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1 Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA
2 Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA; Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA
* To whom correspondence should be addressed. E-mail: shenning{at}bcm.tmc.edu.
In the developing intestine, transcription of 
-glucosidase genes such as sucrase-isomaltase and
trehalase is stimulated by glucocorticoid administration. The consequent increase of their
respective mRNAs is characterized by a 12 hr lag, suggesting that the response to
glucocorticoids represents a secondary effect. We hypothesized that the primary response of the
tissue to glucocorticoids includes induction of one or more intestinal transcription factors. To
investigate this hypothesis we identified a region in the mouse trehalase promoter (located at
nucleotides -406 to -377 from the transcription start site) with potential binding sites for three
transcription factors: Cdx-2, GATA and C/EBP. Gel shifts were performed using labeled
oligonucleotides from this region with nuclear extracts from jejunums of either control 8-day old
mouse pups or littermates treated with dexamethasone (DEX) 4 hr prior to sacrifice. A specific
shifted band was observed with DEX extracts but not with control extracts. Supershift assays
indicated the presence of GATA-4 and GATA-6 but not GATA-5, nor Cdx-2, C/EBP, C/EBP
,
or C/EBP
. GATA binding was further implicated by competition studies with mutated
oligonucleotides. Finally, Western blotting showed GATA-4 and GATA-6 proteins in DEX but
not control nuclear extracts. For GATA-4 the same pattern was demonstrated with whole cell
extracts and with the cytosol fraction. We conclude that expression of GATA-4 and GATA-6
proteins in the suckling mouse jejunum is stimulated by DEX. This novel finding constitutes an
important first step in understanding the molecular mechanism of glucocorticoid action on the
developing intestine.
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