Regulation of the Xenopus laevis transcription factor IIIA gene during oogenesis and early embryogenesis: negative elements repress the O-TFIIIA promoter in embryonic cells.
Expression of the Xenopus laevis transcription factor IIIA (TFIIIA) gene is developmentally regulated. In this study we have used defined nucleotide mutations to map cis-elements involved in transcriptional regulation of the promoter for oocyte-TFIIIA (O-TFIIIA) in stage II-IV oocytes, stage VI oocytes, and tail bud embryos. During oogenesis O-TFIIIA mRNA levels decline 5- to 10-fold, and during early embryogenesis O-TFIIIA mRNA levels decline approximately 10(6)-fold per cell. In stage II-IV oocytes we find evidence for at least three distinct positive-acting cis-elements that contribute to the efficient expression of O-TFIIIA. These elements are located between -1800 to -425, -280 to -235, and -235 to -220. The most distal cis-element(s) appears to be developmentally regulated during oogenesis, since deletion of nucleotide sequences from -1800 to -425 does not reduce O-TFIIIA expression in stage VI oocytes. However, the two cis-elements located between -280 to -235 and -235 to -220 are required for the efficient expression of O-TFIIIA in stage VI oocytes. In tail bud embryos we find evidence for several developmentally regulated positive and negative cis-elements involved in O-TFIIIA expression. The positive-acting cis-elements are located between -159 to -110 and -110 to -58. The negative-acting cis-elements are found at positions -425 to -350 and -200 to -159. In addition to the developmentally regulated elements controlling O-TFIIIA gene expression in tail bud embryos, the positive-acting cis-elements active during oogenesis (located between -280 to -235 and -235 to -220) are also active during early embryogenesis. Thus, transcription from the O-TFIIIA promoter appears to be regulated by a combination of constitutive positive factors and developmentally regulated positive and negative factors during oogenesis and early embryogenesis.
Pfaff
S L
SL
School of Medicine, Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee 37232.
Hall
R K
RK
Hart
G C
GC
Taylor
W L
WL
D000818:Animals; D001483:Base Sequence; D001755:Blastocyst / Q000502:physiology; D015500:Chloramphenicol O-Acetyltransferase / Q000096:biosynthesis; D002872:Chromosome Deletion; D005775:Gastrula / Q000502:physiology; D005786:Gene Expression Regulation; D008969:Molecular Sequence Data; D016297:Mutagenesis, Site-Directed; D009866:Oogenesis / Q000502:physiology*; D010063:Ovum / Q000502:physiology; D011401:Promoter Regions, Genetic / Q000502:physiology*; D012333:RNA, Messenger / Q000096:biosynthesis; D012341:RNA, Ribosomal, 5S / Q000096:biosynthesis*; D035582:Transcription Factor TFIIIA; D014157:Transcription Factors / Q000096:biosynthesis / Q000235:genetics* / Q000502:physiology*; D014158:Transcription, Genetic; D014982:Xenopus laevis / Q000196:embryology*
D012333:RNA, Messenger; D012341:RNA, Ribosomal, 5S; D035582:Transcription Factor TFIIIA; D014157:Transcription Factors; D015500:Chloramphenicol O-Acetyltransferase