title: Retinoic acid-driven Hox1 is required in the epidermis for forming the otic/atrial placodes during ascidian metamorphosis.
abstract: Retinoic acid (RA)-mediated expression of the homeobox gene Hox1 is a hallmark of the chordate central nervous system (CNS). It has been suggested that the RA-Hox1 network also functions in the epidermal ectoderm of chordates. Here, we show that in the urochordate ascidian Ciona intestinalis, RA-Hox1 in the epidermal ectoderm is necessary for formation of the atrial siphon placode (ASP), a structure homologous to the vertebrate otic placode. Loss of Hox1 function resulted in loss of the ASP, which could be rescued by expressing Hox1 in the epidermis. As previous studies showed that RA directly upregulates Hox1 in the epidermis of Ciona larvae, we also examined the role of RA in ASP formation. We showed that abolishment of RA resulted in loss of the ASP, which could be rescued by forced expression of Hox1 in the epidermis. Our results suggest that RA-Hox1 in the epidermal ectoderm played a key role in the acquisition of the otic placode during chordate evolution.
authors.affiliation: Shimoda Marine Research Center, University of Tsukuba, Shimoda, Shizuoka 415-0025, Japan. sasakura@kurofune.shimoda.tsukuba.ac.jp
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Sasakura
authors.forename: Miyuki
authors.initials: M
authors.lastname: Kanda
authors.forename: Taku
authors.initials: T
authors.lastname: Ikeda
authors.forename: Takeo
authors.initials: T
authors.lastname: Horie
authors.forename: Narudo
authors.initials: N
authors.lastname: Kawai
authors.forename: Yosuke
authors.initials: Y
authors.lastname: Ogura
authors.forename: Reiko
authors.initials: R
authors.lastname: Yoshida
authors.forename: Akiko
authors.initials: A
authors.lastname: Hozumi
authors.forename: Nori
authors.initials: N
authors.lastname: Satoh
authors.forename: Shigeki
authors.initials: S
authors.lastname: Fujiwara
mesh_terms: D000818:Animals; D002938:Ciona intestinalis / Q000187:drug effects / Q000254:growth & development*; D004742:Enhancer Elements, Genetic / Q000235:genetics; D004817:Epidermis / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D005880:Gills / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism; D049452:Green Fluorescent Proteins / Q000378:metabolism; D006325:Heart Atria / Q000033:anatomy & histology* / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism; D018398:Homeodomain Proteins / Q000235:genetics / Q000378:metabolism*; D008675:Metamorphosis, Biological / Q000187:drug effects* / Q000235:genetics; D024510:Muscle Development / Q000187:drug effects; D009132:Muscles / Q000187:drug effects; D009154:Mutation / Q000235:genetics; D014212:Tretinoin / Q000494:pharmacology*
chemical_list: D018398:Homeodomain Proteins; D049452:Green Fluorescent Proteins; D014212:Tretinoin