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C A Ettensohn

Publications and source records attributed to C A Ettensohn.

At least 19 recordsLinked to original sources
PubMed2006

A genome-wide analysis of biomineralization-related proteins in the sea urchin Strongylocentrotus purpuratus.

Biomineralization, the biologically controlled formation of mineral deposits, is of widespread importance in biology, medicine, and engineering. Mineralized structures are found in most metazoan phyla and often have supportive, protective, or feeding functions. Among deuterostomes, only echinoderms and vertebrates produce extensive biomineralized structures. Although skeletons appeared independently in these two groups, ancestors of the vertebrates and echinoderms may have utilized similar components of a shared genetic "toolkit" to carry out biomineralization. The present study had two goals. First, we sought to expand our understanding of the proteins involved in biomineralization in the sea urchin, a powerful model system for analyzing the basic cellular and molecular mechanisms that underlie this process. Second, we sought to shed light on the possible evolutionary relationships between biomineralization in echinoderms and vertebrates. We used several computational methods to survey the genome of the purple sea urchin Strongylocentrotus purpuratus for gene products involved in biomineralization. Our analysis has greatly expanded the collection of biomineralization-related proteins. We have found that these proteins are often members of small families encoded by genes that are clustered in the genome. Most of the proteins are sea urchin-specific; that is, they have no apparent homologues in other invertebrate deuterostomes or vertebrates. Similarly, many of the vertebrate proteins that mediate mineral deposition do not have counterparts in the S. purpuratus genome. Our findings therefore reveal substantial differences in the primary sequences of proteins that mediate biomineral formation in echinoderms and vertebrates, possibly reflecting loose constraints on the primary structures of the proteins involved. On the other hand, certain cellular and molecular processes associated with earlier events in skeletogenesis appear similar in echinoderms and vertebrates, leaving open the possibility of deeper evolutionary relationships.

Amino Acid Sequence↗
PubMed2001

A large-scale analysis of mRNAs expressed by primary mesenchyme cells of the sea urchin embryo.

The primary mesenchyme cells (PMCs) of the sea urchin embryo have been an important model system for the analysis of cell behavior during gastrulation. To gain an improved understanding of the molecular basis of PMC behavior, a set of 8293 expressed sequenced tags (ESTs) was derived from an enriched population of mid-gastrula stage PMCs. These ESTs represented approximately 1200 distinct proteins, or about 15% of the mRNAs expressed by the gastrula stage embryo. 655 proteins were similar (P<10(-7) by BLAST comparisons) to other proteins in GenBank, for which some information is available concerning expression and/or function. Another 116 were similar to ESTs identified in other organisms, but not further characterized. We conservatively estimate that sequences encoding at least 435 additional proteins were included in the pool of ESTs that did not yield matches by BLAST analysis. The collection of newly identified proteins includes many candidate regulators of primary mesenchyme morphogenesis, including PMC-specific extracellular matrix proteins, cell surface proteins, spicule matrix proteins and transcription factors. This work provides a basis for linking specific molecular changes to specific cell behaviors during gastrulation. Our analysis has also led to the cloning of several key components of signaling pathways that play crucial roles in early sea urchin development.

Animals↗
PubMed2000

A sea urchin genome project: sequence scan, virtual map, and additional resources.

Results of a first-stage Sea Urchin Genome Project are summarized here. The species chosen was Strongylocentrotus purpuratus, a research model of major importance in developmental and molecular biology. A virtual map of the genome was constructed by sequencing the ends of 76,020 bacterial artificial chromosome (BAC) recombinants (average length, 125 kb). The BAC-end sequence tag connectors (STCs) occur an average of 10 kb apart, and, together with restriction digest patterns recorded for the same BAC clones, they provide immediate access to contigs of several hundred kilobases surrounding any gene of interest. The STCs survey >5% of the genome and provide the estimate that this genome contains approximately 27,350 protein-coding genes. The frequency distribution and canonical sequences of all middle and highly repetitive sequence families in the genome were obtained from the STCs as well. The 500-kb Hox gene complex of this species is being sequenced in its entirety. In addition, arrayed cDNA libraries of >10(5) clones each were constructed from every major stage of embryogenesis, several individual cell types, and adult tissues and are available to the community. The accumulated STC data and an expanding expressed sequence tag database (at present including >12, 000 sequences) have been reported to GenBank and are accessible on public web sites.

Aging↗
PubMed2000

Cell-substrate interactions during sea urchin gastrulation: migrating primary mesenchyme cells interact with and align extracellular matrix fibers that contain ECM3, a molecule with NG2-like and multiple calcium-binding domains.

The migratory primary mesenchyme cells (PMCs) of the sea urchin embryo are a model experimental system for the analysis of cell-extracellular matrix (ECM) interactions. Although the behavior of PMCs during gastrulation has been analyzed in considerable detail, it has proven difficult to identify specific substrate molecules with which these cells interact. Here, using a new monoclonal antibody (2.5C4) generated by an in vitro immunization procedure, we show that migrating PMCs interact with a distinct class of ECM fiber. The 2.5C4-positive fibers are distributed in a vegetal (high) to animal (low) gradient on the basal surface of the ectoderm. Three observations indicate that PMC filopodia interact directly with the fibers: (1) During gastrulation, 2.5C4-positive fibers gradually become oriented in a prominent circumferential belt that corresponds precisely to the position of the subequatorial PMC ring. (2) This fiber pattern is blocked by microsurgical removal of PMCs but is restored if PMCs are reintroduced into the embryo. (3) Examination of immunostained embryo whole mounts by confocal microscopy reveals a striking association between PMC filopodial roots and foci of fiber bundling. Double-immunostaining experiments using 2.5C4 and antibodies against previously identified matrix constituents show that the protein ECM3 is a component of the fibers. We have determined the complete amino acid sequence of ECM3 and find that this large protein (3103 amino acids) consists of an N-terminal domain similar to the mammalian chondroitin sulfate proteoglycan core protein NG2, a central region composed of five tandem repeats of a domain contained within the regulatory Ca2+-binding loop of Na+-Ca2+ exchange proteins, and a C-terminal region with no homology to known proteins. The general structure of ECM3 is similar in several respects to that of a sponge protein, MAFp4. MAFp4 is a major component of aggregation factor, an ECM complex that mediates the calcium-dependent, species-specific sorting of sponge cells. These studies establish ECM3 as a strong candidate for a PMC substrate molecule and point to several possible mechanisms by which interactions between PMC filopodia and ECM3-containing fibers could provide guidance information to migrating PMCs.

Amino Acid Sequence↗
PubMed1999

Cell movements in the sea urchin embryo.

Recent studies show that gastrulation in the sea urchin embryo involves movement of cells over the blastopore lip (involution). Some cells in the vegetal plate of the late blastula become bottle-shaped but they play a limited role in gastrulation. The functions of specific integrins, regulators of cell-cell adhesion, and extracellular matrix components in gastrulation are currently being analyzed. In addition, light-microscopic studies continue to provide a unique picture of dynamic cell behavior in vivo.

Animals↗
PubMed1999

The role of micromere signaling in Notch activation and mesoderm specification during sea urchin embryogenesis.

In the sea urchin embryo, the micromeres act as a vegetal signaling center. These cells have been shown to induce endoderm; however, their role in mesoderm development has been less clear. We demonstrate that the micromeres play an important role in the induction of secondary mesenchyme cells (SMCs), possibly by activating the Notch signaling pathway. After removing the micromeres, we observed a significant delay in the formation of all mesodermal cell types examined. In addition, there was a marked reduction in the numbers of pigment cells, blastocoelar cells and cells expressing the SMC1 antigen, a marker for prospective SMCs. The development of skeletogenic cells and muscle cells, however, was not severely affected. Transplantation of micromeres to animal cells resulted in the induction of SMC1-positive cells, pigment cells, blastocoelar cells and muscle cells. The numbers of these cell types were less than those found in sham transplantation control embryos, suggesting that animal cells are less responsive to the micromere-derived signal than vegetal cells. Previous studies have demonstrated a role for Notch signaling in the development of SMCs. We show that the micromere-derived signal is necessary for the downregulation of the Notch protein, which is correlated with its activation, in prospective SMCs. We propose that the micromeres induce adjacent cells to form SMCs, possibly by presenting a ligand for the Notch receptor.

Animals↗
PubMed1998

The dynamics and regulation of mesenchymal cell fusion in the sea urchin embryo.

Cell-cell fusion occurs in a wide variety of developmental contexts, yet the mechanisms involved are just beginning to be elucidated. In the sea urchin embryo, primary mesenchyme cells (PMCs) fuse to form syncytial filopodial cables within which skeletal spicules are deposited. Taking advantage of the optical transparency and ease of micromanipulation of sea urchin embryos, we have developed methods for directly observing the dynamics of PMC fusion in vivo. A fraction of the PMCs was labeled with fluorescent dextran and transfer of the dye to unlabeled PMCs was followed by time-lapse, fluorescence microscopy. Fusion was first detected about 2 h after PMCs began to migrate within the blastocoel. Fusion proceeded in parallel with the assembly of the PMC ring pattern and was complete by the early gastrula stage. The formation of a single, extensive PMC syncytium was confirmed by DiI labeling of fixed embryos. When single micromeres were isolated and cultured in unsupplemented seawater, they divided and their progeny underwent fusion. This shows that the capacity to fuse is autonomously programmed in the micromere-PMC lineage by the 16-cell stage. PMC transplantations at late embryonic stages revealed that these cells remain fusion-competent long after their fusion is complete. At late stages, other mesenchyme cells (blastocoelar cells) are also present within the blastocoel and are migrating and fusing with one another. Fusion-competent blastocoelar cells and PMCs come into contact but do not fuse with one another, indicating that these two cell types fuse by distinct mechanisms. When secondary mesenchyme cells convert to a skeletogenic fate they alter their fusogenic properties and join the PMC syncytium, as shown by transfer of fluorescent dextran. Our analysis has provided a detailed picture of the cellular basis and regulation of mesodermal cell fusion and has important implications regarding molecular mechanisms that underlie fusion.

Animals↗
PubMed1997

Skeletal morphogenesis in the sea urchin embryo: regulation of primary mesenchyme gene expression and skeletal rod growth by ectoderm-derived cues.

The skeleton of the sea urchin embryo is synthesized by the primary mesenchyme cells (PMCs). Previous studies have shown that local interactions between PMCs and the neighboring ectoderm regulate several aspects of skeletal morphogenesis, including PMC distribution in the blastocoel, the size of the skeleton and its branching pattern. In the present study, we have further examined the regulation of skeletogenesis by the ectoderm. We generated a 'rate map' of skeletal growth, which revealed stereotypical changes in the rates at which specific skeletal elements elongate during development. We showed that three transcripts encoding PMC-specific gene products known to be involved in the synthesis of the skeleton exhibited dynamic, spatially regulated patterns of expression within the PMC syncytium. All three gene products showed high levels of expression at sites of skeletal rod growth, although the specific patterns varied among the genes. We present direct evidence, based upon cell transplantation experiments, that the expression of one of these genes, SM30, is responsive to local, ectoderm-derived cues. Based upon our studies, we suggest that short-range signals from different ectodermal territories may regulate the expression of PMC-specific gene products that are rate-limiting in skeletal biosynthesis, thereby locally influencing skeletal rod growth.

Animals↗
PubMed1996

Expression of S9 and actin CyIIa mRNAs reveals dorso-ventral polarity and mesodermal sublineages in the vegetal plate of the sea urchin embryo.

We have used whole amount in situ hybridization to analyze the patterns of expression of two genes, S9 and actin CyIIa, during the development of the sea urchin, Strongylocentrotus purpuratus. We demonstrate that at the late blastula stage, these two mRNAs are expressed specifically by cells of the vegetal plate. Their domains of expression, however, are different. S9 mRNA is broadly distributed within most of the vegetal plate except for the central region, while CyIIa expression is restricted to a population of 10-15 cells in the ventral region of the plate. S9-expressing secondary mesenchyme cells (SMCs) migrate from the vegetal plate into the blastocoel early in gastrulation and later populate the dorsal ectoderm. The numbers, morphology, and migratory behavior of these cells strongly suggest that they are pigment cells. Throughout gastrulation, CyIIa mRNA is expressed by a population of presumptive SMCs at the ventral aspect of the archenteron tip. The pattern of expression of this mRNA is dynamic, however, and by the early pluteus stage, CyIIa mRNA accumulates in primary mesenchyme cells (PMCs), SMCs, and endodermal cells of the gut. When embryos are treated with NiCl2, a compound that has been shown to ventralize other embryonic tissues, CyIIa mRNA is expressed by an increased number of cells in the vegetal plate in a radially symmetrical pattern. The spatial pattern of CyIIa expression provides the first direct molecular evidence that the vegetal plate is polarized along the dorso-ventral (D-V) axis of the embryo. This gene product should be a valuable marker in future studies of D-V axis specification, as it can be detected at earlier developmental stages than existing molecular markers of this axis. Our observations show that the vegetal plate consists of subterritories of gene expression, and provide further support for the view that diversification of the presumptive, non-skeletogenic mesoderm begins prior to the onset of invagination.

Actins↗
PubMed1996

A fate map of the vegetal plate of the sea urchin (Lytechinus variegatus) mesenchyme blastula.

Previous lineage tracing experiments have shown that the vegetal blastomers of cleavage stage embryos give rise to all the mesoderm and endoderm of the sea urchin larva. In these studies, vegetal blastomers were labeled no later than the sixth cleavage division (60-64 cell stage). In an earlier study we showed that single cells in the vegetal plate of the blastula stage Lytechinus variegatus embryo could be labeled in situ with the fluorescent, lipophilic dye, DiI(C18), and that cells labeled in the central region of the vegetal plate of the mesenchyme blastula primarily gave rise to homogeneous clones consisting of a single secondary mesenchyme cell (SMC) type (Ruffins and Ettensohn (1993) Dev. Biol. 160, 285-288). Our clonal labeling showed that a detailed fate map could be generated using the DiI(C18) labeling technique. Such a fate map could provide information about the spatial relationships between the precursors of specific mesodermal and endodermal cell types and information concerning the movements of these cells during gastrulation and later embryogenesis. We have used this method to construct the first detailed fate map of the vegetal plate of the sea urchin embryo. Ours is a latitudinal map; mapping from the plate center, where the mesodermal precursors reside, through the region which contains the endodermal precursors and across the ectodermal boundary. We found that the precursors of certain SMC types are segregated in the mesenchyme blastula stage vegetal plate and that prospective germ layers reside within specific boundaries. To determine whether the vegetal plate is radially symmetrical with respect to mesodermal cell fates, single blastomeres of four cell stage embryos were injected with lysyl-rhodamine dextran (LRD). The resulting ectodermal labeling patterns were classified and correlated with the SMC types labeled. This analysis indicates that the dorsal and ventral blastomers do not contribute equally to SMC derivatives in L. variegatus.

Animals↗
PubMed1995

Four-dimensional microscopic analysis of the filopodial behavior of primary mesenchyme cells during gastrulation in the sea urchin embryo.

During gastrulation of the sea urchin embryo, primary mesenchyme cells (PMCs) migrate from the vegetal pole to a site below the equator of the embryo where they form a ring-like structure and begin producing the larval skeleton. As these cells migrate, they extend and retract filopodia which appear to interact with the basal lamina and underlying ectoderm. To better characterize this behavior in vivo, we studied PMC migration using differential interference contrast (DIC) microscopy in combination with four-dimensional imaging (x, y, z space and time). We were able to determine the persistence and direction of extension of each filopodium and were also able to observe the dynamic behavior of each using colorized movie loops. This analysis showed that: (1) Most filopodia are quite transient, usually persisting for less than 0.5-6.0 min, during which time they continuously survey their surroundings; (2) PMCs extend an average of 121 filopodia/hr during migration; (3) the initial direction of extension of filopodia from the cell body is random, with just as many filopodia projecting toward as away from the direction of migration; (4) as a consequence of (2) and (3) above, each PMC explores the area surrounding its cell body approximately once every 5 min; (5) PMCs nearer to the target site migrate faster than those located farther away. To further investigate filopodial distribution, confocal microscopy was used to collect z series of PMCs transplanted to different locations in the embryo and fixed during migration. We found that more filopodia tended to be distributed toward the target site as cells approached the ring, suggesting that filopodial distribution may reflect regional differences in directional cues.

Animals↗
PubMed1994

An N-linked carbohydrate-containing extracellular matrix determinant plays a key role in sea urchin gastrulation.

During the process of gastrulation in the sea urchin embryo, the vegetal plate invaginates to form the archenteron, a long narrow tube that extends across the blastocoel. Rearrangement of cells within the archenteron is thought to be a key component of the process of archenteron elongation. While these cell rearrangements have been well described, the mechanism of the rearrangements and the coordination of the movements of individual cells that results in the elongation of the archenteron are not well understood. We have identified a monoclonal antibody, called ECM 1, that recognizes an N-linked carbohydrate-containing epitope on several high-molecular-weight basal lamina glycoproteins. In an attempt to block the function of this determinant in development, the ECM 1 antibody was injected into the blastocoel of living embryos and the effects on morphogenesis were determined. Injection of intact ECM 1 IgG or monovalent Fab fragments blocks cell rearrangements during secondary invagination and cell movements during segmentation of the gut. Glycopeptides derived from the glycoproteins recognized by ECM 1 also inhibit cell rearrangements during secondary invagination when injected into the blastocoel. The inhibitory activity of these peptides is eliminated by digestion with N-glycosidase F or pronase, enzymes that also disrupt the ECM 1 determinant. ECM 1 recognizes a nonuniformly distributed determinant in the basal lamina and blastocoel matrix. This determinant is stored in cytoplasmic granules in the unfertilized egg and is deposited into the basal lamina by the blastula stage. The determinant becomes concentrated in the basal lamina in the vegetal region of the embryo early in gastrulation. At the prism stage, the determinant accumulates in the basal lamina and blastocoel matrix in the ventral region of the embryo. These data indicate that the vegetally localized, N-linked carbohydrate-containing determinant recognized by ECM 1 plays an important role in cell movements during archenteron morphogenesis in the sea urchin embryo.

Animals↗
PubMed1994

Primary mesenchyme cell migration in the sea urchin embryo: distribution of directional cues.

The directional migration of the primary mesenchyme cells (PMCs) of the sea urchin embryo is a critical step in the process of gastrulation. Although interactions between the migrating cells and the blastocoel environment are necessary for guiding the PMCs to their subequatorial target site, the nature of these interactions and the localization of guidance cues involved in directing the cells are not yet known. Previous studies have suggested that PMC migration is the result of random exploration and selective trapping at the target site by a pattern of adhesiveness in the ectoderm or basal lamina. To better characterize the distribution of guidance cues in the blastocoel we used a combination of time-lapse microscopy, microsurgery, and fluorescence photoablation to study the behavior of the migrating cells. By using fluorescence time-lapse microscopy, and a two-dimensional random-walk analysis of cell trajectories, we demonstrated that fluorescently labeled PMCs injected near the animal pole move in a directed fashion over a relatively long distance to reach the target site. This suggests that guidance cues are distributed globally throughout the embryo and are not restricted to the immediate ring area. To further test this hypothesis we investigated the migratory behavior of PMCs that were prevented from interacting directly with the target site. First, we examined the behavior of PMCs injected into animal embryo fragments lacking the target site. We found that PMCs move to the vegetal-most area of such embryo fragments, regardless of their size. Second, we studied the effects of photoablating a stripe of ectoderm between PMCs injected at the animal pole region (APR) and the target site. PMCs were found to accumulate along the ablated stripe and were unable to cross it for up to 6 hr after ablation. We also examined the migratory behavior of endogenous PMCs in embryos treated with lithium, a vegetalizing agent which shifts the position of the PMC ring toward the animal pole. We found that PMCs accumulated along an ablated stripe of ectoderm positioned below the shifted target site, suggesting that endogenous PMCs follow a set of directional cues to the target site which may be similar to those used by PMCs injected into the APR. As a whole, these results suggest that migrating PMCs follow a set of directional cues that are widely distributed throughout the blastocoel and that may be arranged in a gradient.

Animals↗
PubMed1993

A clonal analysis of secondary mesenchyme cell fates in the sea urchin embryo.

The secondary mesenchyme cells (SMCs) give rise to most of the mesoderm of the sea urchin embryo. Although the early embryonic lineage of these cells has been described, the mechanisms that cause SMCs to become restricted to a particular mesodermal cell fate are unknown. To begin to address this question, we performed a clonal analysis of the fates of SMC precursors in the vegetal plate by labeling single cells with the fluorescent dye DiI (C18). Our data show that some presumptive SMCs remain pluripotent at the late blastula stage, since some cells labeled at this stage gave rise to more than one mesodermal cell type. Surprisingly, however, most labeled cells gave rise to homogeneous clones composed of a single cell type. This observation indicates that either many SMC precursors are restricted in their fate before the start of gastrulation or that all the progeny of a single vegetal plate cell are influenced by the same instructional signals during gastrulation, despite the cell divisions and extensive cell movements that occur during this time. The percentage of clones composed of a single cell type increased during the blastula stage, supporting the view that the process of SMC fate specification begins before the onset of gastrulation.

Animals↗
PubMed1993

Mesodermal cell interactions in the sea urchin embryo: properties of skeletogenic secondary mesenchyme cells.

An interaction between the two principal populations of mesodermal cells in the sea urchin embryo, primary and secondary mesenchyme cells (PMCs and SMCs, respectively), regulates SMC fates and the process of skeletogenesis. In the undisturbed embryo, skeletal elements are produced exclusively by PMCs. Certain SMCs also have the ability to express a skeletogenic phenotype; however, signals transmitted by the PMCs direct these cells into alternative developmental pathways. In this study, a combination of fluorescent cell-labeling methods, embryo microsurgery and cell-specific molecular markers have been used to study the lineage, numbers, normal fate(s) and developmental potential of the skeletogenic SMCs. Previous fate-mapping studies have shown that SMCs are derived from the veg2 layer of blastomeres of the 64-cell-stage embryo and from the small micromeres. By specifically labeling the small micromeres with 5-bromodeoxyuridine, we demonstrate that descendants of these cells do not participate in skeletogenesis in PMC-depleted larvae, even though they are the closest lineal relatives of PMCs. Skeletogenic SMCs are therefore derived exclusively from the veg2 blastomeres. Because the SMCs are a heterogeneous population of cells, we have sought to gain information concerning the normal fate(s) of skeletogenic SMCs by determining whether specific cell types are reduced or absent in PMC(-) larvae. Of the four known SMC derivatives: pigment cells, blastocoelar (basal) cells, muscle cells and coelomic pouch cells, only pigment cells show a major reduction (> 50%) in number following SMC skeletogenesis. We therefore propose that the PMC-derived signal regulates a developmental switch, directing SMCs to adopt a pigment cell phenotype instead of a default (skeletogenic) fate. Ablation of SMCs at the late gastrula stage does not result in the recruitment of any additional skeletogenic cells, demonstrating that, by this stage, the number of SMCs with skeletogenic potential is restricted to 60-70 cells. Previous studies showed that during their switch to a skeletogenic fate, SMCs alter their migratory behavior and cell surface properties. In this study, we demonstrate that during conversion, SMCs become insensitive to the PMC-derived signal, while at the same time they acquire PMC-specific signaling properties.

Animals↗
PubMed1993

Size regulation and morphogenesis: a cellular analysis of skeletogenesis in the sea urchin embryo.

The formation of the skeleton is a central event in sea urchin morphogenesis. The skeleton serves as a framework for the larval body and is the primary determinant of its shape. Previous studies have shown that the size of the skeleton is invariant despite wide experimentally induced variations in the number of skeleton-forming primary mesenchyme cells (PMCs). In the present study, we have used PMC transplantation, fluorescent cell markers and confocal laser scanning microscopy to analyze cellular aspects of skeletal patterning. Labeling of embryos with 5-bromodeoxyuridine demonstrates that the entire embryonic phase of skeletal morphogenesis occurs in the absence of PMC division. During embryogenesis, skeletal rods elongate by one of two mechanisms; either preceded by a cluster (plug) of PMCs or by extending along an existing PMC filopodial cable. Elongation of skeletal rods occurs exclusively by the addition of new material at the rod tips, although radial growth (increase in rod thickness) occurs along the length of the rods. Photoablation of a distinctive region of ectoderm cells at the arm tip results in an inhibition of skeletal rod elongation, indicating that a local ectoderm-PMC interaction is required for skeletal growth. The regulation of skeletal patterning was also examined in embryos that had been microinjected with additional PMCs and in half-sized larvae derived from blastomeres isolated at the 2-cell stage. Microinjection of 50-100 PMCs into the blastocoel at the mesenchyme blastula stage leads to an increase in the numbers of PMCs along all skeletal rods and a two-fold increase in the number of cells in the plugs, yet no increase in the length of the skeletal rods. The length of the anal rods can, however, be increased by microinjecting developmentally 'young' PMCs into the arm tips of late stage embryos. We find that the rate of skeletal rod elongation is independent of both the mode of rod growth (chain or plug) and the number of PMCs in the plug at the growing rod tip. Instead, the rate of elongation appears to be strictly regulated by the quantity of ectodermal tissue present in the embryo. These studies provide new information concerning normal mechanisms of skeletal growth and patterning and lead us to propose a model for the regulation of skeleton size based upon an intrinsic PMC 'clock' and an ectoderm-derived signal that regulates the rate of skeletal rod elongation.

Animals↗
PubMed1992

Cell interactions and mesodermal cell fates in the sea urchin embryo.

Cell interactions during gastrulation play a key role in the determination of mesodermal cell fates in the sea urchin embryo. An interaction between primary and secondary mesenchyme cells (PMCs and SMCs, respectively), the two principal populations of mesodermal cells, regulates the expression of SMC fates. PMCs are committed early in cleavage to express a skeletogenic phenotype. During gastrulation, they transmit a signal that suppresses the skeletogenic potential of a subpopulation of SMCs and directs these cells into an alternative developmental pathway. This review summarizes present information concerning the cellular basis of the PMC-SMC interaction, as analyzed by cell transplantation and ablation experiments, fluorescent cell labeling methods and the use of cell type-specific molecular markers. The nature and stability of SMC fate switching, the timing of the PMC-SMC interaction and its quantitative characteristics, and the lineage, numbers and normal fate of the population of skeletogenic SMCs are discussed. Evidence is presented indicating that PMCs and SMCs come into direct filopodial contact during the late gastrula stage, when the signal is transmitted. Finally, evolutionary questions raised by these studies are briefly addressed.

Animals↗