Cell Interactions in the Sea Urchin Embryo

Ettensohn, Charles A.; Guss, Kirsten A.; Malinda, Katherine M.; Miller, Roberta N.; Ruffins, Seth

doi:10.1016/s1064-2722(08)60057-2

Cited by 15 publications

(16 citation statements)

References 148 publications

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“…Microsurgical removal of PMCs at the early-gastrula stage triggers a conversion of non-skeletogenic mesoderm (NSM) cells to the PMC fate. Transfating is followed by the synthesis of a complete, wellpatterned skeleton, albeit in a delayed fashion (reviewed by Ettensohn, 1992). Recent analysis has shown that NSM transfating is associated with the activation of many (probably all) of the downstream biomineralization genes in the micromere-PMC GRN .…”

Section: Ectopic Deployment Of the Skeletogenic Grnmentioning

confidence: 99%

“…foxa also has positive regulatory inputs into endodermal genes, but at later stages of development. The term 'exclusion effect' has been used to describe the linking of a particular GRN network to transcriptional repressors that target regulatory genes required for (Hörstadius, 1939;Ettensohn, 1992). (D-F) Animal cells, derived from mesomeres (blue), can be induced to activate the skeletogenic GRN by LiCl treatment (Livingston and Wilt, 1989), by the mis-expression of Delta (Sweet et al, 2002) or of Pmar1 , or by inductive signals from micromeres (Minokawa et al, 1997).…”

Section: Competition Between Grnsmentioning

confidence: 99%

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Lessons from a gene regulatory network: echinoderm skeletogenesis provides insights into evolution, plasticity and morphogenesis

Ettensohn

2009

Development

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Significant new insights have emerged from the analysis of a gene regulatory network (GRN) that underlies the development of the endoskeleton of the sea urchin embryo. Comparative studies have revealed ways in which this GRN has been modified (and conserved) during echinoderm evolution, and point to mechanisms associated with the evolution of a new cell lineage. The skeletogenic GRN has also recently been used to study the long-standing problem of developmental plasticity. Other recent findings have linked this transcriptional GRN to morphoregulatory proteins that control skeletal anatomy. These new studies highlight powerful new ways in which GRNs can be used to dissect development and the evolution of morphogenesis. IntroductionTo understand how development is encoded in the genome, biologists are turning increasingly to system-level approaches. The concept of transcriptional gene regulatory networks (GRNs) is proving to be a powerful one in this context. GRNs are ensembles of genes that encode transcription factors (TFs) and the genes that these proteins regulate. A central component of GRN analysis is the dissection of the cis-regulatory control systems of genes. Cisregulatory systems consist of non-coding DNA sequences that control when and where genes are transcribed. They are often viewed as modular, information-processing systems (Davidson, 2006). GRN analysis attempts to identify not only the functional interactions among genes, but also the relevant cis-regulatory DNA sequences, the proteins that bind to these sequences, and the logic by which cis-regulatory systems control gene transcription.The GRNs that operate during embryonic development (developmental GRNs) are highly dynamic. New interactions between genes are continually established as old interactions are modified or discarded. Inputs from cell signaling pathways, and intrinsic properties of regulatory networks themselves, contribute to the dynamic nature of GRNs (see Davidson, 2006). The genomic regulatory states of embryonic cells, which are a reflection of the concentrations and activities of hundreds of TFs and the global patterns of gene activity they evoke, are thus ever changing.This review considers recent studies that have applied the GRN concept in new and informative ways to examine developmental plasticity (that is, the ability of embryonic cells to switch developmental pathways), morphogenesis, and the evolution of developmental programs. It focuses on a GRN that controls skeletogenesis in sea urchins, a group of animals belonging to the phylum Echinodermata that has proven to be particularly useful for the analysis of GRNs in early development. GRNs that underlie cell specification are presently understood in greater detail in the sea urchin than in any other metazoan embryo, although work is ongoing in several other experimental models (Koide et al., 2005;Stathopoulos and Levine, 2005;Ge et al., 2006;Satou et al., 2008). For general reviews of GRNs in early sea urchin development, and of the methods used to construct and represe...

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Section: Ectopic Deployment Of the Skeletogenic Grnmentioning

confidence: 99%

Section: Competition Between Grnsmentioning

confidence: 99%

Lessons from a gene regulatory network: echinoderm skeletogenesis provides insights into evolution, plasticity and morphogenesis

Ettensohn

2009

Development

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“…Remarkably, some populations of cells retain the capacity to activate the PMC GRN even after the onset of gastrulation. Microsurgical removal of PMCs at the early gastrula stage causes a subpopulation of non-skeletogenic mesoderm (NSM) cells to switch to the PMC fate (Ettensohn and McClay, 1988;Ettensohn, 1990;Ettensohn, 1992). Surgical removal of both PMCs and NSM cells at the archenteron tip leads to fate-switching by presumptive endoderm cells (McClay and Logan, 1996).…”

Section: Introductionmentioning

confidence: 99%

Gene regulatory networks and developmental plasticity in the early sea urchin embryo: alternative deployment of the skeletogenic gene regulatory network

et al. 2007

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Cell fates in the sea urchin embryo are remarkably labile, despite the fact that maternal polarity and zygotic programs of differential gene expression pattern the embryo from the earliest stages. Recent work has focused on transcriptional gene regulatory networks (GRNs) deployed in specific embryonic territories during early development. The micromere-primary mesenchyme cell (PMC) GRN drives the development of the embryonic skeleton. Although normally deployed only by presumptive PMCs, every lineage of the early embryo has the potential to activate this pathway. Here, we focus on one striking example of regulative activation of the skeletogenic GRN; the transfating of non-skeletogenic mesoderm (NSM) cells to a PMC fate during gastrulation. We show that transfating is accompanied by the de novo expression of terminal, biomineralization-related genes in the PMC GRN, as well as genes encoding two upstream transcription factors, Lvalx1 and Lvtbr. We report that Lvalx1, a key component of the skeletogenic GRN in the PMC lineage, plays an essential role in the regulative pathway both in NSM cells and in animal blastomeres. MAPK signaling is required for the expression of Lvalx1 and downstream skeletogenic genes in NSM cells, mirroring its role in the PMC lineage. We also demonstrate that Lvalx1 regulates the signal from PMCs that normally suppresses NSM transfating. Significantly, misexpression of Lvalx1 in macromeres (the progenitors of NSM cells) is sufficient to activate the skeletogenic GRN. We suggest that NSM cells normally deploy a basal mesodermal pathway and require only an Lvalx1-mediated sub-program to express a PMC fate. Finally, we provide evidence that, in contrast to the normal pathway, activation of the skeletogenic GRN in NSM cells is independent of Lvpmar1. Our studies reveal that, although most features of the micromere-PMC GRN are recapitulated in transfating NSM cells, different inputs activate this GRN during normal and regulative development.

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“…Processes of PMC differentiation have been well characterized owing to its unique lineage, migratory behavior and skeletogenic properties (Ettensohn, 1992;Wilt, 1999). Another population of mesenchyme cells, SMCs, differentiates into four types of cells, pigment, blastocoelar Burke, 1989, 1992), circum esophageal muscle (Burke and Alvarez, 1988) and coelomic pouch cells.…”

Section: Introductionmentioning

confidence: 99%