Activation of posterior gap gene expression in the Drosophila blastoderm

Rivera‐Pomar, Rolando; Lu, Xiangyi; Perrimon, Norbert; Taubert, Heike; Jäckle, Herbert

doi:10.1038/376253a0

Cited by 184 publications

(199 citation statements)

References 27 publications

Supporting

Mentioning

190

Contrasting

Order By: Relevance

“…To determine whether dCBP may participate in enhancerspecific activities of Bcd, we took advantage of another reporter gene, kni-CAT, which contains the 64-bp Bcd-responsive kni enhancer element (17). Our co-transfection experiments showed that, whereas dCBP increased the activity of Bcd on hb-CAT reporter by 19 fold (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Despite its critical biological role and extensive previous studies, it remains unclear how Bcd activates transcription and what other factors participate in the activation process (15,16). Another important issue on Bcd as a molecular morphogen relates to its special ability to activate different target genes in distinctive manners (13,(17)(18)(19). Only recent studies have begun to shed light on this important issue, suggesting that enhancer architecture can influence how Bcd binds DNA and activates transcription (20).…”

mentioning

confidence: 99%

See 1 more Smart Citation

The Co-activator CREB-binding Protein Participates in Enhancer-dependent Activities of Bicoid

Wen

2004

Journal of Biological Chemistry

View full text Add to dashboard Cite

Bicoid (Bcd) is a transcriptional activator required for early embryonic patterning in Drosophila. Despite extensive studies, it currently remains unclear how Bcd activates transcription and what proteins participate in its activation process. In this report, we describe experiments to analyze the role of the Drosophila co-activator dCBP in Bcd-mediated activation. In Drosophila S2 cells, the Bcd activity is increased by the co-transfection of plasmids expressing dCBP and reduced by doublestranded RNA-mediated interference against dCBP. We further show that Bcd and dCBP can interact with each other and that Bcd-interacting domains of dCBP can cause dominant negative effects on Bcd activity in S2 cells. Our comparison of two Bcd-responsive enhancers, hunchback (hb) and knirps (kni), reveals a differential role of dCBP in facilitating Bcd activation. A dCBP mutant defective in its histone acetyltransferase activity exhibits a reduced, but not abolished, co-activator function for Bcd. Our chromatin immunoprecipitation experiments show that dCBP can increase not only the occupancy of Bcd itself at the enhancers but also the recruitment of general transcription factors to the promoter. Together, these experiments suggest that dCBP is an enhancer-dependent co-activator of Bcd, facilitating its activation through multiple mechanisms.

show abstract

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

The Co-activator CREB-binding Protein Participates in Enhancer-dependent Activities of Bicoid

Wen

2004

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…1). Possibly, Ma-bcd is repressing translation of a Megaselia caudal homolog more posteriorly than in the Drosophila embryo (50,51) and/or Ma-bcd has a stronger inf luence on the activation of posterior gap genes such as Krüppel and knirps (7,52). However, the additional requirement for bicoid might not be linked to increased hunchback function in the more primitive f ly species, because the relevant expression of this gene is conserved (Fig.…”

Section: Ma-bcd Rnai Causes Symmetrical Double Abdomen In Megaseliamentioning

confidence: 99%

“…The head and thorax are replaced by duplicated posterior terminal structures of reversed polarity (4). The morphogen-like function of Bicoid requires cooperation with the zinc finger type transcription factor Hunchback in determining the anterior segment pattern; posteriorly, Bicoid complements the homeodomain transcription factor caudal in a partially redundant manner (5)(6)(7)(8).…”

mentioning

confidence: 99%

Function of bicoid and hunchback homologs in the basal cyclorrhaphan fly Megaselia (Phoridae)

Stauber

Taubert

Schmidt‐Ott

2000

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

View full text Add to dashboard Cite

The Drosophila gene bicoid functions at the beginning of a gene cascade that specifies anterior structures in the embryo. Its transcripts are localized at the anterior pole of the oocyte, giving rise to a Bicoid protein gradient, which regulates the spatially restricted expression of target genes along the anterior-posterior axis of the embryo in a concentration-dependent manner. The morphogen function of Bicoid requires the coactivity of the zinc finger transcription factor Hunchback, which is expressed in a Bicoid-dependent fashion in the anterior half of the embryo. Whereas hunchback is conserved throughout insects, bicoid homologs are known only from cyclorrhaphan flies. Thus far, identification of hunchback and bicoid homologs rests only on sequence comparison. In this study, we used double-stranded RNA interference (RNAi) to address the function of bicoid and hunchback homologs in embryos of the lower cyclorrhaphan fly Megaselia abdita (Phoridae). Megaselia-hunchback RNAi causes hunchback-like phenotypes as observed in Drosophila, but Megaselia-bicoid RNAi causes phenotypes different from corresponding RNAi experiments in Drosophila and bicoid mutant embryos. Megaselia-bicoid is required not only for the head and thorax but also for the development of four abdominal segments. This difference between Megaselia and Drosophila suggests that the range of functional bicoid activity has been reduced in higher flies.

show abstract

“…Several CRMs (including kni and hairy 7) also contain clusters of binding sites for Caudal (Cad), which is expressed in a posterior gradient (38). Previous work suggests that Cad functions with Bcd to activate expression of these CRMs (39,40).…”

Section: Ap Positioning By Combinations Of Activators Andmentioning

confidence: 99%

The role of binding site cluster strength in Bicoid-dependent patterning in Drosophila

Ochoa-Espinosa

Yücel

Kaplan

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

168

171

View full text Add to dashboard Cite

The maternal morphogen Bicoid (Bcd) is distributed in an embryonic gradient that is critical for patterning the anterior-posterior (AP) body plan in Drosophila. Previous work identified several target genes that respond directly to Bcd-dependent activation. Positioning of these targets along the AP axis is thought to be controlled by cis-regulatory modules (CRMs) that contain clusters of Bcd-binding sites of different ''strengths.'' Here we use a combination of Bcd-site cluster analysis and evolutionary conservation to predict Bcd-dependent CRMs. We tested 14 predicted CRMs by in vivo reporter gene assays; 11 show Bcd-dependent activation, which brings the total number of known Bcd target elements to 21. Some CRMs drive expression patterns that are restricted to the most anterior part of the embryo, whereas others extend into middle and posterior regions. However, we do not detect a strong correlation between AP position of target gene expression and the strength of Bcd site clusters alone. Rather, we find that binding sites for other activators, including Hunchback and Caudal correlate with CRM expression in middle and posterior body regions. Also, many Bcd-dependent CRMs contain clusters of sites for the gap protein Kruppel, which may limit the posterior extent of activation by the Bcd gradient. We propose that the key design principle in AP patterning is the differential integration of positive and negative transcriptional information at the level of individual CRMs for each target gene.morphogen ͉ network ͉ transcription G radients of two transcription factors, Bicoid (Bcd) and Dorsal (Dl), are critical for patterning the major body plan axes in the Drosophila embryo. This studied focused on Bcd, a maternal effect gene whose mRNA is initially localized at the anterior pole of the oocyte (Fig. 1A) (1). Upon egg deposition, the trapped bcd RNA is translated, and a nuclear gradient forms, with highest concentrations near the anterior pole and progressively lower concentrations in more posterior regions (Fig. 1B) (2). Bcd protein distribution matches its biological activity, with high levels required for the positioning of the most anterior structures, intermediate levels for head structures, and low levels for the thoracic and anterior abdominal segments. Varying the shape of the Bcd gradient has a direct effect on positional identity in the blastoderm (3). Increasing the maternal input of bcd can shift morphological landmarks posteriorly, whereas decreasing it shifts them anteriorly. These experiments suggest that the concentration of Bcd protein present at each position along the length of the embryo (EL) determines the destiny of cells that will occupy that region.Bcd protein contains a homeodomain and functions as a morphogen by activating the transcription of multiple target genes in different positions along the anterior-posterior (AP) axis (reviewed in refs. 4 and 5). Driever, Thoma, and Nüsslein-Volhard (6) first proposed that differential positioning could occur by means of gene-specific regulatory ele...

show abstract

Activation of posterior gap gene expression in the Drosophila blastoderm

Cited by 184 publications

References 27 publications

The Co-activator CREB-binding Protein Participates in Enhancer-dependent Activities of Bicoid

The Co-activator CREB-binding Protein Participates in Enhancer-dependent Activities of Bicoid

Function of bicoid and hunchback homologs in the basal cyclorrhaphan fly Megaselia (Phoridae)

The role of binding site cluster strength in Bicoid-dependent patterning in Drosophila

Contact Info

Product

Resources

About