Stripe forming architecture of the gap gene system

Reinitz, John; Kosman, David; Vanario-Alonso, Carlos E.; Sharp, David H.

doi:10.1002/(sici)1520-6408(1998)23:1<11::aid-dvg2>3.0.co;2-9

Cited by 57 publications

(22 citation statements)

References 40 publications

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“…Gene circuits fail to reproduce expression patterns unless a complete (i.e., sufficient) set of regulators is represented in the model Jaeger et al, 2004b). This fact was exploited in a study where gene circuits including gap genes and the pair-rule gene even-skipped (eve) were fit to patterns of eve gene expression which had been shifted anteriorly or posteriorly by one or more nuclei (Reinitz et al, 1998). In contrast to the original eve pattern, none of these shifted patterns were reproduced correctly by the model, indicating that the expression pattern of eve is the only pair-rule pattern which can be formed by regulatory input from gap genes alone.…”

Section: Introductionmentioning

confidence: 93%

“…Reinitz et al, 1998). Early, mRNA expression patterns of Kr were shifted anteriorly or posteriorly to obtain a series of artificial data sets by displacing the Kr domain to different positions along the A-P axis (Fig.…”

Section: Spatial Constraints For Maternal Regulation Of Gap Gene Domainsmentioning

confidence: 99%

“…A similar, context-dependent mechanism is involved in regulation of eve stripes two and three (see Fig. 7 in Reinitz et al, 1998), where Hb activates stripe two with Bcd as its co-activator, while it represses stripe three on its own (Stanojevic et al, 1989(Stanojevic et al, , 1991Small et al, 1992Small et al, , 1996.…”

Section: Balance Between Bcd Activation and Hb Repressionmentioning

confidence: 99%

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Known maternal gradients are not sufficient for the establishment of gap domains in Drosophila melanogaster

Jaeger

Sharp

Reinitz

2007

Mechanisms of Development

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129

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Gap genes are among the first transcriptional targets of maternal morphogen gradients in the early Drosophila embryo. However, it remains unclear whether these gradients are indeed sufficient to establish the boundaries of localized gap gene expression patterns. In this study, we address this question using gap gene circuits, which are data-driven mathematical tools for extracting regulatory information from quantitative wild-type gene expression data. We present new, quantitative data on the mRNA expression patterns for the gap genes Krüppel (Kr), knirps (kni) and giant (gt) during the early blastoderm stage of Drosophila development. This data set shows significant differences in timing of gap gene expression compared to previous observations, and reveals that early gap gene expression is highly variable in both space and time. Gene circuit models fit to this data set were used for a detailed regulatory analysis of early gap gene expression. Our analysis shows that the proper balance of maternal repression and activation is essential for the correct positioning of gap domains, and that such balance can only be achieved for early expression of kni. In contrast, our results suggest that early expression of gt requires local neutralization of repressive input in the anterior region of the embryo, and that known maternal gradients are completely insufficient to position the boundaries of the early central Kr domain, or in fact any Kr-like domain in the central region of the blastoderm embryo. Based on this, we propose that unknown additional regulators must be involved in early gap gene regulation.

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Section: Introductionmentioning

confidence: 93%

Section: Spatial Constraints For Maternal Regulation Of Gap Gene Domainsmentioning

confidence: 99%

Section: Balance Between Bcd Activation and Hb Repressionmentioning

confidence: 99%

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Known maternal gradients are not sufficient for the establishment of gap domains in Drosophila melanogaster

Jaeger

Sharp

Reinitz

2007

Mechanisms of Development

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129

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“…To date, it is unclear what biological mechanism in D. melanogaster might explain how a TF switches from activator to repressor or vice versa (see Reinitz et al [12] for a review). One hypothesis is that the TF itself does not switch its function, but that the altered outcome is an emergent property of the complex interactions of the system.…”

Section: Introductionmentioning

confidence: 99%

Dual-functioning transcription factors in the developmental gene network of Drosophila melanogaster

2010

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BackgroundQuantitative models for transcriptional regulation have shown great promise for advancing our understanding of the biological mechanisms underlying gene regulation. However, all of the models to date assume a transcription factor (TF) to have either activating or repressing function towards all the genes it is regulating.ResultsIn this paper we demonstrate, on the example of the developmental gene network in D. melanogaster, that the data-fit can be improved by up to 40% if the model is allowing certain TFs to have dual function, that is, acting as activator for some genes and as repressor for others. We demonstrate that the improvement is not due to additional flexibility in the model but rather derived from the data itself. We also found no evidence for the involvement of other known site-specific TFs in regulating this network. Finally, we propose SUMOylation as a candidate biological mechanism allowing TFs to switch their role when a small ubiquitin-like modifier (SUMO) is covalently attached to the TF. We strengthen this hypothesis by demonstrating that the TFs predicted to have dual function also contain the known SUMO consensus motif, while TFs predicted to have only one role lack this motif.ConclusionsWe argue that a SUMOylation-dependent mechanism allowing TFs to have dual function represents a promising area for further research and might be another step towards uncovering the biological mechanisms underlying transcriptional regulation.

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“…This in turn produces a heterogeneous distribution of the associated proteins. These proteins act as TFs for other developmental genes, known as pair-rule genes, which exhibit a stripe-patterned expression [65]. The even-skipped (eve) gene belongs to the family of pair-rule genes and displays a seven-striped pattern (Fig.…”

Section: Embryosmentioning

confidence: 99%

The 3D Genome Shapes the Regulatory Code of Developmental Genes

Mozziconacci

Merle

Lesne

2020

Journal of Molecular Biology

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mots)We revisit the notion of gene regulatory code in embryonic development in the light of recent findings about genome spatial organisation. By analogy with the genetic code, we posit that the concept of code can only be used if the corresponding adaptor can clearly be identified. An adaptor is here defined as an intermediary physical entity mediating the correspondence between codewords and objects in a gratuitous and evolvable way. In the context of the gene regulatory code, the encoded objects are the gene expression levels, while the concentrations of specific transcription factors in the cell nucleus provide the codewords. The notion of code is meaningful in the absence of direct physicochemical relationships between the objects and the codewords, when the mediation by an adaptor is required. We propose that a plausible adaptor for this code is the gene domain, that is, the genome segment delimited by topological insulators and comprising the gene and its enhancer regulatory sequences. We review recent evidences, based on genome-wide chromosome conformation capture experiments, showing that preferential contact domains found in metazoan genomes are the physical traces of gene domains. Accordingly, genome 3D folding plays a direct role in shaping the developmental gene regulatory code.

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Stripe forming architecture of the gap gene system

Cited by 57 publications

References 40 publications

Known maternal gradients are not sufficient for the establishment of gap domains in Drosophila melanogaster

Known maternal gradients are not sufficient for the establishment of gap domains in Drosophila melanogaster

Dual-functioning transcription factors in the developmental gene network of Drosophila melanogaster

The 3D Genome Shapes the Regulatory Code of Developmental Genes

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