ABSTRACT
The mouse alpha-fetoprotein gene is expressed at high levels in the fetal liver and is transcriptionally silenced at birth. The repression is governed, at least in part, by the 250 base pair (bp) AFP promoter. We show here that the AFP promoter is dramatically repressed by HNF3 in HepG2 hepatoma cells. This repression is governed by the region between -205 and -150. Furthermore, this fragment can confer HNF3-mediated repression on a heterologous promoter. The repression is abolished by a mutation that is centered at -165. EMSA analyses using in vivo and in vitro synthesized proteins indicate that HNF3 proteins do not bind DNA from the -205 to -150 region. We propose that HNF3 represses AFP promoter activity through indirect mechanisms that modulate the binding or activity of a liver-enriched factor that interacts with the -165 region of the AFP promoter.
Subject(s)
DNA-Binding Proteins/physiology , Gene Silencing , Nuclear Proteins/physiology , Promoter Regions, Genetic , Transcription Factors , alpha-Fetoproteins/genetics , Animals , Base Sequence , Binding Sites , Carcinoma, Hepatocellular , HeLa Cells , Hepatocyte Nuclear Factor 3-alpha , Hepatocyte Nuclear Factor 3-beta , Humans , Mice , Mutation , Repressor Proteins/physiology , Tumor Cells, CulturedABSTRACT
Few studies in the domain of reading have explored the relation between time limitations and reading comprehension. Time limitations may enhance reading comprehension by promoting mindfulness in students, a construct which involves exertion of more effort and motivation. This study explored the effects of time constraints on reading comprehension in adult readers. Mild time constraints should create greater mindfulness in readers, resulting in enhanced comprehension. College students read passages under no time pressure, under mild time pressure, or under severe time pressure. Reading comprehension was assessed in each condition. The best reading comprehension was observed under mild time pressure. Implications are discussed. Copyright 1999 Academic Press.