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The centrohelid heliozoan Raphidocystis contractilis has many radiating axopodia, each containing axopodial microtubules. The axopodia show rapid contraction at nearly a video rate (30 frames per second) in response to mechanical stimuli. The axopodial contraction is accompanied by cytoskeletal microtubule depolymerization, but the molecular mechanism of this phenomenon has not been elucidated. In this study, we performed de novo transcriptome sequencing of R. contractilis to identify genes involved in microtubule dynamics such as the rapid axopodial contraction. The transcriptome sequencing generated 7.15‐Gbp clean reads in total, which were assembled as 31,771 unigenes. Using the obtained gene sets, we identified several microtubule‐severing proteins which might be involved in the rapid axopodial contraction, and kinesin‐like genes that occur in gene duplication. On the other hand, some genes for microtubule motor proteins involved in the formation and motility of flagella were not found in R. contractilis, suggesting that the gene repertoire of R. contractilis reflected the morphological features of nonflagellated protists. Our transcriptome analysis provides basic information for the analysis of the molecular mechanism underlying microtubule dynamics in R. contractilis. [ABSTRACT FROM AUTHOR]

Ecological developmental biology (eco-devo) explores the mechanistic relationships between the processes of individual development and environmental factors. Recent studies imply that some of these relationships have deep evolutionary origins, and may even pre-date the divergences of the simplest extant animals, including cnidarians and sponges. Development of these early diverging metazoans is often sensitive to environmental factors, and these interactions occur in the context of conserved signaling pathways and mechanisms of tissue homeostasis whose detailed molecular logic remain elusive. Efficient methods for transgenesis in cnidarians together with the ease of experimental manipulation in cnidarians and sponges make them ideal models for understanding causal relationships between environmental factors and developmental mechanisms. Here, we identify major questions at the interface between animal evolution and development and outline a road map for research aimed at identifying the mechanisms that link environmental factors to developmental mechanisms in early diverging metazoans. Also watch the . [ABSTRACT FROM AUTHOR]

Specification of early embryonic cells of animals is established by maternally provided factors and interactions of neighboring cells. The present study addressed a question of autonomous versus non-autonomous specification of embryonic cells by using the Ciona intestinalis embryo, in particular the genetic cascade of zygotic expression of transcription factor genes responsible for notochord specification. To examine this issue, we combined the classic experiment of continuous dissociation of embryonic cells with the modern technique of oligonucleotide-based microarrays. We measured early zygotic expression of 389 core transcription factors genes and 118 major signal molecule genes in embryonic cells that were fully dissociated from the first cleavage. Our results indicated that even if cells are free from contact with neighbors, the major transcription factor genes that have primary roles in embryonic cell specification commence their zygotic expression at the same time as in normal embryos. Dissociation of embryonic cells did not affect extracellular signal-regulated kinases (ERK) activity. Although normal embryos treated with U0126 failed to express Bra and Twist-like-1, dissociated embryonic cells treated with U0126 expressed the genes. These results are discussed in relation to the grade of autonomous versus non-autonomous genetic cascades that are responsible for the specification of early Ciona embryonic cells. [ABSTRACT FROM AUTHOR]

We report here characterization of five genes for novel components of the canonical Wnt/ β-catenin signaling pathway. These genes were identified in the ascidian Ciona intestinalis through a loss-of-function screening for genes required for embryogenesis with morpholinos, and four of them have counterparts in vertebrates. The five genes we studied are as follows: Ci-PGAP1, a Ciona orthologue of human PGAP1, which encodes GPI (glycosylphosphatidylinositol) inositol-deacylase, Ci-ZF278, a gene encoding a C2H2 zinc-finger protein, Ci-C10orf11, a Ciona orthologue of human C10orf11 that encodes a protein with leucine-rich repeats, Ci-Spatial/C4orf17, a single counterpart for two human genes Spatial and C4orf17, and Ci-FLJ10634, a Ciona orthologue of human FLJ10634 that encodes a member of the J-protein family. Knockdown of each of the genes mimicked β-catenin knockdown and resulted in suppression of the expression of β-catenin downstream genes ( Ci-FoxD, Ci-Lhx3, Ci-Otx and Ci-Fgf9/16/20) and subsequent endoderm formation. For every gene, defects in knockdown embryos were rescued by overexpression of a constitutively active form, but not wild-type, of Ci- β-catenin. Dosage-sensitive interactions were found between Ci-β-catenin and each of the genes. These results suggest that these five genes act upstream of or parallel to Ci- β-catenin in the Wnt/ β-catenin signaling pathway in early Ciona embryos. [ABSTRACT FROM AUTHOR]

Primary mesenchyme cells (PMC), the skeletogenic cells derived from the micromeres of the sea urchin embryo, are involved in the differentiation of the gut. When PMC were deleted from the mesenchyme blastula, both formation of the constrictions in the gut and expression of endoderm-specific alkaline phosphatase were significantly delayed. Therefore, the correct timing of gut differentiation depends on the existence of PMC, probably via a type of promotive signal. To date, the only role of PMC in other tissue differentiation has been a suppressive signal for the conversion of secondary mesenchyme cells (SMC) into skeletogenic cells. The present experiments using PMC ablation and transplantation showed that both signaling processes occurred in the same short period during gastrulation, but the embryos kept their competence for gut differentiation until a later stage. Further investigations indicated that conversion of SMC did not cause delay in gut differentiation and that SMC did not mediate the PMC signal to the endoderm. Therefore, the effect of PMC on gut differentiation could be a new role that is independent of the suppressive effect for SMC conversion. [ABSTRACT FROM AUTHOR]