Location of P element insertions in the proximal promoter region of Hsp70A is consequential for gene expression and correlated with fecundity in Drosophila melanogaster

2005 ◽  
Vol preprint (2007) ◽  
pp. 1
Author(s):  
Bing Chen ◽  
Victoria Shilova ◽  
Olga Zatsepina ◽  
Michael Evgen'ev ◽  
Martin Feder
2004 ◽  
Vol 287 (3) ◽  
pp. F460-F468 ◽  
Author(s):  
Christie P. Thomas ◽  
Randy W. Loftus ◽  
Kang Z. Liu

VIT32, a vasopressin-induced transcript, inhibits Na+ transport when coexpressed with the epithelial sodium channel in Xenopus laevis oocytes ( EMBO J 21: 5109–5117, 2002). To understand the mechanism of VIT32 gene regulation, we examined the effect of DDAVP and cAMP stimulation on VIT32 expression in M-1 mouse collecting duct cells and in H441 human airway epithelial cells. Elevation of cAMP with forskolin and IBMX increased VIT32 gene expression with a peak effect at 2 h. The increase in gene expression was abolished by H89 and by actinomycin D, suggesting that cAMP stimulates VIT32 mRNA expression by a PKA-mediated increase in gene transcription. An ∼1.5-kb fragment of the 5′-flanking region of VIT32 was cloned and was able to confer cAMP-stimulated reporter gene activity when transfected into M-1 and H441 cells. By deletion analysis and site-directed mutagenesis, a cAMP response element (CRE) was identified within the proximal promoter region that was sufficient to account for the increase in VIT32 gene expression seen with DDAVP and elevation of cAMP. Furthermore, DDAVP-stimulated VIT32 promoter-reporter activity was inhibited by H89 and by a dominant negative CREB construct. Finally, we were able to identify CREB as a nuclear protein that bound to the VIT32 CRE in gel mobility shift assays. In summary, DDAVP stimulates transcription of VIT32 via a CRE within the proximal promoter region of the VIT32 gene.


Mitochondrion ◽  
2001 ◽  
Vol 1 (3) ◽  
pp. 225-236 ◽  
Author(s):  
Cristina Ugalde ◽  
Pilar Ochoa ◽  
Marı́a Luz Pérez ◽  
Miguel Angel Fernández-Moreno ◽  
Manuel Calleja ◽  
...  

1993 ◽  
Vol 23 (3) ◽  
pp. 553-565 ◽  
Author(s):  
Norihiro Ohtsubo ◽  
Takuya Nakayama ◽  
Rie Terada ◽  
Ko Shimamoto ◽  
Masaki Iwabuchi

1992 ◽  
Vol 20 (5) ◽  
pp. 1061-1068 ◽  
Author(s):  
Valerie Rossi ◽  
Jean Francois Rouayrenc ◽  
Laurent Paquereau ◽  
Marie Joseé Vilarem ◽  
Alphonse Le Cam

Development ◽  
1988 ◽  
Vol 104 (Supplement) ◽  
pp. 85-93 ◽  
Author(s):  
Stephen J. Poole ◽  
Thomas B. Kornberg

The engrailed gene is required for segmentation of the Drosophila embryo and is expressed in cells constituting the posterior developmental compartments. In mutant embryos lacking engrailed function, portions of the cuticular pattern in each segment are deleted, resulting in fusion of adjacent denticle bands. Using P-element-mediated transposition, we generated flies that express the engrailed gene under the control of an hsp70 promoter, and found that ectopic, heat-shock-induced, engrailed expression caused pattern defects similar to those in embryos lacking engrailed function. Sensitivity to heat shock was only during the cellular blastoderm and early gastrulation periods. This window of sensitivity corresponds to the time when wildtype engrailed protein localizes into segmentally reiterated stripes and represents only a small portion of the normal period of engrailed gene expression.


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