Pair-rule expression of the Drosophila fushi tarazu gene: a nuclear receptor response element mediates the opposing regulatory effects of runt and hairy

Development ◽  
1995 ◽  
Vol 121 (2) ◽  
pp. 453-462 ◽  
Author(s):  
C. Tsai ◽  
P. Gergen
Keyword(s):  
Nuclear Receptor ◽  
Transcriptional Activation ◽  
Reporter Genes ◽  
Orphan Nuclear Receptor ◽  
Fushi Tarazu ◽  
Pair Rule Gene ◽  
Dna Elements ◽  
Regulatory Effects ◽  
Opposing Effects ◽  
Pair Rule

The segmentation genes runt and hairy are required for the proper transcriptional regulation of the pair-rule gene fushi tarazu during the blastoderm stage of Drosophila embryogenesis. The expression of different fushi tarazu reporter genes was examined in runt and hairy mutant embryos, as well as in runt over-expressing embryos in order to identify DNA elements responsible for mediating these regulatory effects. The results indicated that runt and hairy act through a common 32 base-pair element. This element, designated as fDE1, contains a binding site for a small family of orphan nuclear receptor proteins that are uniformly expressed in blastoderm embryos. The pair-rule expression of reporter gene constructs containing multimerized fDE1 elements depends on activation by runt and repression by hairy. Examination of reporter genes with mutated fDE1 elements provided further evidence that this element mediates both transcriptional activation and repression. Genetic experiments indicated that the opposing effects of runt and hairy were not due solely to cross-regulatory interactions between these two genes and that fDE1-dependent expression is regulated by factors in addition to runt and hairy.

Ftz-F1 is a cofactor in Ftz activation of the Drosophila engrailed gene

Development ◽  
1997 ◽  
Vol 124 (4) ◽  
pp. 839-847 ◽  
Author(s):  
B. Florence ◽  
A. Guichet ◽  
A. Ephrussi ◽  
A. Laughon
Keyword(s):  
Transcriptional Activation ◽  
Binding Sites ◽  
Direct Contact ◽  
Regulatory Element ◽  
Drosophila Embryo ◽  
Homeodomain Protein ◽  
Reporter Expression ◽  
Fushi Tarazu ◽  
Pair Rule Gene ◽  
Pair Rule

The fushi tarazu pair-rule gene is required for the formation of alternating parasegmental boundaries in the Drosophila embryo. fushi tarazu encodes a homeodomain protein necessary for transcription of the engrailed gene in even-numbered parasegments. Here we report that, within an engrailed enhancer, adjacent and conserved binding sites for the Fushi tarazu protein and a cofactor are each necessary, and together sufficient, for transcriptional activation. Footprinting shows that the cofactor site can be bound specifically by Ftz-F1, a member of the nuclear receptor superfamily. Ftz-F1 and the Fushi tarazu homeodomain bind the sites with 4- to 8-fold cooperativity, suggesting that direct contact between the two proteins may contribute to target recognition. Even parasegmental reporter expression is dependent on Fushi tarazu and maternal Ftz-F1, suggesting that these two proteins are indeed the factors that act upon the two sites in embryos. The two adjacent binding sites are also required for continued activity of the engrailed enhancer after Fushi tarazu protein is no longer detectable, including the period when engrailed, and the enhancer, become dependent upon wingless. We also report the existence of a separate negative regulatory element that apparently responds to odd-skipped.

The orphan nuclear receptor NGFI-B regulates expression of the gene encoding steroid 21-hydroxylase

1993 ◽  
Vol 13 (2) ◽  
pp. 861-868
Author(s):  
T E Wilson ◽  
A R Mouw ◽  
C A Weaver ◽  
J Milbrandt ◽  
K L Parker
Keyword(s):  
Nuclear Receptor ◽  
Transcriptional Activation ◽  
Core Promoter ◽  
Orphan Nuclear Receptor ◽  
Recognition Sequence ◽  
Mobility Shift ◽  
Adrenocortical Cells ◽  
Gene Encoding ◽  
Adult Rat ◽  
Gel Mobility Shift

As part of its trophic action to maintain the steroidogenic capacity of adrenocortical cells, corticotropin (ACTH) increases the transcription of the cytochrome P-450 steroid hydroxylase genes, including the gene encoding steroid 21-hydroxylase (21-OHase). We previously identified several promoter elements that regulate 21-OHase gene expression in mouse Y1 adrenocortical tumor cells. One of these elements, located at nucleotide -65, closely resembles the recognition sequence of the orphan nuclear receptor NGFI-B, suggesting that NGFI-B regulates this essential steroidogenic enzyme. To explore this possibility, we first used in situ hybridization to demonstrate high levels of NGFI-B transcripts in the adrenal cortex of the adult rat. In cultured mouse Y1 adrenocortical cells, treatment with ACTH, the major regulator of 21-OHase transcription, rapidly increased NGFI-B expression. Gel mobility shift and DNase I footprinting experiments showed that recombinantly expressed NGFI-B interacts specifically with the 21-OHase -65 element and identified one complex formed by Y1 extracts and the 21-OHase -65 element that contains NGFI-B. Expression of NGFI-B significantly augmented the activity of the intact 21-OHase promoter, while mutations of the -65 element that abolish NGFI-B binding markedly diminished NGFI-B-mediated transcriptional activation. Specific mutations of NGFI-B shown previously to impair either DNA binding or transcriptional activation diminished the effect of NGFI-B coexpression on 21-OHase expression. Finally, an oligonucleotide containing the NGFI-B response element conferred ACTH response to a core promoter from the prolactin gene, showing that this element is sufficient for ACTH induction. Collectively, these results identify a cellular promoter element that is regulated by NGFI-B and implicate NGFI-B in the transcriptional induction of 21-OHase by ACTH.

Transcriptional regulation of cytoskeletal functions and segmentation by a novel maternal pair-rule gene, lilliputian

Development ◽  
2001 ◽  
Vol 128 (5) ◽  
pp. 801-813 ◽  
Author(s):  
A.H. Tang ◽  
T.P. Neufeld ◽  
G.M. Rubin ◽  
H.A. Muller
Keyword(s):  
Transcriptional Control ◽  
Fragile X ◽  
Transcriptional Regulator ◽  
Regulator Gene ◽  
Embryonic Patterning ◽  
Fushi Tarazu ◽  
Fragile X Mental Retardation ◽  
Pair Rule Gene ◽  
Mutant Phenotypes ◽  
Pair Rule

Transcriptional control during early Drosophila development is governed by maternal and zygotic factors. We have identified a novel maternal transcriptional regulator gene, lilliputian (lilli), which contains an HMG1 (AT-hook) motif and a domain with similarity to the human fragile X mental retardation FMR2 protein and the AF4 proto-oncoprotein. Embryos lacking maternal lilli expression show specific defects in the establishment of a functional cytoskeleton during cellularization, and exhibit a pair-rule segmentation phenotype. These mutant phenotypes correlate with markedly reduced expression of the early zygotic genes serendipity alpha, fushi tarazu and huckebein, which are essential for cellularization and embryonic patterning. In addition, loss of lilli in adult photoreceptor and bristle cells results in a significant decrease in cell size. Our results indicate that lilli represents a novel pair-rule gene that acts in cytoskeleton regulation, segmentation and morphogenesis.

scholarly journals The HMG-box protein Lilliputian is required for Runt-dependent activation of the pair-rule gene fushi–tarazu

2007 ◽  
Vol 301 (2) ◽  
pp. 350-360 ◽  
Author(s):  
Christine J. VanderZwan-Butler ◽  
Lisa M. Prazak ◽  
J. Peter Gergen
Keyword(s):  
Fushi Tarazu ◽  
Hmg Box ◽  
Pair Rule Gene ◽  
Pair Rule

scholarly journals Dax1 Up-Regulates Oct4 Expression in Mouse Embryonic Stem Cells via LRH-1 and SRA

2010 ◽  
Vol 24 (12) ◽  
pp. 2281-2291 ◽  
Author(s):  
Victoria R. Kelly ◽  
Bin Xu ◽  
Rork Kuick ◽  
Ronald J. Koenig ◽  
Gary D. Hammer
Keyword(s):  
Nuclear Receptor ◽  
Transcriptional Activation ◽  
Chromatin Immunoprecipitation ◽  
Target Genes ◽  
Embryonic Stem ◽  
Steroid Receptor ◽  
Orphan Nuclear Receptor ◽  
Steroidogenic Factor 1 ◽  
Oct4 Expression ◽  
Mes Cells

Abstract Dax1 (Nr0b1) is an atypical orphan nuclear receptor that has recently been shown to play a role in mouse embryonic stem (mES) cell pluripotency. Here we describe a mechanism by which Dax1 maintains pluripotency. In steroidogenic cells, Dax1 protein interacts with the NR5A nuclear receptor steroidogenic factor 1 (Nr5a1) to inhibit transcription of target genes. In mES cells, liver receptor homolog 1 (LRH-1, Nr5a2), the other NR5A family member, is expressed, and LRH-1 has been shown to interact with Dax1. We demonstrate by coimmunoprecipitation that Dax1 is, indeed, able to form a complex with LRH-1 in mES cells. Because Dax1 was historically characterized as an inhibitor of steroidogenic factor 1-mediated transcriptional activation, we hypothesized that Dax1 would inhibit LRH-1 action in mES cells. Therefore, we examined the effect of Dax1 on the LRH-1-mediated activation of the critical ES cell factor Oct4 (Pou5f1). Chromatin immunoprecipitation localized Dax1 to the Oct4 promoter at the LRH-1 binding site, and luciferase assays together with Dax1 overexpression and knockdown experiments revealed that, rather than repress, Dax1 accentuated LRH-1-mediated activation of the Oct4 gene. Similar to our previously published studies that defined the RNA coactivator steroid receptor RNA activator as the critical mediator of Dax1 coactivation function, Dax1 augmentation of LRH-1-mediated Oct4 activation is dependent upon steroid receptor RNA activator. Finally, utilizing published chromatin immunoprecipitation data of whole-genome binding sites of LRH-1 and Dax1, we show that LRH-1 and Dax1 commonly colocalize at 288 genes (43% of LRH-1 target genes), many of which are involved in mES cell pluripotency. Thus, our results indicate that Dax1 plays an important role in the maintenance of pluripotency in mES cells through interaction with LRH-1 and transcriptional activation of Oct4 and other genes.

Decoding positional information: regulation of the pair-rule gene hairy

Development ◽  
1990 ◽  
Vol 110 (4) ◽  
pp. 1223-1231 ◽  
Author(s):  
K.R. Howard ◽  
G. Struhl
Keyword(s):  
Transcriptional Activation ◽  
Transcriptional Repression ◽  
Expression Patterns ◽  
Positional Information ◽  
Regulatory Elements ◽  
Regulatory Factors ◽  
Cis Acting ◽  
Pair Rule Gene ◽  
Necessary And Sufficient ◽  
Pair Rule

In the series of local gene activations that occur during early Drosophila development, the striped expression patterns of the pair-rule genes provide the first indication of segmental periodicity. The experiments that we report here address the question of how these patterns arise, by studying the regulation of one of these genes, hairy. We show that each of the seven stripes of hairy expression is controlled by a distinct subset of cis-acting regulatory elements, some mediating transcriptional activation and others transcriptional repression. In general, elements necessary and sufficient for triggering a particular stripe response are clustered on the DNA and appear to overlap or be interspersed with elements involved in at least one other stripe response. Our results extend previous findings suggesting that periodic hairy expression arises by a decoding process in which each stripe is triggered by particular combinations or concentrations of regulatory factors. These regulatory factors are likely to include the products of the gap class of segmentation genes that are required for activating or positioning particular subsets of hairy stripes and are expressed with overlapping distributions during early embryogenesis.

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