The genetics and molecular structure of the Drosophila pair-rule gene odd Oz (odz)

Levine, Anna; Gartenberg, Devorah; Yakov, Rivka; Lieberman, Yael; Budai-Hadrian, Ofra; Bashan-Ahrend, Ayelet; Wides, Ron

doi:10.1016/s0378-1119(97)00375-2

Cited by 15 publications

(16 citation statements)

References 31 publications

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“…These presented themselves as cuticles with a limited number of pairwise 'fusions' that were in the segmental register observed for odz hypomorphic alleles (Fig. 3A, b; see Levine et al, 1997a). We assume that these non-amorphic phenotypes appear because of the non-null nature of the Ten-a 367 allele mutation, and/or due to partial zygotic rescue bestowed by the fathers to female embryos.…”

Section: Germ Line Clone Derived Ten-a à Embryos Display Segmentationmentioning

confidence: 79%

“…Approximately 11% of this dead population is expected to give a weak cuticle phenotype due to the incomplete penetrance of odz 844 alone. This is because only approximately 20% of odz 844 / odz 844 homozygotes give a discernable weak segmentation phenotype, rather than an apparently wild type cuticle (see Section 4; Levine et al, 1997a). Among the population of lethal embryos (n = 1525), 5% showed a weak phenotype, and 2.7% showed a strong full pair-rule phenotype, which is never seen (<0.1%) for odz 844 homozygotes alone.…”

Section: R E T R a C T E Dmentioning

confidence: 99%

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RETRACTED: Drosophila Ten-a is a maternal pair-rule and patterning gene

Rakovitsky

Buganim

Swissa

et al. 2007

Mechanisms of Development

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The Ten-a gene of Drosophila melanogaster encodes several alternative variants of a full length member of the Odz/Tenm protein family. A number of Ten-a mutants created by inexact excisions of a resident P-element insertion are embryonic lethal, but show no pair-rule phenotype. In contrast, these mutants, and deficiencies removing Ten-a, do enhance the segmentation phenotype of a weak allele of the paralog gene odz (or Ten-m) to the odz amorphic phenotype. Germ line clone derived Ten-a(-) embryos display a pair-rule phenotype which phenocopies that of odz. Post segmentation eye patterning phenotypes of Ten-a mutants establish it as a pleiotropic patterning co-partner of odz.

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Section: Germ Line Clone Derived Ten-a à Embryos Display Segmentationmentioning

confidence: 79%

Section: R E T R a C T E Dmentioning

confidence: 99%

RETRACTED: Drosophila Ten-a is a maternal pair-rule and patterning gene

Rakovitsky

Buganim

Swissa

et al. 2007

Mechanisms of Development

Self Cite

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“…During the later stages of development, Ten-a and Tenm/Odz are predominantly expressed in the nervous system (Levine et al, 1997;Minet et al, 1999;Fascetti and Baumgartner, 2002). The predominant neuronal expression is conserved in the vertebrate homologues ten-m1, 2, 3 and 4 in the mouse (Oohashi et al, 1999;Ben-Zur et al, 2000), neurestin in the rat (Otaki and Firestein, 1999) and ten-m3 and ten-m4 in zebrafish (Mieda et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

The intracellular domain of teneurin-2 has a nuclear function and represses zic-1-mediated transcription

Bagutti

Forro

Ferralli

et al. 2003

Journal of Cell Science

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Teneurin-2, a vertebrate homologue of the Drosophila pairrule gene ten-m/odz, is revealed to be a membrane-bound transcription regulator. In the nucleus, the intracellular domain of teneurin-2 colocalizes with promyelocytic leukemia (PML) protein in nuclear bodies implicated in transcription control. Since Drosophila ten-m acts epistatically to another pair-rule gene opa, we investigated whether gene regulation by the mammalian opa homologue zic-1 was influenced by the intracellular domain of teneurin-2. We found that zic-mediated transcription from the apolipoprotein E promoter was inhibited. Release of the intracellular domain of teneurin-2 could be stimulated by homophilic interaction of the extracellular domain, and the intracellular domain was stabilized by proteasome inhibitors. We have previously shown that teneurin-2 is expressed by neurons belonging to the same functional circuit. Therefore, we hypothesize that homophilic interaction enables neurons to identify their targets and that the release of the intracellular domain of teneurin-2 provides them with a signal to switch their gene expression program from growth towards differentiation once the proper contact has been made.

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“…It enhances a weak allele combination of odz, which leads to very subtle segmentation defects (Fig. 2a;and Levine et al, 1997a), to a full fledged P-R phenotype (compare Fig. 2a and 2b), essentially phenocopying an odz null phenotype.…”

Section: Carboxy-terminal Truncated Variant Of the Odz Protein Exhibimentioning

confidence: 99%

“…The sublines, once isolated, were outcrossed to unlink other third chromosome lethals, then were tested and proven not to complement other known odz alleles and deficiencies. The odz 628 (w Ϫ ; odz 628 FRT80B}/ TM3 Sb) line used in this work bears a mutation on the FRT chromosome that is lethal but that has a very weak P-R cuticle phenotype, like many other lethal odz hypomorphic alleles (Levine et al, 1997a). Line odz 628 was balanced with a TM3 Sb ftz-LacZ chromosome, allowing for selection of homozygous odz embryos that are not stained blue in the presence of X-Gal.…”

Section: Mutagenesis and Screening: Creation Of An Frt-odz Mutant Chrmentioning

confidence: 99%