ArticleDevelopment genes and evolution2004
Ets-mediated brain induction in embryos of the ascidian Halocynthia roretzi.
Article in Development genes and evolution, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 16 citations in OpenAlex.
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- Identification, Characterization, and Expression Analysis Reveal Diverse Regulated Roles of Three MAPK Genes inFrontiers in physiology · 2021Article
- An otx/nodal regulatory signature for posterior neural development in ascidians.PLoS genetics · 2014Article
- Erk2 in ovarian development of green mud crab Scylla paramamosain.DNA and cell biology · 2012Article
- FGF9/16/20 and Wnt-5alpha signals are involved in specification of secondary muscle fate in embryos of the ascidian, Halocynthia roretzi.Development genes and evolution · 2007Article
- Brain induction in ascidian embryos is dependent on juxtaposition of FGF9/16/20-producing and -receiving cells.Development genes and evolution · 2007Article
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2 authors at 1 institution in 1 country.
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Abstract
The larval ascidian brain (sensory vesicle) is located on the dorsal side of the trunk region and forms part of the anterior central nervous system. Sensory organs such as the otolith, ocellus, and hydrostatic-pressure organ reside in the brain. The brain coordinates the core roles of the larval nervous system. The brain is derived from anterior animal a-line blastomeres. The default fate of these blastomeres is epidermis, and the inductive signals from anterior vegetal blastomeres convert the fate into brain. It remains unclear, however, when these inductive interactions take place. To determine when, we examined whether partial embryos derived from brain-lineage blastomeres isolated at various stages express neural and epidermal marker genes. Partial embryos derived from brain-lineage blastomeres isolated after the 32-cell stage expressed all the neural marker genes examined. The expression of the epidermal marker gene was first reduced in partial embryos when blastomeres were isolated at the 64-cell stage. Moreover, the process for brain specification seemed to continue after the 110-cell stage. We also investigated the function of HrEts, an ascidian homolog of Ets transcription factors, to elucidate the molecular mechanism of brain induction. HrEts functions were inhibited by the use of antisense morpholino oligonucleotides. Loss of Ets functions resulted in loss of the expression of some of the neural marker genes and the ectopic expression of the epidermal marker gene in brain precursor cells. These results suggest that HrEts is an essential transcription factor that mediates ascidian brain induction.
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