title: Antimorphic PV.1 causes secondary axis by inducing ectopic organizer.
abstract: Xenopus homeobox gene, PV.1 ventralizes activin-induced dorsal mesoderm and inhibits neuralization of ectoderm in animal cap when overexpressed. Here we generated PV.1/engrailed fusion construct (N-PV1-EnR) to perform loss-of-function study for this transcription factor. N-PV1-EnR showed an extremely antimorphic effect, causing a partial secondary embryonic axis when expressed at ventral marginal zone of blastula. In ventral marginal zone cells, this chimeric protein induced organizer genes and suppressed ventral markers mimicking those effects reported for dominant negative BMP-4 receptor (DNBR). Moreover, N-PV1-EnR rescued the ventralized embryos caused by the ectopic dorsal expression of PV.1 but not by that of Xvent-2. These results suggested that PV.1 functions at downstream of BMP-4 as a ventralizing effector which acts separately from Xvent-2 and the dominant negative effect gained by this specific mutant is applicable for the further studies of BMP-4 downstream pathway.
authors.affiliation: Department of Anatomy, School of Medicine, Kyungpook National University, Taegu, 700-422, South Korea.
authors.forename: Yoo-Seok
authors.initials: YS
authors.lastname: Hwang
authors.forename: Jeong-Jae
authors.initials: JJ
authors.lastname: Seo
authors.forename: Sang-Wook
authors.initials: SW
authors.lastname: Cha
authors.forename: Hyun-Shik
authors.initials: HS
authors.lastname: Lee
authors.forename: Sung-Young
authors.initials: SY
authors.lastname: Lee
authors.forename: Dong-Hyun
authors.initials: DH
authors.lastname: Roh
authors.forename: Hsiang-fu
authors.initials: HF
authors.lastname: Kung Hf
authors.forename: Jaebong
authors.initials: J
authors.lastname: Kim
authors.forename: Mae
authors.initials: M
authors.lastname: Ja Park
mesh_terms: D030201:Activin Receptors, Type I / Q000235:genetics / Q000378:metabolism; D000818:Animals; D019521:Body Patterning / Q000187:drug effects / Q000502:physiology*; D052005:Bone Morphogenetic Protein Receptors, Type I; D004625:Embryo, Nonmammalian / Q000187:drug effects / Q000196:embryology / Q000502:physiology; D004627:Embryonic Induction / Q000187:drug effects; D005799:Genes, Dominant; D018398:Homeodomain Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000494:pharmacology*; D066298:In Vitro Techniques; D008845:Microinjections; D020897:Organizers, Embryonic / Q000187:drug effects / Q000378:metabolism*; D010641:Phenotype; D017346:Protein Serine-Threonine Kinases; D012333:RNA, Messenger / Q000008:administration & dosage / Q000235:genetics; D017978:Receptors, Growth Factor; D011993:Recombinant Fusion Proteins / Q000096:biosynthesis / Q000235:genetics / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology; D014157:Transcription Factors; D014981:Xenopus; D029867:Xenopus Proteins
chemical_list: D018398:Homeodomain Proteins; D012333:RNA, Messenger; D017978:Receptors, Growth Factor; D011993:Recombinant Fusion Proteins; D014157:Transcription Factors; D029867:Xenopus Proteins; C106185:engrailed homeobox proteins; C109693:ventx1.1 protein, Xenopus; D017346:Protein Serine-Threonine Kinases; D030201:Activin Receptors, Type I; D052005:Bone Morphogenetic Protein Receptors, Type I