1, a heparan sulfate 6-O-endosulfatase, inhibits fibroblast growth factor signaling in mesoderm induction and angiogenesis.

The signaling activities of multiple developmental ligands require sulfated heparan sulfate (HS) proteoglycans as coreceptors. QSulf1 and its mammalian orthologs are cell surface HS 6-O-endosulfatases that are expressed in embryonic mesodermal and neural progenitors and promote Wnt signal transduction. In this study, we have investigated the function of QSulf1 in fibroblast growth factor (FGF) signaling, which requires 6-O-sulfated HS for FGF receptor (FGFR) dimerization and tyrosine kinase activation. Here, we report that QSulf1 inhibits FGF2- and FGF4-induced mesoderm formation in the Xenopus embryo and FGF-dependent angiogenesis in the chicken embryo through 6-O-desulfation of cell surface HS. QSulf1 regulates FGF signaling through inhibition of HS-mediated FGFR1 activation by interfering with FGF-HS-FGFR1 ternary complex formation. Furthermore, QSulf1 can produce enzymatically modified soluble heparin that acts as a potent inhibitor of FGF2-induced angiogenesis in the chicken embryo. QSulf1, therefore, has dual regulatory functions as a negative regulator of FGF signaling and a positive regulator of Wnt signaling. Therefore, QSulf1 provides another reagent to produce enzymatically modified heparin compounds, in vivo and in vitro, to modulate cellular signaling in stem cell-based therapies to promote tissue regeneration and in cancer therapies to control cell growth and block angiogenesis.

Animals↗
PubMed1996

Specific induction of apoptosis in P19 embryonal carcinoma cells by retinoic acid and BMP2 or BMP4.

Retinoic acid (RA) affects the response of many cells to growth factors, including the bone morphogenetic proteins (BMPs). The BMPs are members of the TGF-beta, family of growth factors, originally identified by their bone-inducing activities. Their widespread expression suggests many roles other than that in osteogenesis. Because RA modulates the cell's response to growth factors, this may be a means by which the retinoids exert some of their known teratogenic effects. One such cellular response may be apoptosis. While apoptosis is required for normal development, the location and timing of its induction must be carefully controlled. Recently, several TGF-beta family members have been implicated in the induction of apoptosis in certain cell types. We show here, using P19 embryonal carcinoma cells, that the combination of RA and BMP2 or BMP4 synergistically induces apoptosis in 40% of the population within 24 hr. In contrast, RA alone induces apoptosis in only 10-15% of the population and each of the BMPs alone minimally induces apoptosis. Apoptosis depends on the dose of both the RA and the BMP as well as on new protein synthesis. Further, the induction of apoptosis prevents the formation of fully differentiated neurons and glial cells and instead leads to primarily smooth muscle cell differentiation. These results suggest that some of the malformations caused by retinoids may be due to the induction of inappropriate apoptosis in cells exposed to BMPs.

Apoptosis↗
PubMed1994

Effects of truncated activin and FGF receptors and of follistatin on the inducing activities of BVg1 and activin: does activin play a role in mesoderm induction?

Activin and Vg1, two members of the TGF-beta family, are believed to play roles in mesoderm induction and axis formation in the amphibian embryo. Both molecules are provided maternally, either as protein (activin) or as RNA and protein (Vg1), and experiments with a truncated form of a type IIB activin receptor have led to the conclusion that activin is required for induction of mesoderm in vivo. In this paper we first show that truncated versions of two different Xenopus activin receptors also have severe effects on the activity of the mature region of Vg1, suggesting that such receptors may block the function of several members of the TGF-beta family. We go on to demonstrate that follistatin, a secreted protein which binds activin and blocks its activity, does not interfere with Vg1 signalling. Furthermore, overexpression of follistatin mRNA in Xenopus embryos does not perturb mesoderm formation. Taken together, our data show that the effects of truncated activin receptors on Xenopus development can be explained by the inhibition of Vg1 activity, while the lack of effect of follistatin argues against a function for activin in mesoderm induction.

Activin Receptors↗
PubMed1992

Interaction of Wnt and activin in dorsal mesoderm induction in Xenopus.

Both the activin and Wnt families of peptide growth factors are capable of inducing dorsal mesoderm in Xenopus embryos. Presumptive ventral ectoderm cells isolated from embryos injected with Xwnt8 mRNA were cultured in the presence of activin A to study the possible interactions between these two classes of signaling proteins. We find that overexpression of Xwnt8 RNA alters the response of ventral ectoderm to activin such that ventral explants differentiate dorsoanterior structures including notochord and eyes. This response is similar to the response of dorsal ectoderm to activin alone. When embryos are irradiated with uv light to inhibit dorsal axis formation, ectodermal explants differentiate notochord when they are induced by a combination of both signaling factors, but not when cells receive only one inducing signal (activin or Xwnt8). This result is further supported by the observation that goosecoid (gsc) mRNA, an early marker for dorsal mesoderm, is expressed in these explants only when they are injected with Xwnt8 mRNA followed by exposure to activin. Early morphogenetic movements of the induced cells and activation of muscle-specific actin and Brachyury (Xbra) genes also reveal a cooperation of activin A and Xwnt8 in mesoderm induction.

Actins↗
PubMedDate not supplied

Mesodermal induction defect as a possible cause of ear malformations.

Deafness due to inner ear anomalies is rarely associated with malformations of the auricles. We describe two brothers with profound congenital sensorineural deafness, abnormal vestibular function, normal ossicles, and delayed motor development. Since the external and inner ear originate from distinctly separate structures, the embryogenesis of this malformation association is less clear than in the more common association of external and middle anomalies, where the latter two structures are derived from the first and second branchial arches. The combination of auricular and inner ear anomalies, with sparing of the middle ear structures, can be explained on the assumption that mesodermal induction is responsible for normal differentiation of both the otocyst and of the branchial arch ectoderm. A recessive mutant gene may lead to a deficiency of a mesodermal inducer substance of a target tissue receptor site. A similar mechanism may be involved in other multiple malformation syndromes, whereby a mutant gene acting during a specific period of organogenesis causes disruption of the normal induction-competence relationship.

Cell Differentiation↗
PubMed1990

The Xenopus MyoD gene: an unlocalised maternal mRNA predates lineage-restricted expression in the early embryo.

Expression of the mouse MyoD gene appears to represent a critical point in the commitment of cultured cells to muscle. In Xenopus, myogenic commitment begins during mesoderm induction which is initiated early in development by endogenous growth factors. To study MyoD gene expression during induction, a Xenopus MyoD gene and homologous cDNAs were selected from Xenopus libraries and analysed. Two different cDNAs have been sequenced. They code for proteins closely related to each other and to mouse MyoD and are likely to be expressed from duplicated Xenopus MyoD genes. Surprisingly, MyoD mRNA is first detected during oogenesis and the maternal species is not localized exclusively to the region of the blastula fated to muscle. Zygotic MyoD mRNA accumulates slowly above maternal levels beginning at the MBT and new transcripts are localized to the somitic mesoderm. Expression outside of somites has been detected in developing heads of tailbud embryos and can be induced in blastula animal pole explants treated with mesoderm-inducing factors. The early expression of MyoD in Xenopus development suggests that it may play a part in the induction of muscle mesoderm and generally strengthens the evidence that MyoD is determinative in muscle commitment. In addition, the initiation of MyoD transcription at the MBT and its stimulation by mesoderm-inducing factors implies that MyoD gene expression is an immediate early response to mesoderm induction.

Amino Acid Sequence↗
PubMed1991

Hensen's node induces neural tissue in Xenopus ectoderm. Implications for the action of the organizer in neural induction.

The development of the vertebrate nervous system is initiated in amphibia by inductive interactions between ectoderm and a region of the embryo called the organizer. The organizer tissue in the dorsal lip of the blastopore of Xenopus and Hensen's node in chick embryos have similar neural inducing properties when transplanted into ectopic sites in their respective embryos. To begin to determine the nature of the inducing signals of the organizer and whether they are conserved across species we have examined the ability of Hensen's node to induce neural tissue in Xenopus ectoderm. We show that Hensen's node induces large amounts of neural tissue in Xenopus ectoderm. Neural induction proceeds in the absence of mesodermal differentiation and is accompanied by tissue movements which may reflect notoplate induction. The competence of the ectoderm to respond to Hensen's node extends much later in development than that to activin-A or to induction by vegetal cells, and parallels the extended competence to neural induction by axial mesoderm. The actions of activin-A and Hensen's node are further distinguished by their effects on lithium-treated ectoderm. These results suggest that neural induction can occur efficiently in response to inducing signals from organizer tissue arrested at a stage prior to gastrulation, and that such early interactions in the blastula may be an important component of neural induction in vertebrate embryos.

Activins↗
PubMed1994

A role for cytoplasmic determinants in mesoderm patterning: cell-autonomous activation of the goosecoid and Xwnt-8 genes along the dorsoventral axis of early Xenopus embryos.

Although an induction event is required for the formation of mesoderm in Xenopus embryos, it is not clear that this induction is wholly sufficient to give rise to a correctly patterned mesodermal layer. We have studied the expression of the two genes, goosecoid and Xwnt-8, in Xenopus gastrulae in which cell-cell communication, and therefore mesoderm induction, has been prevented by frequent cell dispersion. Although neither the early panmesodermal marker Xbra nor the muscle-specific alpha-actin gene were activated under these conditions, goosecoid and Xwnt-8 were activated in cells of dorsal and ventrolateral origin respectively, thus correctly reflecting their distribution during normal development. We also show that the spatial pattern of expression of these two genes along the animal-vegetal axis is similar in normal and in dissociated early gastrulae: goosecoid is mainly expressed in future mesoderm while the domain of expression of Xwnt-8 spans the mesoderm-endoderm boundary. These results show that, during the blastula and early gastrula stages, gene activation can be controlled cell-autonomously along both the animal-vegetal and dorsoventral embryo axes. This suggests that the inheritance of localised maternal cytoplasmic determinants is a key event for the patterning of mesoderm. We present a modified model of mesoderm formation in which the different mesoderm cell types are produced as a result of cooperation between induction-dependent and induction-independent immediate-early genes.

Animals↗