Function of the spalt/spalt-related gene complex in positioning the veins in the Drosophila wing

Celis, José F. de; Barrio, Rosa

doi:10.1016/s0925-4773(99)00261-0

Cited by 118 publications

(136 citation statements)

References 41 publications

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“…Genetic evidence in Drosophila has demonstrated a cell autonomous role for spalt as a transcriptional repressor (7)(8)(9). Similarly, in recent work we revealed that Sall proteins contain an N-terminal repression domain that recruits the nucleosome remodeling and deacetylase (NuRD) 2 complex, revealing a strong correlation between repression and NuRD complex interaction (10).…”

mentioning

confidence: 69%

“…Sall1 and Gbx2 are well defined transcriptional regulators that are critical for embryonic development (7)(8)(9)(35)(36)(37)(38). Gbx2 is a homeobox-containing transcription factor that is required for the proper determination of the mid-hindbrain boundary in the neural tube (36,38).…”

Section: Discussionmentioning

confidence: 99%

“…In contrast to transcriptional repression mediated by Sall proteins, it has been shown that Sall proteins can function as transcriptional activators in some contexts (8,15). The ability of Sall1 to function as a transcriptional activator, despite a strong interaction with the NuRD corepressor complex, suggests the possibility that a molecular switch likely coordinates the transcriptional repression and activation activities of Sall1.…”

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confidence: 99%

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A Phosphomimetic Mutation in the Sall1 Repression Motif Disrupts Recruitment of the Nucleosome Remodeling and Deacetylase Complex and Repression of Gbx2

Lauberth

Bilyeu

Firulli

et al. 2007

Journal of Biological Chemistry

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confidence: 69%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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A Phosphomimetic Mutation in the Sall1 Repression Motif Disrupts Recruitment of the Nucleosome Remodeling and Deacetylase Complex and Repression of Gbx2

Lauberth

Bilyeu

Firulli

et al. 2007

Journal of Biological Chemistry

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“…total), Caudal (15), Ftz (25), Hunchback (43), Knirps (47), Krüppel (21), and Tramtrak (7). We also narrowed down the number of regulatory regions to 10, each containing at least two of the seven types of sites: engrailed intron (enint; Kassis et al 1989;Florence et al 1997), even-skipped stripe 2 (eve2; Stanojevic et al 1991;Small et al 1992;Arnosti et al 1996), even-skipped stripe 3+7 (eve3+7; Small et al 1996), fushi-tarazu proximal enhancer (ftzprox; Han et al 1993Han et al , 1998Yu et al 1999), hairy stripe 6 enhancer (hairy6; Langeland et al 1994), hairy stripe 7 enhancer (hairy7; La Rosee et al 1997Rosee et al , 1999, abdominal-A enhancer (iab2; Shimell et al 2000), Krüppel region 730 (kr730; Hoch et al 1991), spalt early enhancer (sal; Kuhnlein et al 1997;Barrio et al 1999;de Celis et al 1999), and tailless enhancer (tll; Hoch et al 1992;Liaw et al 1995).…”

Section: Developmental Enhancers: Maps Of Binding-site Distributionmentioning

confidence: 99%

Extraction of Functional Binding Sites from Unique Regulatory Regions: The Drosophila Early Developmental Enhancers

Papatsenko¹,

Makeev

Lifanov³

et al. 2002

Genome Res.

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The early developmental enhancers of Drosophila melanogaster comprise one of the most sophisticated regulatory systems in higher eukaryotes. An elaborate code in their DNA sequence translates both maternal and early embryonic regulatory signals into spatial distribution of transcription factors. One of the most striking features of this code is the redundancy of binding sites for these transcription factors (BSTF). Using this redundancy, we explored the possibility of predicting functional binding sites in a single enhancer region without any prior consensus/matrix description or evolutionary sequence comparisons. We developed a conceptually simple algorithm, Scanseq, that employs an original statistical evaluation for identifying the most redundant motifs and locates the position of potential BSTF in a given regulatory region. To estimate the biological relevance of our predictions, we built thorough literature-based annotations for the best-known Drosophila developmental enhancers and we generated detailed distribution maps for the most robust binding sites. The high statistical correlation between the location of BSTF in these experiment-based maps and the location predicted in silico by Scanseq confirmed the relevance of our approach. We also discuss the definition of true binding sites and the possible biological principles that govern patterning of regulatory regions and the distribution of transcriptional signals.

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“…Heterozygous mutant mice recapitulate phenotypic features of Okihiro syndrome including deafness, lower anogenital tract abnormalities, renal hypoplasia, anencephaly, Hirschprung's disease, and skeletal defects. This phenotype shows important differences in cardiac and ear manifestations to previously characterized Sall4 mutant alleles and should prove useful for the investigation of the influence of modifier alleles and protein interactions on the transcriptional regulatory function of Sall4.Keywords bacterial recombineering; Sall4; Okihiro syndrome; mouse; organogenesis; embryonic stem cells SALL4 is a member of the SALL gene family of zinc finger transcription factors (Kohlhase et al, 1996), containing multiple C2H2 double zinc finger domains, homologous to the Drosophila spalt (sal) homeotic gene important in pattern formation and cell specification (de Celis et al, 1996(de Celis et al, , 1999Jurgens, 1988;Kuhnlein et al, 1994). Murine Sall4 (Kohlhase et al, 2002a) is required for inner cell mass proliferation in early embryonic development (Sakaki-Yumoto et al, 2006).…”

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confidence: 99%

A Sall4 mutant mouse model useful for studying the role of Sall4 in early embryonic development and organogenesis

Warren¹,

Wang²,

Spiden³

et al. 2007

Genesis

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SummarySALL4 is a homologue of the Drosophila homeotic gene spalt, a zinc finger transcription factor, required for inner cell mass proliferation in early embryonic development. It also interacts with other transcription factors to control the development of the anorectal region, kidney, heart, limbs, and brain. Truncating mutations in SALL4 cause Okihiro syndrome, manifest as Duane anomaly, radial ray defects and sensorineural and conductive deafness. We report the characterization of a novel murine Sall4 null allele created by bacterial recombineering in ES cells. Homozygous mutant mice exhibit early embryonic lethality. Heterozygous mutant mice recapitulate phenotypic features of Okihiro syndrome including deafness, lower anogenital tract abnormalities, renal hypoplasia, anencephaly, Hirschprung's disease, and skeletal defects. This phenotype shows important differences in cardiac and ear manifestations to previously characterized Sall4 mutant alleles and should prove useful for the investigation of the influence of modifier alleles and protein interactions on the transcriptional regulatory function of Sall4.Keywords bacterial recombineering; Sall4; Okihiro syndrome; mouse; organogenesis; embryonic stem cells SALL4 is a member of the SALL gene family of zinc finger transcription factors (Kohlhase et al., 1996), containing multiple C2H2 double zinc finger domains, homologous to the Drosophila spalt (sal) homeotic gene important in pattern formation and cell specification (de Celis et al., 1996(de Celis et al., , 1999Jurgens, 1988;Kuhnlein et al., 1994). Murine Sall4 (Kohlhase et al., 2002a) is required for inner cell mass proliferation in early embryonic development (Sakaki-Yumoto et al., 2006). It also interacts with other transcription factors, such as Sall1 and the Tbx family of transcription factors to control the development of the anorectal region, kidney, heart, limbs and brain, by acting on downstream targets including Fgf10 (Kiefer et al., 2003;Koshiba-Takeuchi et al., 2006;Sakaki-Yumoto et al., 2006). Mutations in SALL1 are associated with Townes-Brock syndrome (OMIM 107480) (Kohlhase, 2000;Powell and Michaelis, 1999) RESULTSTo inactivate Sall4 we generated a targeting vector (Sall4-TV1) by bacterial recombineering which was designed to delete exons 2-4 ( Fig. 1a). This deletion removes all zinc finger domains of the protein and is expected to result in a null allele. The Sall4-TV1 was used to target the locus in AB2.2 ES cells. Targeted clones were obtained at a rate of 15% (Fig. 1b). Two of these targeted clones were used to establish the Sall4 Brdm1 allele in mice (Fig. 1c).PCR analysis of E3.5 blastocysts identified all three genotypes to be present (Fig. 1d). RT-PCR was performed on E8.5 embryos (Fig. 1e). A reduction of mRNA transcript was evident in Sall4 m1/+ embryos compared with Sall4 +/+ embryos. Whole mount analysis of Sall4 m1/+ embryos at E10.5 revealed that Sall4 mRNA was expressed with the expected tissue distribution, namely midbrain, branchial arch, and limb bud mesenchyme (Kohlhas...

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Function of the spalt/spalt-related gene complex in positioning the veins in the Drosophila wing

Cited by 118 publications

References 41 publications

A Phosphomimetic Mutation in the Sall1 Repression Motif Disrupts Recruitment of the Nucleosome Remodeling and Deacetylase Complex and Repression of Gbx2

A Phosphomimetic Mutation in the Sall1 Repression Motif Disrupts Recruitment of the Nucleosome Remodeling and Deacetylase Complex and Repression of Gbx2

Extraction of Functional Binding Sites from Unique Regulatory Regions: The Drosophila Early Developmental Enhancers

A Sall4 mutant mouse model useful for studying the role of Sall4 in early embryonic development and organogenesis

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